The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index; 15 of the 24 sources its claims cite were checked for support.
The IL-6–gp130–STAT3 pathway in hepatocytes triggers liver protection in T cell–mediated liver injury
Open accessAbstract
Increasing evidence demonstrates that IL-6 has a protective role during liver injury. IL-6 activates intracellular pathways via the gp130 receptor. In order to identify IL-6-gp130 pathways involved in mediating liver protection, we analyzed hepatocyte-specific gp130 knockout mice in a concanavalin A-induced (Con A-induced) model of immune-mediated hepatitis. We demonstrated that IL-6-gp130-dependent pathways in hepatocytes alone are sufficient for triggering protection in Con A-induced hepatitis. gp130-STAT3 signaling in hepatocytes mediates the IL-6-triggered protective effect. This was demonstrated by analysis of IL-6-induced protection in mice selectively deficient for gp130-dependent STAT1/3 or gp130-SHP2-RAS signaling in hepatocytes. To identify IL-6-gp130-STAT1/3 dependently expressed liver-protective factors, we performed gene array analysis of hepatic gene expression in hepatocyte-specific gp130(-/-) mice as well as in gp130-STAT1/3- and gp130-SHP2-RAS-MAPK-deficient mice. The mouse IL-8 ortholog KC (also known as Gro-alpha) and serum amyloid A2 (SAA2) was identified as differentially IL-6-gp130-STAT3-regulated genes. Hepatic expression of KC and SAA2 mediate the liver-protective potential of IL-6, since treatment with recombinant KC or serum SAA2 effectively reduced liver injury during Con A-induced hepatitis. In summary, this study defines IL-6-gp130-STAT3-dependent gene expression in hepatocytes that mediates IL-6-triggered protection in immune-mediated Con A-induced hepatitis. Additionally, we identified the IL-6-gp130-STAT3-dependent proteins KC and SAA2 as new candidates for therapeutic targets in liver diseases.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In a mouse Con A model of T cell–mediated hepatitis, IL-6–gp130–STAT3 signaling specifically in hepatocytes is necessary and sufficient for IL-6-triggered liver protection. The authors identify KC and SAA2 as IL-6–gp130–STAT3–dependent hepatocyte proteins that can themselves reduce Con A–induced liver injury.
Key findings
- Hepatocyte gp130 is required for IL-6 protection: IL-6 pretreatment completely blocked AST increases in wild-type mice, but failed to protect hepatocyte-specific gp130-null mice; all `alfpCre gp130 LoxP/LoxP` mice died within the first 20 hours after Con A, whereas NaCl- and IL-6-treated wild-type animals survived.
- The protective signal is gp130-STAT3, not gp130-SHP2-RAS-MAPK: IL-6 pretreatment completely prevented liver damage in `alfpCre gp130 Y757F/LoxP` mice, while all `alfpCre gp130 ΔSTAT/LoxP` mice died within 8 hours after Con A regardless of IL-6, versus 100% survival in the Y757F group.
- Gene array analysis identified KC and SAA2 as differentially IL-6–gp130-STAT3–regulated genes. Recombinant SAA (0.8 mg/kg) significantly reduced AST increases, and recombinant KC (40 µg/kg) significantly reduced AST levels and led to 100% survival versus 70% in NaCl-treated animals.
- IL-6 treatment significantly reduced PMN infiltration 4 hours after Con A injection, and IL-6 stimulation induced KC serum levels by approximately 100-fold.
Methods
- Male BALB/c mice, 8–10 weeks old, were used. Hepatocyte-specific gp130 mutants were generated by crossing `alfpCre` mice with `gp130 LoxP`, `gp130 ΔSTAT/ΔSTAT`, or `gp130 Y757F/Y757F` mice. Con A hepatitis was induced with 32.5 mg/kg i.v.; IL-6 (200 µg/kg) was given i.p. 3 hours before Con A; recombinant SAA (0.8 mg/kg) or KC (40 µg/kg) was given i.v. 1 hour before Con A.
- Liver injury was quantified by serum AST; cytokine levels by ELISA; STAT1/STAT3/ERK activation by Western blot and immunofluorescence; PMN infiltration by H&E counts.
- Gene expression profiling used Affymetrix mouse genome GeneChips on pooled liver RNA from 3 mice per group treated with IL-6 or NaCl; primary hepatocytes were isolated by collagenase perfusion and stimulated with 200 ng/ml IL-6.
Limitations
- The paper does not state a limitations section. Evident from the text: all experiments are in mice using the Con A model, so human relevance remains extrapolative.
- Gene expression profiling used pooled RNA from 3 mice per group, limiting assessment of inter-individual variability.
- Some supporting observations are reported as “data not shown” (e.g., hepatic mRNA expression and KC-dependent PMN influx), so they cannot be independently verified from the paper.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
15 of 24 cited sources checked · 8 supported · 0 flagged · accuracy not yet measured
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Increasing evidence demonstrates that IL-6 has a protective role during liver injury.”
- Also stated in: § Introduction · p. 1 · plain
“IL-6 is a pleiotropic cytokine with beneficial effects for the liver. This cytokine promotes liver regeneration and protects against a multitude of liver-damaging influences such as alcohol and CCl4 intoxication (1-4).”
What the sources say
- Supportedcites [1] source
The Discussion (p. 1534) reports that IL-6 conferred almost complete protection against Con A-induced hepatitis in mice when administered at least three hours before disease induction. The paper also notes that IL-6 given after Con A injection increased liver-injury markers, so the protective role shown here depends on timing. (LLM, conf=0.90)
- Supportedcites [2] source
The Discussion reports that IL-6 treatment reduced CCl4-induced liver injury in mice, including mice with an intact IL-6 response. It also reports greater injury in IL-6-deficient mice, supporting the attributed protective role in the liver-injury model studied. (LLM, conf=0.93)
- Supportedcites [3] source
The Introduction states that IL-6 plays a protective role in the mouse concanavalin A liver-injury model when administered before injury. The Discussion also reports protection in several mouse models of liver-cell damage, while noting that protection in human liver disease remains unestablished. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [4] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Introduction · p. 1 · plain
Every source the paper cites for this claim was checked and supports it.
