The DOI matches its Crossref record; 79 of the 81 references it cites were found in a registry or an index.
TLR-Activated B Cells Suppress T Cell-Mediated Autoimmunity
Abstract
TLR sense microbial infections, and control activation of immune responses. Dendritic cells, macrophages, and B lymphocytes express TLR and the TLR-signaling adaptor protein MyD88. The impact of TLR-activated B cells on T cell-mediated inflammation is unknown. In this study, we have used mice carrying B cell-restricted deficiencies in MyD88 or in distinct TLR to examine the impact of TLR-activated B cells on a T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis (EAE). We demonstrate that TLR-signaling in B cells suppresses inflammatory T cell responses (both Th1 and Th17), and stimulates recovery from EAE. Only certain TLR are required on B cells for resolution of EAE, and these are dispensable for disease initiation, indicating that a category of TLR agonists preferentially triggers a suppressive function in B cells and thereby limits autoimmune disease. The TLR agonists controlling the regulatory function of B cells are provided by components of Mycobacterium tuberculosis present in the adjuvant. Thus, MyD88 signaling in B cells antagonizes MyD88 signaling in other cells, which drives differentiation of Th17 cells and is required for induction of EAE. Altogether, our data indicate that B cells link recognition of microbial products via TLR to suppression of a T cell-mediated autoimmune disease.
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“Bregs is a generic term used to define B cells endowed with regulatory and immunosuppressive functions. They play a crucial role in maintain ing immunological homeostasis by producing anti-inflammatory cyto kines such as interleukin-10 (IL-10), IL-35, and transforming growth factor-beta (TGFβ ), thereby suppressing immunopathology.”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [58]
In the citing paper
“Their differentiation is influenced by signals such as CD40 ligation, TLR stimulation, and cytokine exposure [58,63,64].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [58]
In the citing paper
“Bregs inhibit the expansion of pathogenic T cells and other pro-inflammatory immune cells, thereby preventing excessive immune activation [55 -58].”
From Is there a role for B cells in Alzheimer's disease? (2026) · cites this paper as [58]
Citations
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“CD1dhiCD5+ B10 Breg cells have been identified in the context of experimental autoimmune encephalomyelitis (EAE) [6], allergy [7], chronic colitis [8] and infections [9,10].”
BackgroundInfluentialNLRP6 deficiency expands a novel CD103+ B cell population that confers immune tolerance in NOD mice
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Shen, P. (2012) · Frontiers in Bioscience-Elite · doi:10.2741/e597 · Cited by 9
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Neziraj, T., Siewert, L. K., Pössnecker, E., & Pröbstel, A. (2023) · European Journal of Immunology · doi:10.1002/eji.202250033 · Cited by 13
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TLR9 Signaling Suppresses the Canonical Plasma Cell Differentiation Program in Follicular B Cells
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Loss of Gαq impairs regulatory B-cell function
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Influence of drug molecules on regulatory B cells
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Enteroantigen‐presenting B cells efficiently stimulate CD4+ T cells in vitro
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“TLR2 promotes IL-10-producing Treg cells [86,87].”
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“Work from Casey Weaver’s laboratory suggested that Th17 cells start producing IFN-γ when restimulated in the presence of IL-23 and in the absence of TGF-β (Lee et al. 2009).”
InfluentialThe circulating IL‐35+ regulatory B cells are associated with thyroid associated opthalmopathy
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“33 CD19 + CD25 + CD71 + CD73 − Bregs have been identified to produce substantial amounts of IL ‐ 10 in response to CpG stimulation, effectively inhibiting the proliferation of antigen ‐ specific T ‐ cells in an IL ‐ 10 ‐ dependent manner.”
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Regulation of Germinal Center Reactions by B and T Cells
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“Interestingly, mice deficient in TLR2 and TLR4, or MyD88 in B cells, show a significantly delayed recovery from EAE, indicating that those TLR signals activate the regulatory function of B cells [168].”
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“IL-10 production by Breg cells requires LPS-induced TLR signaling (36).”
BackgroundB Cells with Regulatory Function in Animal Models of Autoimmune and Non-Autoimmune Diseases
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Regulatory B Cells - Implications in Autoimmune and Allergic Disorders
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Activation of Toll‐like receptor 4 by thyroid hormone triggers abnormal B‐cell activation
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Identification of IL-10 competent B cells in swine.
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“In one experiment, despite normal Breg development in MyD88-de fi cient mice, these mice failed to secrete suf fi cient IL-10 upon LPS stimulation (127).”
Expansion of B10 cells in vitro: Pathways, techniques and applications in transplantation (Review)
Zhao, D., Huai, G., Yuan, Y., Cui, Y., Yuan, Y.-L., & Zhao, G. (2024) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2024.5470 · Cited by 3
“TLR agonists, such as LPS from gram‑negative bacteria, peptidoglycan from gram‑positive bacteria or CpG‑containing oligonucleotides that mimic bacterial DNA (115), are potent factors in inducing IL‑10 production by naïve B cells (32,37).”
Cerrillos-Gutíerrez, J. I., Medina-Pérez, M., Andrade-Sierra, J., García-Sánchez, A., Cardona-Muñoz, E., Campos-Pérez, W., Martínez-López, E., Sánchez-Lozano, D. I., Campos-Bayardo, T. I., Román-Rojas, D., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25137023 · Cited by 3
“TLR7 and TLR9 are intracellular receptors not directly accessible to natural extracellular nucleic acids such as B cells because they do not internalize extracellular material through micropinocytosis or endocytosis [11].”
