Cutting edge: IL-21 and TLR signaling regulate germinal center responses in a B cell-intrinsic manner.

Journal article

IL-21 produced by follicular Th (Tfh) cells is an important regulator of Tfh cell development and B cell responses, including germinal center (GC) formation. However, whether defective GC formation and Ab responses are a consequence of impaired Tfh cells development or a B cell-intrinsic defect in IL-21-deficient mice requires clarification. To address this question, we generated chimeric mice lacking IL-21R exclusively on B cells. In this study, we demonstrate that GC reaction and B cell responses induced by immunization with virus-like particles were strongly reduced in both global and B cell-specific IL-21R-deficient mice. Interestingly, the presence of TLR7 ligand within virus-like particles largely restored defective GC reaction and Ab responses in global as well as in B cell-specific IL-21R-deficient mice. Hence, IL-21 acts directly on B cells and cooperates with TLR signaling for optimal B cell responses.

Authors: Bessa, J; Kopf, M; Bachmann, M

• Publication status: Published
• Journal: Journal of Immunology
• Volume: 184
• Issue: 9
• Pages: 4615-4619
• Publication date: 2010-05-01
• DOI: 10.4049/jimmunol.0903949
• EISSN: 1550-6606
• ISSN: 0022-1767
• Language: English
• Keywords: Allolevivirus; Virion; Receptors, Interleukin-21; Ligands; Germinal Center; Antibodies, Viral; Mice, Inbred C57BL; Immunity, Innate; Immunoglobulin G; Toll-Like Receptor 8; B-Lymphocyte Subsets; Gene Expression Regulation, Viral; Mice; Interleukins; Gene Products, env; Signal Transduction; Membrane Glycoproteins; Toll-Like Receptor 7; Epitopes, T-Lymphocyte; Mice, Knockout; Animals; T-Lymphocytes, Helper-Inducer; Recombinant Proteins