In the paper
“IL-6 activates intracellular pathways via the gp130 receptor.”
- Also stated in: § Introduction · p. 1 · boosted
“The initiated intracellular signaling is strictly dependent on the function of gp130 (19).”
What the sources say
- Supportedcites [19] Ishihara, 2002, Biochim. Biophys. Acta. source
Section 2 describes gp130 as the signal-transducing subunit of the IL-6 receptor complex and says IL-6 binding triggers its association with gp130. The same section identifies two major downstream pathways generated through gp130. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Introduction · p. 1 · boosted
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, KC alone is not sufficient for the activation of infiltrated cells, and high systemic KC levels lead to impaired PMN activation via desensitization of the PMN CXC-receptor 2 (46).”
What the sources say
- Supportedcites [46] source
The Summary (p. 2039) reports that N51/KC expression recruited neutrophils without inflammatory activation. The Discussion (p. 2046) further suggests that activation such as degranulation requires other inflammatory mediators, supporting the claim that KC alone is insufficient. (LLM, conf=0.90)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, KC alone is not sufficient for the activation of infiltrated cells, and high systemic KC levels lead to impaired PMN activation via desensitization of the PMN CXC-receptor 2 (46).”
What the sources say
- Partly supportedcites [46] sourceExperimental — accuracy not yet measured
The Discussion (p. 2046) says chronic N51/KC expression recruits neutrophils without inflammatory activation and suggests that activation such as degranulation requires other mediators. It does not report that high systemic KC impairs PMN activation or that CXC-receptor 2 desensitization causes such impairment. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Earlier studies demonstrated that IL-6 attenuated liver injury in Con A-induced hepatitis (1).”
What the sources say
- Partly supportedcites [1] sourceExperimental — accuracy not yet measured
The Results (p. 1533) show that recombinant IL-6 given before Con A injection protected mice from liver injury. The timing qualification matters: IL-6 given at the same time had no protective effect, and administration afterward increased injury. The unqualified claim therefore overstates the finding. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We demonstrated that IL-6-gp130-dependent pathways in hepatocytes alone are sufficient for triggering protection in Con A-induced hepatitis.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“gp130-STAT3 signaling in hepatocytes mediates the IL-6-triggered protective effect.”
- Also stated in: § Figure 3 · p. 4 · plain
“IL-6 pretreatment of alfpCre gp130 Y757F/LoxP mice resulted in complete prevention of liver cell damage (Figure 5A). In contrast, alfpCre gp130 Δ STAT/LoxP animals showed enhanced sensitivity toward Con A when compared to wild-type mice (Figure 5B).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Figure 3 · p. 4 · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mouse IL-8 ortholog KC (also known as Groα ) and serum amyloid A2 (SAA2) was identified as differentially IL-6-gp130-STAT3-regulated genes.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-6-treated mice showed a significant reduction in PMN infiltration during Con Ainduced hepatitis (Figure 7D).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-6 serum concentrations correlated with survival rates.”
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- Probably not a substantial claim. 14
- It may state two separate claims as one. 15
- The quote only partly states this claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The phosphorylation of gp130 leads to dimerization of gp130 and activation of STAT1 and STAT3 as well as the SHP2-RAS-MAPK pathway (where SHP2 is Src homology 2 [SH2] domain-containing protein tyrosine phosphatase) (20-22).”
What the sources say
- Not checked — no full text of the sourcecites [20] source
- Partly supportedcites [21] Nakajima, 1996, EMBO J. sourceExperimental — accuracy not yet measured
The Abstract describes IL-6-induced Stat activation, particularly Stat3, in M1 leukemia cells. The available passages do not establish that gp130 phosphorylation causes gp130 dimerization or activates STAT1 and the SHP2–RAS–MAPK pathway; those parts of the attributed claim are unsupported. (LLM, conf=0.78)
- Not checked — no full text of the sourcecites [22] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For signal transduction, IL-6 binds the membrane-bound IL-6 receptor α (gp80). The IL-6-gp80 dimer interacts with gp130, the signal transducing unit in this complex.”
What the sources say
- Partly supportedcites [19] Ishihara, 2002, Biochim. Biophys. Acta. sourceExperimental — accuracy not yet measured
Section 2 (page unavailable) says IL-6 binds IL-6Rα, triggering its association with gp130, which the paper identifies as the signal-transducing subunit. The paper distinguishes cell-expressed IL-6Rα from its soluble form, but the available passages do not identify IL-6Rα as “gp80”; that specific label is unsupported by our copy. (LLM, conf=0.82)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Activation of PMNs during Con A-induced liver failure is an essential step for disease progression (12).”
What the sources say
- Partly supportedcites [12] Bonder, 2004, J. Immunol. sourceExperimental — accuracy not yet measured
The Discussion (page not provided) says Con A activates neutrophils and calls their activation an important step in Con A-induced hepatitis. It describes neutrophil recruitment as paramount and shows that depletion prevents liver injury, but it does not establish that activation itself is essential. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Additionally, recent reports demonstrated that other IL-6 family members, e.g., IL-11 and CT-1, also confer protection in this model (35, 36).”
What the sources say
- Supportedcites [35] source
The cited paper supports the CT-1 example in the sentence. In “Treatment With AdCT-1 Protects Mice From Liver Damage Induced by Concanavalin A,” it reports that CT-1 treatment reduced liver injury in mice challenged with Con-A. The separate IL-11 example is not attributed to this source. (LLM, conf=0.94)
- Partly supportedcites [36] Mahboubi, 2000, J. Immunol. sourceExperimental — accuracy not yet measured
The Abstract identifies IL-11 as an IL-6-family cytokine, and the section on CTL- and complement-mediated cytolysis reports that IL-11 partially protects human endothelial cells from immune-mediated injury. The paper does not report protection by IL-11 or CT-1 in Con A-induced hepatitis; its experiments concern endothelial cells, not that hepatitis model. (LLM, conf=0.84)
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“During the early stages, TNFα and IFNγ directly mediate liver cell damage (11).”