BackgroundThe Role of Toll-Like Receptors in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis
Gran, B., Nyirenda, M. H., & Crooks, J. E. (2013) · Springer eBooks · doi:10.1007/978-1-4614-7953-6_8 · Cited by 4
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“Notably, MyD88 − / − mice exhibit complete resistance to EAE [13–16].”
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Deficiency in TLR4 impairs regulatory B cells production induced by Schistosome soluble egg antigen
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Stimulation with FITC-labeled antigens confers B cells with regulatory properties
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Proinsulin-Loaded Nanoparticles Suppress Insulitis and Induce Temporary Diabetes Remission
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Self-citationMicrobial metabolite effects on TLR to develop autoimmune diseases
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Skewed B cell differentiation affects lymphoid organogenesis but not T cell‐mediated autoimmunity
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Linfocitos B reguladores en enfermedades humanas y modelos murinos de autoinmunidad
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B cells set trends: Lessons from multiple sclerosis
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“In other immune-mediated conditions, such as RA and SLE, patients treated with rituximab showed an increased risk of the rare complication of progressive multifocal leukoencephalopathy, mediated by the JC virus.217,218 Although these patients were on other concomitant immune therapies, of interest has been the conside…”
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“2006) and TLR activation of B cells may control autoimmune T cell responses (Lenert et al. 2005; Lampropoulou et al. 2008).”
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Self-citationTh17 cells and neutrophils: exploiting their crosstalk for multiple sclerosis therapeutics
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Ocrelizumab Modulates Both B and T Cell Immune Capacities in Multiple Sclerosis
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“Breg cells are shown to be expanded by toll-like receptor (TLR) ligands such as lipopolysaccharide (LPS) [21,34] and cytokines such as IL-6 [35,36] and IL-21 [37].”
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B cell counterpart of Treg cells: As a new target for autoimmune disease therapy
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“[53] Mice with B cell‑specific deletion of STIM proteins exhibited marked exacerbation of EAE development, and B cells lacking both STIM proteins failed to secrete BCR‑mediated IL‑10.”
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“Ensuite, une étude a démontré que le transfert syngénique de LB activés par le BCR (par stimulation anti-IgM) dans des souris NOD protège ces dernières contre le développement de diabète de type I en sécrétant de l’IL-10 et en augmentant la réponse immunitaire Th2 au dépend de la réponse Th1 [203].”
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Regulatory Role of Peritoneal B Cells in EAE
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B Cells and Regulatory B Cells in Cancer Escape
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A double-edged sword in B-cell-targeted therapy for inflammatory diseases
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B-Cells in Cancer Immunology: For or Against Cancer Growth?
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Phenotypes, Origins and Functions of Regulatory B Cells in Autoimmune and Inflammatory Diseases
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“Mivel tudjuk, hogy ezen szignálok (BCR/TLR9) a regulátor B-sejtek differenciálódásának fontos indukáló faktorai [6, 12] - és annak analógiájára, hogy a T-bet a CD4 regulátor T-sejtek egy kis populációjának szuppresszív funkciójának szabályozásában fontos szerepept tölt be [9] - kíváncsiak voltunk, hogy ezeken a recept…”
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Cytokine-Producing Effector B Cells
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Role of B Cells in the Pathogenesis of Multiple Sclerosis
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Self-citation
Metadata
- Authors
- Lampropoulou, V., Hoehlig, K., Roch, T., Neves, P., Gómez, E. C., Sweenie, C. H., Hao, Y., Freitas, A. A., Steinhoff, U., Anderton, S. M., & Fillatreau, S.
- Affiliations
- German Rheumatism Research Centre (DE)
- Deutsches Rheuma-ForschungsZentrum , Berlin ,
- University of Edinburgh (GB)
- Centre National de la Recherche Scientifique (FR)
- Unité de Recherche Associée Centre National de la Recherche Scientifique 1961, Institut Pasteur , Paris ,
- Max Planck Institute for Infection Biology (DE)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-04-01
- Volume
- 180
- Issue
- 7
- Pages
- 4763-4773
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1918941126
- Cited by
- 436
- References
- 81
- Citations by year
- 2026: 11 · 2025: 7 · 2024: 11 · 2023: 13 · 2022: 17 · 2021: 23 · 2020: 13 · 2019: 17 · 2018: 24 · 2017: 24 · 2016: 41 · 2015: 31 · 2014: 34 · 2013: 40 · 2012: 33
- FWCI
- 13.45
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Keywords
- MyD88, T cell-mediated autoimmunity, experimental autoimmune encephalomyelitis, Th17 cells, Th1 cells, B cell suppression, TLR agonists, dendritic cells, macrophages
- MeSH terms
- Animals, B-Lymphocytes, Dendritic Cells, Encephalomyelitis, Autoimmune, Experimental, Lymphocyte Activation, Mice, Inbred C57BL, Mycobacterium tuberculosis, T-Lymphocytes, Signal Transduction, Autoimmunity, Interleukin-10, Mice, Knockout, Toll-Like Receptors, Mice, Myeloid Differentiation Factor 88
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