Interleukin-6/STAT3 signaling regulates the ability of naive T cells to acquire B-cell help capacities
Copyright policy )Interleukin-6/STAT3 signaling regulates the ability of naive T cells to acquire B-cell help capacities
AbstractThe conditions leading to the activation/differentiation of T-helper (Th) cells dedicated for B-cell antibody production are still poorly characterized. We now demonstrate that interleukin-6 (IL-6) promotes the differentiation of naive T lymphocytes into helper cells able to promote B-cell activation and antibody secretion. IL-6–driven acquisition of B-cell help capacity requires expression of the signal transducer and activator of transcription 3 (STAT3), but not STAT4 or STAT6 transcription factors, suggesting that the ability to provide help to B cells is not restricted to a well-defined Th1 or Th2 effector population. T cell–specific STAT3-deficient mice displayed reduced humoral responses in vivo that could not be related to an altered expansion of CXCR5-expressing helper T cells. IL-6 was shown to promote IL-21 secretion, a cytokine that was similarly found to promote the differentiation of naive T cells into potent B-cell helper cells. Collectively, these data indicate that the ability to provide B-cell help is regulated by IL-6/IL-21 through STAT3 activation, independently of Th1, Th2, Th17, or follicular helper T cell (TFH) differentiation.
- Université Libre de Bruxelles Belgium
- National Institute of Health Pakistan
- National Institutes of Health United States
- University of Liège Belgium
Interleukin-6 -- physiology, T-Lymphocytes, Lymphocyte Activation -- genetics, Tnf, nicotinamide, Inbred C57BL, Lymphocyte Activation, Interleukin-21, STAT3 Transcription Factor -- physiology, B-Lymphocytes -- drug effects, Mice, Laboratory medicine & medical technology, T-Lymphocytes -- physiology, Receptors, Cell Differentiation -- immunology, Human health sciences, Inbred BALB C, Mice, Knockout, B-Lymphocytes, Mice, Inbred BALB C, Antibody Formation -- genetics, T-Lymphocytes -- drug effects, Cell Differentiation, Interleukin-6 -- pharmacology, T-Lymphocytes, Helper-Inducer, Sciences bio-médicales et agricoles, CXCR5 -- metabolism, Interleukin-6 -- genetics, Médecine de laboratoire & technologie médicale, B-Lymphocytes -- immunology, Signal Transduction, Receptors, CXCR5, STAT3 Transcription Factor, Knockout, STAT3 Transcription Factor -- genetics, Sciences de la santé humaine, Signal Transduction -- genetics, Interleukins -- physiology, Animals, Signal Transduction -- physiology, Interleukin-6, Interleukins, Helper-Inducer -- immunology, Mice, Inbred C57BL, Interleukins -- secretion, inflammation, Antibody Formation, Helper-Inducer -- physiology, Antibody Formation -- drug effects, T-Lymphocytes -- immunology
Interleukin-6 -- physiology, T-Lymphocytes, Lymphocyte Activation -- genetics, Tnf, nicotinamide, Inbred C57BL, Lymphocyte Activation, Interleukin-21, STAT3 Transcription Factor -- physiology, B-Lymphocytes -- drug effects, Mice, Laboratory medicine & medical technology, T-Lymphocytes -- physiology, Receptors, Cell Differentiation -- immunology, Human health sciences, Inbred BALB C, Mice, Knockout, B-Lymphocytes, Mice, Inbred BALB C, Antibody Formation -- genetics, T-Lymphocytes -- drug effects, Cell Differentiation, Interleukin-6 -- pharmacology, T-Lymphocytes, Helper-Inducer, Sciences bio-médicales et agricoles, CXCR5 -- metabolism, Interleukin-6 -- genetics, Médecine de laboratoire & technologie médicale, B-Lymphocytes -- immunology, Signal Transduction, Receptors, CXCR5, STAT3 Transcription Factor, Knockout, STAT3 Transcription Factor -- genetics, Sciences de la santé humaine, Signal Transduction -- genetics, Interleukins -- physiology, Animals, Signal Transduction -- physiology, Interleukin-6, Interleukins, Helper-Inducer -- immunology, Mice, Inbred C57BL, Interleukins -- secretion, inflammation, Antibody Formation, Helper-Inducer -- physiology, Antibody Formation -- drug effects, T-Lymphocytes -- immunology
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