What the sources say
- Partly supportedcites [11] sourceExperimental — accuracy not yet measured
The introduction (page not supplied) reports that TNF levels rise early after Con A injection and that anti-TNF treatment blocks liver injury. The Discussion (page not supplied) says IFNγ is critical for apoptosis but finds no clear evidence that it directly induces it; the authors consider it more likely to modulate TNF-triggered pathways. Thus, the claim that both cytokines directly mediate early liver cell damage overstates the source. (LLM, conf=0.88)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Gp130 is the common signal transducer used by the IL-6 family of cytokines, which includes IL-6, leukemia inhibitory factor (LIF), IL-11, cardiotrophin-1 (CT-1), oncostatin-M (OSM), and the ciliary neurotrophic factor (19).”
What the sources say
- Supportedcites [19] Ishihara, 2002, Biochim. Biophys. Acta. source
Section 2, “Cell specificity at the level of the cytokine receptor” (page not provided), calls gp130 a common signal-transducing subunit of IL-6-family cytokine receptors. It also lists gp130 as shared by the receptors for CNTF, LIF, OSM, IL-11, and CT-1. (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Additionally, recent studies showed effects of KC expression on monocyte recruitment during development of experimental atherosclerosis (47).”
What the sources say
- Supportedcites [47] Huo, 2001, J. Clin. Invest. source
The Discussion reports that KC is expressed on early atherosclerotic endothelium and significantly contributes to monocyte arrest. In the experimental apoE-deficient mouse artery model, blocking KC reduced monocyte accumulation, while adding KC increased it (Discussion, p. 1312; results, p. 1310). (LLM, conf=0.92)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“High IL-6 serum concentrations after Con A injection were detectable in animals with a disruption of the IL-6gp130-STAT3 pathway and correlated with increased morbidity.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hepatocytes of IL-6-pretreated wild-type mice showed STAT3 activation 3 hours after IL-6 injection. Up to 4 hours after initiation of Con A-induced hepatitis, these cells were not able to activate STAT3, although high IL-6 serum levels were detectable (Figures 3D and 2E).”
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, alfpCre gp130 Δ STAT/LoxP animals showed enhanced sensitivity toward Con A when compared to wild-type mice (Figure 5B). Independently of IL-6 pretreatment, all alfpCre gp130 Δ STAT/LoxP mice died within 8 hours after Con A injection in contrast to a 100% survival rate for all analyzed alfpCre gp130 Y757F/LoxP animals.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IFNγ levels in alfpCre gp130 Y757F/LoxP and wild-type mice were not affected by pretreatment with IL-6, despite our observation that both strains showed protection from Con A-induced liver damage (Figure 2, C and D; Figure 5, C and D).”
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-6 pretreatment completely blocked liver cell damage. No increase in transaminases was evident (Figure 1A).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-6 stimulation induces KC serum levels by approximately 100-fold, correlating with a pronounced upregulating of KC mRNA in the liver (Figure 6).”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Figure 6 depicts a selection of genes that are significantly regulated by gp130-dependent pathways in hepatocytes in vivo.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In wild-type mice, TNFα levels were reduced after IL-6 stimulation. But in alfpCre gp130 Y757F/LoxP mice, which retained sensitivity to IL-6-dependent liver protection, no changes in TNFα levels were detected.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, all alfpCre gp130 LoxP/LoxP mice died within the first 20 hours after Con A injection. In contrast, all NaCL- and IL-6-treated wild-type animals survived during this phase, indicating a higher sensitivity of alfpCre gp130 LoxP/LoxP mice toward Con A.”
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“It has been shown that SOCS-3 negatively regulates IL-6 signaling in vivo (43).”
What the sources say
- Not checked — no full text of the sourcecites [43] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The increased number of STAT3-positive cells likely reflects IL-6induced sensitization of NK cells, monocytes, or Kupffer cells to STAT3-activating pathways.”
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Con A-induced liver damage is a well-defined experimental animal model of acute hepatitis. It mimics human viral and autoimmune hepatitis in many aspects (8-10).”
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“IL-6 pretreatment inhibited the increase of STAT3 activation in hepatocytes of wild-type mice, probably by inducing negative feedback mechanisms, e.g., induction of SOCS-3 in hepatocytes (Figure 6).”
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“A variety of factors, such as LPS or PDGF, induce tissue-specific expression of KC (45), which in turn promotes localized PMN migration.”
What the sources say
- Not checked — no full text of the sourcecites [45] Bozic, 1995, J. Immunol. source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, serum levels of TNFα and IFNγ showed no correlation with the capacity of IL-6 to provide protection from liver damage, indicating that alterations in concentrations of these cytokines are unlikely to explain protection.”
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“To verify equal loading of protein samples, a Coomassie-blue stained SDS Gel was quantified.”
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both proteins are potent inhibitors of Con Ainduced hepatitis and might also be of interest in the treatment of immune-mediated liver diseases in humans.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Additionally, nuclear proteins were isolated from each liver, and the activation of STAT3 and ERK1/2 was analyzed by Western blot to verify the integrity of IL-6 signaling in each mouse.”
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“To ensure that infiltrated cells in livers of Con A-treated mice were not eliminated, we washed the organs intensively by shaking the organs for 15 minutes in cold PBS.”
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
The overall extent of hepatic gp130 inactivation in alfpCre gp130 LoxP/LoxP mice reflects complete gp130 deletion in hepatocytes.
“Since nonparenchymal cells show no gp130 deletion, the overall extent of hepatic gp130 inactivation is likely to reflect complete gp130 deletion in hepatocytes.”
The paper relies on this without support.
KC controls chemotaxis and activation of polymorph nuclear cells (PMNs) in areas of inflammation.
“KC controls chemotaxis and activation of polymorph nuclear cells (PMNs) in areas of inflammation.”
The paper relies on this without support.
SAA2 is a target of MMP.
“SAA2 is a known target of MMP and MMP activity induced during T cell-mediated hepatitis.”
The paper relies on this without support.
