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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.

Original publication




Journal article


J Immunol

Publication Date





4615 - 4619


Allolevivirus, Animals, Antibodies, Viral, B-Lymphocyte Subsets, Epitopes, T-Lymphocyte, Gene Expression Regulation, Viral, Gene Products, env, Germinal Center, Immunity, Innate, Immunoglobulin G, Interleukins, Ligands, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Knockout, Receptors, Interleukin-21, Recombinant Proteins, Signal Transduction, T-Lymphocytes, Helper-Inducer, Toll-Like Receptor 7, Toll-Like Receptor 8, Virion