ArticleJournal of immunology (Baltimore, Md. : 1950)2013
IL-17RA is essential for optimal localization of follicular Th cells in the germinal center light zone to promote autoantibody-producing B cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 86 citations in OpenAlex.
- Functional and Transcriptomic Characterization of Peritoneal Immune-Modulation by Addition of Alanyl-Glutamine to Dialysis Fluid.Scientific reports · 2017Trial
- An "old" cytokine's new trick: IL-1β in B cells and the germinal center.Function (Oxford, England) · 2026Review
- IL-4 alters TLR7-induced B cell developmental program in lupus.Clinical immunology (Orlando, Fla.) · 2025Article
- TIGITFrontiers in immunology · 2024Article
- Increased development of T-betClinical immunology (Orlando, Fla.) · 2023Article
- Ets1 and IL17RA cooperate to regulate autoimmune responses and skin immunity toFrontiers in immunology · 2023Article
- Symbiotic bacteria-dependent expansion of MR1-reactive T cells causes autoimmunity in the absence of Bcl11b.Nature communications · 2022Article
- T Cell-Intrinsic Interleukin 17 Receptor A Signaling Supports the Establishment of Chronic Murine Gammaherpesvirus 68 Infection.Journal of virology · 2022Article
- T cell help in the autoreactive germinal center.Scandinavian journal of immunology · 2022Review
- Host Genetics But Not Commensal Microbiota Determines the Initial Development of Systemic Autoimmune Disease in BXD2 Mice.Arthritis & rheumatology (Hoboken, N.J.) · 2022Article
- Functions of regulators of G protein signaling 16 in immunity, inflammation, and other diseases.Frontiers in molecular biosciences · 2022Review
- IL-17-dependent fibroblastic reticular cell training boosts tissue protective mucosal immunity through IL-10-producing B cells.Science immunology · 2021Article
- CD4Trends in immunology · 2021Review
- Cytokine-skewed Tfh cells: functional consequences for B cell help.Trends in immunology · 2021Review
- Gammaherpesvirus Usurps Host IL-17 Signaling To Support the Establishment of Chronic Infection.mBio · 2021Article
- Immune Skew of Circulating Follicular Helper T Cells Associates With Myasthenia Gravis Severity.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis.Frontiers in medicine · 2021Review
- Emerging Complexity in CD4Frontiers in immunology · 2021Review
- Role of Tonsillar Chronic Inflammation and Commensal Bacteria in the Pathogenesis of Pediatric OSA.Frontiers in immunology · 2021Article
- The Potential of Harnessing IL-2-Mediated Immunosuppression to Prevent Pathogenic B Cell Responses.Frontiers in immunology · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Germinal centers (GCs) provide a microenvironment that promotes and regulates the interactions of B cells with follicular Th (TFH) cells. In this study, we show that there are significantly higher frequencies of CXCR5(+)ICOS(+) TFH cells in autoimmune BXD2 mice, and these cells express both IL-21R and IL-17RA. Although IL-17 and IL-21 are both important for the formation of spontaneous GCs and development of pathogenic autoantibodies, IL-21, but not IL-17, is required for the proper development of TFH cells in BXD2 mice. The total numbers of TFH cells and their ability to induce B cell responses in vitro were not affected by a deficiency of IL-17RA in BXD2-Il17ra(-/-) mice, the majority of CXCR5(+) TFH cells from BXD2-Il17ra(-/-) mice were, however, not localized in the GC light zone (LZ). Interruption of IL-17 signaling, either acutely by AdIL-17R:Fc or chronically by Il17ra(-/-), disrupted TFH-B interactions and abrogated the generation of autoantibody-forming B cells in BXD2 mice. IL-17 upregulated the expression of regulator of G-protein signaling 16 (RGS16) to promote the ability of TFH to form conjugates with B cells, which was abolished in TFH cells from BXD2-Rgs16(-/-) mice. The results suggests that IL-17 is an extrinsic stop signal that it acts on postdifferentiated IL-17RA(+) TFH to enable its interaction with responder B cells in the LZ niche. These data suggest a novel concept that TFH differentiation and its stabilization in the LZ are two separate checkpoints and that IL-21 and IL-17 act at each checkpoint to enable pathogenic GC development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.