KC is an immediate early gene with low or no detectable expression in most tissues.
“KC is an immediate early gene with low or no detectable expression in most tissues.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“binding to its receptor has been shown to protect hepatocytes during acute hepatic injury [11]”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [11]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Importantly, this indicates that under the appropriate circumstances, regulation of the endogenous hepatocellular IL-6 receptor can be autocrine instead of endrocrine/paracrine [11].”
From Synthesis of IL-6 by Hepatocytes Is a Normal Response to Common Hepatic Stimuli (2014) · cites this paper as [11]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
KC is identified as both Groα and keratinocyte growth factor
MinorThe paper identifies KC as the mouse IL-8 ortholog Groα, but its abbreviations list defines KC as keratinocyte growth factor. These are different names for different factors.
“The mouse IL-8 ortholog KC (also known as Groα )”
“KC, keratinocyte growth factor”
Citations
Cites
Interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway
HEINRICH, P. C., BEHRMANN, I., MÜLLER-NEWEN, G., SCHAPER, F., & GRAEVE, L. (1998) · Biochemical Journal · doi:10.1042/bj3340297 · Cited by 2,130
gp 130 AND THE INTERLEUKIN-6 FAMILY OF CYTOKINES
Taga, T., & Kishimoto, T. (1997) · Annual Review of Immunology · doi:10.1146/annurev.immunol.15.1.797 · Cited by 1,468
Stahl, N., Farruggella, T. J., Boulton, T. G., Zhong, Z., Darnell, J. E., & Yancopoulos, G. D. (1995) · Science · doi:10.1126/science.7871433 · Cited by 979
SOCS3 negatively regulates IL-6 signaling in vivo
Croker, B. A., Krebs, D. L., Zhang, J.-G., Wormald, S., Willson, T. A., Stanley, E. G., Robb, L., Greenhalgh, C. J., Förster, I., Clausen, B. E., et al. (2003) · Nature Immunology · doi:10.1038/ni931 · Cited by 840
Neutrophil and Kupffer cell-induced oxidant stress and ischemia-reperfusion injury in rat liver
Jaeschke, H., & Farhood, A. I. (1991) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.1991.260.3.g355 · Cited by 662
Fukada, T., Hibi, M., Yamanaka, Y., Takahashi-Tezuka, M., Fujitani, Y., Yamaguchi, T., Nakajima, K., & Hirano, T. (1996) · Immunity · doi:10.1016/s1074-7613(00)80501-4 · Cited by 652
Nakajima, K., Yamanaka, Y., Nakae, K., Kojima, H., Ichiba, M., Kiuchi, N., Kitaoka, T., Fukada, T., Hibi, M., & Hirano, T. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00734.x · Cited by 565
Mizuhara, H., O'Neill, E., Seki, N., Ogawa, T., Kusunoki, C., Otsuka, K., Satoh, S., Niwa, M., Senoh, H., & Fujiwara, H. (1994) · The Journal of Experimental Medicine · doi:10.1084/jem.179.5.1529 · Cited by 517
Concanavalin A?induced T-cell?Mediated hepatic injury in mice: The role of tumor necrosis factor*1
Gantner, F. (1995) · Hepatology · doi:10.1016/0270-9139(95)90428-x · Cited by 487
Tebbutt, N. C., Giraud, A. S., Inglese, M., Jenkins, B., Waring, P., Clay, F. J., Malki, S., Alderman, B. M., Grail, D., Hollande, F., et al. (2002) · Nature Medicine · doi:10.1038/nm763 · Cited by 474
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Flagged first, then by citations
Research works printed but not linked: 1
- Gantner, 1995, Hepatology., 21, 190
Cited by
Sorted by citations
Items 101–200 of 200
Murthy, A., Shao, Y. W., Defamie, V., Wedeles, C. J., Smookler, D. S., & Khokha, R. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1102199 · Cited by 33
Regulation of systemic metabolism by tissue-resident immune cell circuits
Li, J. H., Hepworth, M. R., & O’Sullivan, T. E. (2023) · Immunity · doi:10.1016/j.immuni.2023.05.001 · Cited by 36
Ai, G., Wu, X., Dou, Y., Huang, R., Zhong, L., Liu, Y., Xian, Y., Lin, Z., Li, Y., Su, Z., et al. (2022) · Food and Chemical Toxicology · doi:10.1016/j.fct.2022.113215 · Cited by 32
Pharmacokinetics of Natural and Engineered Secreted Factors Delivered by Mesenchymal Stromal Cells
Elman, J. S., Murray, R., Wang, F.-J., Shen, K., Gao, S., Conway, K. E., Yarmush, M., Tannous, B., Weissleder, R., & Parekkadan, B. (2014) · PLoS ONE · doi:10.1371/journal.pone.0089882 · Cited by 31
Dembek, A., Laggai, S., Kessler, S. M., Czepukojc, B., Simon, Y., Kiemer, A. K., & Hoppstädter, J. (2017) · Immunobiology · doi:10.1016/j.imbio.2017.01.003 · Cited by 31
Gavito, A., Bautista, D., Suárez, J., Badran, S., Arco, R., Pavón, F. J., Serrano, A., Rivera, P., Decara, J. M., Cuesta, A. L., et al. (2016) · PLoS ONE · doi:10.1371/journal.pone.0157956 · Cited by 28
Serum Amyloid A Proteins and Their Impact on Metastasis and Immune Biology in Cancer
Lee, J., & Beatty, G. L. (2021) · Cancers · doi:10.3390/cancers13133179 · Cited by 28
Neuron navigator 3a regulates liver organogenesis during zebrafish embryogenesis
Klein, C., Mikutta, J., Krueger, J., Scholz, K., Brinkmann, J. F. F., Liu, D., Veerkamp, J., Siegel, D., Abdelilah‐Seyfried, S., & le Noble, F. A. C. (2011) · Development · doi:10.1242/dev.056861 · Cited by 27
