The DOI matches its Crossref record; 56 of the 57 references it cites were found in a registry or an index.
Iron Overload Alters Innate and T Helper Cell Responses to Candida albicans in Mice
Abstract
The effect of iron overload on susceptibility of mice to Candida albicans infection and on the type of T helper (Th) immunity elicited was investigated. Iron overload greatly increased susceptibility to disseminated infection with low-virulence C. albicans cells of exogenous origin. The candidacidal activity and the ability to release nitric oxide and bioactive interleukin (IL)-12 were greatly impaired in neutrophils and macrophages from infected mice. CD4 T cells from spleens of iron-overloaded mice were found to produce high levels of IL-4 and IL-10 and low levels of interferon-gamma. Treatment of iron-overloaded mice with the iron chelator, deferoxamine, resulted in the cure of mice from infection, restored the antifungal effector and immunomodulatory functions of the phagocytic cells, and allowed the occurrence of CD4 Th1 protective antifungal responses. These data indicate that iron overload may negatively affect CD4 Th1 development in mice with candidiasis, a function efficiently restored by therapy with deferoxamine.
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“However, immune control of Candida infection could be restored by the iron chelator deferoxamine (DFO) (Mencacci et al., 1997).”
From Iron in infection and immunity (2020) · cites this paper as Mencacci et al., 1997
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Thus, macrophages loaded with iron lose their ability to clear infections with intracellular pathogens, such as Salmonella, Mycobacteria, Chlamydia, Candida, or Legionella (Mencacci et al., 1997; Chlosta et al., 2006; Nairz et al., 2007; Paradkar et al., 2008; Botella et al., 2012; Bellmann-Weiler et al., 2013) whereas reduction of iron levels or addition of iron chelators can improve infection”
From Iron at the interface of immunity and infection (2014) · cites this paper as Mencacci et al., 1997
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In the citing paper
“Iron overload in mice can hamper the protective Th1 response and ability to clear C. albicans infection (Mencacci et al., 1997; Ishida and Johansen, 2014).”
From Iron at the Centre of Candida albicans Interactions (2018) · cites this paper as Mencacci et al., 1997
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“This pathway appears to be partly responsible for the beneficial clinical effects of iron chelators observed in several experimental infection systems (Mencacci et al., 1997; Fritsche et al., 2001; Ibrahim et al., 2007; Bellmann-Weiler et al., 2013; Nairz et al., 2013).”
From Iron at the interface of immunity and infection (2014) · cites this paper as Mencacci et al., 1997
In the citing paper
“Inhibition of TFR affects the proliferation of T cell subtypes differently with TH1 immune responses being more sensitive to intracellular iron depletion than TH2 (Thorson et al., 1991; Mencacci et al., 1997).”
From The Role of Iron Regulation in Immunometabolism and Immune-Related Disease (2019) · cites this paper as Mencacci et al., 1997
In the citing paper
“Moreover, accumulation of intracellular Fe in T cells mitigates the activation, differentiation, and proliferation of T H 1 cells while fostering T H type 2 (T H 2) responses, as illustrated in the context of Candida albicans infection in mice [69,71].”
From The Iron age of host–microbe interactions (2015) · cites this paper as [69]
In the citing paper
“Specifically, the intracellular Fe content of Mø modulates their response to interferon c (IFNc) [68,69], a cytokine produced by activated natural killer (NK) cells and T helper type 1 (T H 1) cells, which plays a central role in driving Mø microbicidal activity [70].”
From The Iron age of host–microbe interactions (2015) · cites this paper as [69]
In the citing paper
“This is in a line with observation that iron supplementation skews T-cell differentiation towards a Th-2 response [130,131] which is largely referred to a negative regulatory effect of iron on the activity of the central Th-1 cytokine interferon-gamma (IFN-γ) [132].”
From Iron in immune cell function and host defense (2021) · cites this paper as [130]
In the citing paper
“On one hand, macrophage iron overload is associated with the inhibition of IFN-γ-driven antimicrobial immune effector pathways such as nitric oxide synthase 2 (Nos2) expression, resulting in impaired control of intracellular microbes (Weiss et al., 1994; Mencacci et al., 1997; Oexle et al., 2003).”
From Genetic and Dietary Iron Overload Differentially Affect the Course of Salmonella Typhimurium Infection (2017) · cites this paper as Mencacci et al., 1997
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Citations
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- Romani L, Mencacci A, Cenci E, et al. Impaired neutrophil response and CD4 / Th1 development in IL-6 -deficient mice infected with Candida Whatever the mechanisms through which iron regulates Th albicans. J Exp Med 1996; 183:1345 -55.
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“The candidacidal activity of neutrophils and macrophages was greatly impaired, and DFO treatment restored the protective functions including release of g-IFN (Mencacci et al., 1997).”
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“Mencacci et al. (1997) indicated that iron overload may negatively affect CD4 Th1 development in mice with candidiasis, a function efficiently restored by therapy with deferoxamine, an iron chelator.”
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“Unlike AlfpCre Hfe mice in steady state,(25) we herein exclusively report on the setting of Salmonella infection and observed that Salmonella-infected AlfpCre Hfe mice show normal iron content in the spleen and bone marrow macrophages, suggesting that high serum iron levels impair IFN-g production and its antimicrobia…”
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Metadata
- Authors
- Mencacci, A., Cenci, E., Boelaert, J. R., Bucci, P., Mosci, P., d'Ostiani, C. F., Bistoni, F., & Romani, L.
- Affiliations
- University of Perugia (IT)
- Venue
- The Journal of Infectious Diseases
- Publisher
- Oxford University Press (OUP)
- Published
- 1997-06
- Volume
- 175
- Issue
- 6
- Pages
- 1467-1476
- ISSN
- 0022-1899 (ISSN-L)
- 1537-6613
- OpenAlex
- W2150374661
- Semantic Scholar
- 599845e36faeaa77f8bb9150b69754059dcae780
- Cited by
- 169
- References
- 57
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 6 · 2020: 10 · 2019: 4 · 2018: 6 · 2017: 3 · 2016: 6 · 2015: 7 · 2014: 4 · 2013: 9 · 2012: 8
- FWCI
- 6.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Infectious Diseases (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Health Sciences › Medicine › Infectious Diseases › Fungal Infections and Studies
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Keywords
- iron overload, Candida albicans, candidiasis, deferoxamine, iron chelation, Th1 cells, CD4+ T cells, neutrophils, macrophages, nitric oxide, IL-12, IL-4, IL-10, interferon-gamma, antifungal immunity, disseminated fungal infection, immunomodulation
- MeSH terms
- Animals, Candida albicans, Candidiasis, Deferoxamine, Disease Susceptibility, Ferric Compounds, Immunoglobulin E, Iron, Iron Chelating Agents, Kidney, Liver, Macrophages, Mice, Inbred BALB C, Neutrophils, Nitrates, Nitric Oxide, RNA, Gene Expression, Cytokines, Th1 Cells, Nitric Oxide Synthase, Iron Overload, Mice
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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.
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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