Self-citationWang, F., Xue, Y., Yang, J., et al. (2016) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2016.08.018 · Cited by 28
Miyaaki, H., Ichikawa, T., Nakao, K., Matsuzaki, T., Muraoka, T., Honda, T., Takeshita, S., Shibata, H., Ozawa, E., Akiyama, M., et al. (2009) · Hepatology Research · doi:10.1111/j.1872-034x.2009.00529.x · Cited by 26
Inflammatory pathways in liver homeostasis and liver injury
Luedde, T., Tacke, F., & Trautwein, C. (2008) · Springer eBooks · doi:10.1007/978-1-4020-8656-4_4 · Cited by 26
Self-citationDepke, M., Steil, L., Domańska, G., Völker, U., Schütt, C., & Kiank, C. (2009) · Molecular Immunology · doi:10.1016/j.molimm.2009.06.014 · Cited by 23
Wang, J., Sun, Q.-H., Zhang, J., Wang, H., & Liu, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23042019 · Cited by 24
The liver metastatic niche: modelling the extracellular matrix in metastasis
Drew, J., & Machesky, L. M. (2021) · Disease Models & Mechanisms · doi:10.1242/dmm.048801 · Cited by 24
Matrine attenuates endotoxin-induced acute liver injury after hepatic ischemia/reperfusion in rats
Zhang, F., Wang, X., Tong, L., Qiao, H., Li, X., You, L., Jiang, H., & Sun, X. (2011) · Surgery Today · doi:10.1007/s00595-010-4423-9 · Cited by 23
Lend, K., van Vollenhoven, R., Lampa, J., Hetland, M. L., Haavardsholm, E. A., Nordström, D., Nurmohamed, M. T., Guðbjörnsson, B., Rudin, A., Østergaard, M., et al. (2022) · The Lancet Rheumatology · doi:10.1016/s2665-9913(22)00186-2 · Cited by 23
Luchtefeld, M., Preuss, C., Rühle, F., Bogalle, E. P., Sietmann, A., Figura, S., Müller, W., Grote, K., Schieffer, B., & Stoll, M. (2011) · PLoS ONE · doi:10.1371/journal.pone.0019427 · Cited by 21
Membrane trafficking as an active regulator of constitutively secreted cytokines
Revelo, N. H., ter Beest, M., & van den Bogaart, G. (2019) · Journal of Cell Science · doi:10.1242/jcs.234781 · Cited by 24
Cytokine profile during occult hepatitis B virus infection in chronic hepatitis C patients
Ribeiro, C. R. D. A., de Almeida, N. A. A., Martinelli, K. G., Pires, M. M. A., Brandão‐Mello, C. E., de Barros, J. J. F., & de Paula, V. S. (2021) · Virology Journal · doi:10.1186/s12985-021-01487-2 · Cited by 22
Comparison of lactate and β-hydroxybutyrate in the treatment of concanavalin-A induced hepatitis
Hazem, S. H., Hamed, M. F., Saad, M. A., & Gameil, N. M. (2018) · International Immunopharmacology · doi:10.1016/j.intimp.2018.06.026 · Cited by 21
Warshow, U. M., Riva, A., Hegazy, D., et al. (2012) · Journal of Viral Hepatitis · doi:10.1111/j.1365-2893.2011.01574.x · Cited by 21
Zhao, J., Wang, Y., Wu, X., Tong, P., Yue, Y., Gao, S., Huang, D., & Huang, J. (2018) · Molecular Medicine Reports · doi:10.3892/mmr.2018.9490 · Cited by 21
Definition of the Chemical and Immunological Signals Involved in Drug-Induced Liver Injury
Ali, S.-E., Waddington, J. C., Park, B. K., & Meng, X. (2019) · Chemical Research in Toxicology · doi:10.1021/acs.chemrestox.9b00275 · Cited by 22
Wang, X., & Ning, Q. (2014) · Europe PMC (PubMed Central) · doi:10.17877/de290r-6940 · Cited by 23
Modeling toxicodynamic effects of trichloroethylene on liver in mouse model of autoimmune hepatitis
Gilbert, K. M., Reisfeld, B., Zurlinden, T. J., Kreps, M. N., Erickson, S. W., & Blossom, S. J. (2014) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2014.07.003 · Cited by 20
Jiang, S., Hu, X., & Liu, P. (2015) · Journal of Chinese Integrative Medicine · doi:10.1016/s2095-4964(15)60185-6 · Cited by 19
Inflammatory networks cultivate cancer cell metastasis to the liver
Lee, J. W., & Beatty, G. L. (2020) · Cell Cycle · doi:10.1080/15384101.2020.1728013 · Cited by 18
Heat stress stimulates hepcidin mRNA expression and C/EBPα protein expression in aged rodent liver
Bloomer, S. A., Kregel, K. C., & Brown, K. E. (2013) · Archives of Gerontology and Geriatrics · doi:10.1016/j.archger.2013.07.012 · Cited by 19
Myeloid cells require gp130 signaling for protective anti‐inflammatory functions during sepsis
Sackett, S. D., Otto, T., Mohs, A., Sander, L. E., Strauch, S., Streetz, K. L., Kroy, D. C., & Trautwein, C. (2019) · The FASEB Journal · doi:10.1096/fj.201802118r · Cited by 18
Self-citationBodeman, C. E., Dzierlenga, A. L., Tally, C. M., Mulligan, R. M., Lake, A. D., Cherrington, N. J., & McKarns, S. C. (2013) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.113.205369 · Cited by 18
Arefhosseini, S., Tutunchi, H., Nomi-Golzar, S., Mahboob, S., Pouretedal, Z., & Ebrahimi‐Mameghani, M. (2022) · Food & Function · doi:10.1039/d1fo03685h · Cited by 19
Manna, P., Sinha, M., & Sil, P. C. (2007) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.20154 · Cited by 17
Interleukin-6 as a biomarker in patients with hepatobiliary cancers
Gosain, R., Anwar, S., Miller, A., et al. (2019) · Journal of Gastrointestinal Oncology · doi:10.21037/jgo.2019.01.09 · Cited by 17
Li, S., Wang, N., Tan, H., Hong, M., Yuen, M., Li, H., & Feng, Y. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01524 · Cited by 16
Frequent in-frame somatic deletions activate gp130 in inflammatory hepatocellular tumors #
Spannbauer, M., & Trautwein, C. (2009) · Hepatology · doi:10.1002/hep.22902 · Cited by 16
Self-citationInterleukin-6: a therapeutic Jekyll and Hyde in gastrointestinal and hepatic diseases
Danese, S., & Gao, B. (2010) · Gut · doi:10.1136/gut.2008.173534 · Cited by 16
The two facets of gp130 signalling in liver tumorigenesis
Schmidt‐Arras, D., Galun, E., & Rose‐John, S. (2021) · Seminars in Immunopathology · doi:10.1007/s00281-021-00861-0 · Cited by 15
Self-citationAutocrine IL-6 regulates GRO-α production in thymic epithelial cells
Tseng, Y., Wu, M., Yang, H.-C., Wang, C., & Lin, C. (2010) · Cytokine · doi:10.1016/j.cyto.2010.05.002 · Cited by 16
Pelosof, L. C., Davis, P. H., Zhang, Z., Zhang, X., & Stanley, S. L. (2005) · Cellular Microbiology · doi:10.1111/j.1462-5822.2005.00642.x · Cited by 16
Nakagawa, J., Koyama, Y., Kawakami, A., Ueki, Y., Tsukamoto, H., Horiuchi, T., Nagano, S., Uchino, A., Ota, T., Akahoshi, M., et al. (2017) · Arthritis Research & Therapy · doi:10.1186/s13075-017-1387-9 · Cited by 15
Purinergic signaling in liver disease: calcium signaling and induction of inflammation
Ulrich, H., Glaser, T., & Thomas, A. P. (2024) · Purinergic Signalling · doi:10.1007/s11302-024-10044-9 · Cited by 14
Lack of xanthine dehydrogenase leads to a remarkable renal decline in a novel hypouricemic rat model
Dissanayake, L. V., Zietara, A. P., Levchenko, V., Spires, D. R., Angulo, M. B., El‐Meanawy, A., Geurts, A. M., Dwinell, M. R., Palygin, O., & Staruschenko, A. (2022) · iScience · doi:10.1016/j.isci.2022.104887 · Cited by 15
Shi, Y., Song, Q., Hu, D., Zhuang, X., & Yu, S. (2015) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2015.03.177 · Cited by 13
Ma, B., Zhu, J., Tan, J., Mao, Y., Tang, L., Shen, C., Zhang, H., Kuang, Y., Fei, J., Yang, X. Y., et al. (2017) · PubMed Central · Cited by 13
Modulatory effects of NDP-MSH in the regenerating liver after partial hepatectomy in rats
Lonati, C., Carlin, A., Leonardi, P., Valenza, F., Bòsari, S., Catania, A., & Gatti, S. (2013) · Peptides · doi:10.1016/j.peptides.2013.10.014 · Cited by 13
Contribution of organokines in the development of NAFLD/NASH associated hepatocellular carcinoma
Vachher, M., Bansal, S., Kumar, B., Yadav, S., Arora, T. K., Wali, N. M., & Burman, A. (2022) · Journal of Cellular Biochemistry · doi:10.1002/jcb.30252 · Cited by 11
Mahsoub, H. M., Heffron, C. L., Hassebroek, A. M., et al. (2023) · mBio · doi:10.1128/mbio.00418-23 · Cited by 11
Protective Effect of Baicalin on Chlorpyrifos-Induced Liver Injury and Its Mechanism
Wang, R., Zhang, K., Liu, K., et al. (2023) · Molecules · doi:10.3390/molecules28237771 · Cited by 11
Lutz, H. H., Sackett, S. D., Kroy, D. C., Gaßler, N., & Trautwein, C. (2011) · European Journal of Cell Biology · doi:10.1016/j.ejcb.2011.09.006 · Cited by 11
Self-citationGiebeler, A., Brandenburg, L., Kaldenbach, M., Erschfeld, S., Wasmuth, H. E., Wruck, C. J., Trautwein, C., & Streetz, K. L. (2012) · Laboratory Investigation · doi:10.1038/labinvest.2012.122 · Cited by 11
Self-citationInhaled Argon Impedes Hepatic Regeneration after Ischemia/Reperfusion Injury in Rats
Schmitz, S. M., Dohmeier, H., Stoppe, C., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21155457 · Cited by 10
Gavito, A., Cabello, R., Suárez, J., Serrano, A., Pavón, F. J., Vida, M., Romero, M. D. M., Pardo, V., Bautista, D., Arrabal, S., et al. (2016) · British Journal of Pharmacology · doi:10.1111/bph.13423 · Cited by 10
Rashidi, S., Farhadi, L., Ghasemi, F., Sheikhesmaeili, F., & Mohammadi, A. (2020) · Infection Genetics and Evolution · doi:10.1016/j.meegid.2020.104580 · Cited by 9
Allogeneic Transplantation, Fas Signaling, and Dysregulation of Hepcidin
Li, X., Xu, F., Karoopongse, E., Marcondes, A. M., Lee, K., Kowdley, K. V., Miao, C. H., Trobridge, G. D., Campbell, J. S., & Deeg, H. J. (2013) · Transplantation and Cellular Therapy · doi:10.1016/j.bbmt.2013.05.012 · Cited by 9
Cytotoxic Doses of Ketoconazole Affect Expression of a Subset of Hepatic Genes
Casley, W. L., Ogrodowczyk, C., Larocque, L., Jaentschke, B., LeBlanc-Westwood, C. A., Menzies, J. A., Whitehouse, L. W., Hefford, M. A., Aubin, R. A., Thorn, C. F., et al. (2007) · Journal of Toxicology and Environmental Health · doi:10.1080/15287390701551407 · Cited by 9
Clusterin inhibits lipopolysaccharide induced liver injury
Seo, H.-Y., Park, J. Y., Lee, S. H., Cho, S. H., Han, E., Hwang, J. S., Kim, M. K., & Jang, B. K. (2025) · Scientific Reports · doi:10.1038/s41598-024-80903-3 · Cited by 10
Casillas-Ramírez, A., Micó-Carnero, M., Sánchez-González, A., Maroto-Serrat, C., Trostchansky, A., & Peralta, C. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1178909 · Cited by 8
Stat3 role in the protective effect of FXR Agonist in parenteral nutrition-associated cholestasis
Ghosh, S., Devereaux, M. W., Anderson, A. L., Kasmi, K. C. E., & Sokol, R. J. (2023) · Hepatology Communications · doi:10.1097/hc9.0000000000000056 · Cited by 8
O'Daly, J. A., Gleason, J., Peña, G., & Colorado, I. (2010) · Archives of Dermatological Research · doi:10.1007/s00403-009-1026-7 · Cited by 7
Wang, H., Wan, M., Li, W., Zhang, Y., Pang, Y., Wen, L., Cai, Y., Shen, C., Wang, Q., Li, D., et al. (2025) · Environment International · doi:10.1016/j.envint.2025.109703 · Cited by 6
Pretreatment with lipopolysaccharide amelioratesPseudomonasexotoxin A-induced hepatotoxicity in rats
Chiu, C.-C., Huang, Y.-T., Wang, Y., et al. (2013) · Immunopharmacology and Immunotoxicology · doi:10.3109/08923973.2013.764503 · Cited by 5
Coculture With Ischemia/Reperfusion-Preconditioned Hepatocytes Improves Islet Function and Survival
Lee, J. G., Lee, J. I., Kim, J. Y., et al. (2018) · Transplantation Proceedings · doi:10.1016/j.transproceed.2018.07.007 · Cited by 5
IL6 Signaling in Cancer: Not Always Bad News
Huynh, J., & Ernst, M. (2021) · Cancer Research · doi:10.1158/0008-5472.can-21-2137 · Cited by 5
Self-citationEffect of interleukin‑31 on septic shock through regulating inflammasomes and interleukin‑1β
Gu, X., Chen, W., Zhu, X., Lu, F., Sheng, B., & Zang, X. (2018) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2018.6181 · Cited by 4
HBV and targeted synthetic (ts)DMARDs: what have we learned from bDMARDs and tsDMARDs?
Gremese, E., Gasbarrini, A., & Ferraccioli, G. (2020) · RMD Open · doi:10.1136/rmdopen-2020-001171 · Cited by 4
STAT3 Mediates Protection From Liver Inflammation After Partial Hepatectomy
Xu, Y., Feng, D., Wang, Y., Luo, Q., & Xu, L. (2009) · Cellular Physiology and Biochemistry · doi:10.1159/000218184 · Cited by 4
Han, Y., Gu, L., Liu, J., et al. (2017) · The Journal of Infectious Diseases · doi:10.1093/infdis/jix097 · Cited by 4
Miltefosine reduces coxsackievirus B3 lethality of mice with enhanced STAT3 activation
Zhang, C. Y., Hung, C.-J., Hsiao, Y.-L., Chang, T.-M., Su, Y., Wang, L.-C., Wang, S., & Chen, S. (2024) · Antiviral Research · doi:10.1016/j.antiviral.2024.105824 · Cited by 3
Mandrekar, P., & Szabó, G. (2010) · Molecular pathology library · doi:10.1007/978-1-4419-7107-4_27 · Cited by 3
Zhou, F., Zhou, B., Qu, Y., Zhong, S., Liu, T., Liu, Y., Zhao, X., Tian, X., Hao, X., & Jiang, P. (2025) · Frontiers in Medicine · doi:10.3389/fmed.2025.1694320 · Cited by 2
YTHDF1 shapes immune-mediated hepatitis via regulating inflammatory cell recruitment and response
Li, H., Yu, K., Zhang, X., et al. (2024) · Genes & Diseases · doi:10.1016/j.gendis.2024.101327 · Cited by 2
Zhang, Z., Shi, D., Dou, H., Wan, R., Yuan, Q., Tu, P., & Xin, D. (2024) · Microbial Pathogenesis · doi:10.1016/j.micpath.2024.107072 · Cited by 3
Animal Models of Autoimmune Liver Diseases
Biburger, M., & Tiegs, G. (2008) · Humana Press eBooks · doi:10.1007/978-1-59745-518-3_24 · Cited by 2
Yang, R., Wan, J.-L., Pi, C.-Q., et al. (2024) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2024.1421370 · Cited by 2
Mutated neuron navigator 3 as a candidate gene for a rare neurodevelopmental disorder
Umair, M., Alharbi, M., Aloyouni, E., et al. (2024) · Molecular Genetics & Genomic Medicine · doi:10.1002/mgg3.2473 · Cited by 2
Head-out immersion in hot water does not increase serum CXCL1 in healthy men
Sakurai, Y., Umemoto, Y., Kawasaki, T., Kojima, D., Kinoshita, T., Yamashiro, M., Banno, M., Arakawa, H., & Tajima, F. (2017) · Trends in Immunotherapy · doi:10.24294/ti.v1.i1.37 · Cited by 2
The Promising Role of Anti-Fibrotic Agent Halofuginone in Liver Fibrosis/Cirrhosis
Karakoyun, B. (2017) · InTech eBooks · doi:10.5772/intechopen.68641 · Cited by 2
Joo, D. J., Kim, J. Y., Lee, J. I., et al. (2012) · Transplantation Proceedings · doi:10.1016/j.transproceed.2012.02.024 · Cited by 1
Miyatani, Y., Choi, D., Aronsohn, A. I., Pillai, A. A., Cohen, R. D., & Rubin, D. T. (2025) · Digestive Diseases and Sciences · doi:10.1007/s10620-025-09569-9 · Cited by 1
Innate Immunity and Disorders of the Liver
Heikenwälder, M. F., Knolle, P. A., & Protzer, U. (2013) · Springer eBooks · doi:10.1007/978-3-319-02096-9_6 · Cited by 1
Bösch, R. V. (2010) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.10.2010.tde-03082010-120238
Luedde, T., Trautwein, C., Mehal, W. Z., Imaeda, A. B., & Mehal, W. Z. (2007) · Wiley eBooks · doi:10.1002/9780470691861.ch2g
Self-citationRole of interleukin-30 as a modulator of transcription signaling in liver injury
Fujita, T. (2012) · Hepatology · doi:10.1002/hep.25864
The regulation of gp130 surface expression on monocytes : implications in chronic inflammation
Honke, N., Idm, P., Fischer, R., & Tenbrock, K. (2014) · RWTH Publications (RWTH Aachen)
Regulation of Metalloproteinase-dependent Ectodomain Shedding in Cytokine Biology and Inflammation
Murthy, A. (2012) · Library and Archives Canada (Government of Canada)
Webster, C. R. L. (2009) · Wiley eBooks · doi:10.1002/9780470747919.ch48
Pivotal Role of Signal-Transducing Adaptor Protein-2 in Pathogenesis of Autoimmune Hepatitis
Sasaki, Y., Saitoh, K., Kagohashi, K., et al. (2021) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b21-00595
Acute liver failure — mechanisms of liver cell destruction
Trautwein, C., Liedtke, C., Streetz, K. L., Luedde, T., & Klein, C. (2007) · Springer eBooks · doi:10.1007/1-4020-4144-6_25
Self-citationHead-out immersion in hot water does not increase serum CXCL1 in healthy men
Sakurai, Y., Umemoto, Y., Kawasaki, T., Kojima, D., Kinoshita, T., Yamashiro, M., Banno, M., Arakawa, H., & Tajima, F. (2019) · Trends in Immunotherapy · doi:10.24294/ti.v3.i1.37
Criddle, D. N., & Javed, M. A. (2013) · Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature · doi:10.3410/f.717980878.793473612
Mitra, A., Cutrera, J. J., Mishra, L., et al. (2012) · Hepatology · doi:10.1002/hep.25862
Insights into Virus-Induced Immune Mediated Liver Pathology
Hamdan, T. A., Ashraf, F., & Bhat, H. (2022) · Cellular Physiology and Biochemistry · doi:10.33594/000000554
Wang, S., Sui, Z., Peng, K., & Cheng, H. (2023) · Tropical Journal of Pharmaceutical Research · doi:10.4314/tjpr.v22i9.22
Capaccia, C., Ciancabilla, F., Porcellato, I., Brachelente, C., Zerani, M., Maranesi, M., & Guelfi, G. (2024) · Current Issues in Molecular Biology · doi:10.3390/cimb46080542
Hamidi, T., Jiang, Y., Robinson, T. P., Kronbergs, A., Au, E. D., Rupert, J. E., Zhong, X., Lal, S., Liang, T. W., Robling, A. G., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.04.01.646698
da Silva, F. A., da Vieira‐da‐Silva, A. L., Esteca, M. V., Costa, S. D. O., Lopes, P. K. F., Batista, I. L., Zimmermann, L. I. D. S., Milanski, M., Torsoni, M. A., & Torsoni, A. S. (2026) · Annals of Hepatology · doi:10.1016/j.aohep.2026.102234
cGAS-mediated immunogenicity impairs the stability and safety of LNP-encapsulated DNA in vivo
Wang, X., Liu, T., Long, B., Li, M., Yao, Y., Fu, Y., Xie, S., Gu, Y., Yue, W., Pan, Y., et al. (2026) · Molecular Therapy — Nucleic Acids · doi:10.1016/j.omtn.2026.103118
Giebeler, A., & Spehr, M. (2011) · RWTH Publications (RWTH Aachen)
Wegenka, U. M., Dikopoulos, N., Reimann, J., Adler, G., & Wahl, C. (2007) · Journal of Hepatology · doi:10.1016/j.jhep.2006.08.009 · Cited by 30
Klein, C., Medina, E., Sander, L., Dierssen, U., Roskams, T., Mueller, W., Trautwein, C., & Goldmann, O. (2007) · The Journal of Infectious Diseases · doi:10.1086/520090 · Cited by 11
Self-citation
Metadata
- Authors
- Klein, C., Wüstefeld, T., Assmus, U., Roskams, T., Rose-John, S., Müller, M., Manns, M. P., Ernst, M., & Trautwein, C.
- Affiliations
- Medizinische Hochschule Hannover (DE)
- KU Leuven (BE)
- Wageningen University & Research (NL)
- The Royal Melbourne Hospital (AU)
- Venue
- Journal of Clinical Investigation
- Published
- 2005-03-03
- Volume
- 115
- Issue
- 4
- Pages
- 860-869
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2020798985
- Cited by
- 200
- References
- 52
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 8 · 2023: 7 · 2022: 7 · 2021: 11 · 2020: 9 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 5 · 2015: 8 · 2014: 12 · 2013: 15 · 2012: 12
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Open access
- green
- research.wur.nl
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed (publishedVersion)
- Socio-Environmental Systems Modeling (acceptedVersion)
- PubMed Central (submittedVersion)
- RWTH Publications (RWTH Aachen) (submittedVersion)
- UEA Digital Repository (University of East Anglia) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- Deutsche Forschungsgemeinschaft (SFB 566, Project B8)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- interleukin-6, gp130, STAT3, hepatocytes, liver injury, immune-mediated hepatitis, concanavalin A-induced hepatitis, hepatoprotection, SAA2, STAT1, hepatocyte-specific knockout mice, therapeutic target
- MeSH terms
- Serum Amyloid A Protein, Animals, Concanavalin A, DNA-Binding Proteins, Enzyme Activation, Hepatitis, Interferon-gamma, Liver, Male, Membrane Glycoproteins, Mice, Inbred BALB C, T-Lymphocytes, Tumor Necrosis Factor-alpha, Signal Transduction, Trans-Activators, Antigens, CD, Interleukin-6, Mice, Knockout, Gene Expression Profiling, Hepatocytes, Extracellular Signal-Regulated MAP Kinases, STAT1 Transcription Factor, STAT3 Transcription Factor, Cytokine Receptor gp130, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-23, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-23 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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