![[feed]](/style/images/feed-icon-14x14.png){kind=icon}
Tools
Tools
| Item Type: | Article |
|---|---|
| Title: | B-cell-intrinsic STAT6 signaling controls germinal center formation |
| Creators Name: | Turqueti-Neves, A., Otte, M., da Costa, O.P., Höpken, U.E., Lipp, M., Buch, T. and Voehringer, D. |
| Abstract: | Infection with helminths and exposure to antigens induce a strong type 2 immune response resulting in the secretion of the cytokines IL-4 and IL-13 by CD4(+) T cells and several innate cell types. IL-4 and IL-13 promote class switch recombination to IgG1 and IgE while their role for germinal center (GC) formation is poorly understood. We found a dramatic reduction in the numbers of GC B cells when investigating different type 2 immune responses in IL-4/IL-13-deficient mice. IL-4/IL-13 from T cells located outside B-cell follicles was sufficient for GC formation. We further revealed that IL-4/IL-13 acts directly on B cells for the formation of a robust GC response. The frequency of apoptotic GC B cells was not altered in the absence of IL-4/IL-13 and proliferation was even enhanced. However, deficiency of STAT6 signaling in B cells resulted in failure to downregulate the chemotactic receptor Gpr183 (Ebi2) and downregulation of this receptor has been shown to be essential for proper GC B cell differentiation. Thus, T cell derived extrafollicular IL-4/IL-13 and STAT6-regulated genes in B cells play a critical role for orchestration of the GC response in type 2 immunity. |
| Keywords: | B Cells, Germinal Center, IL-4, IL-13, STAT6, Animals, Mice |
| Source: | European Journal of Immunology |
| ISSN: | 0014-2980 |
| Publisher: | Wiley |
| Volume: | 44 |
| Number: | 7 |
| Page Range: | 2130-2138 |
| Date: | July 2014 |
| Official Publication: | https://doi.org/10.1002/eji.201344203 |
| PubMed: | View item in PubMed |
Repository Staff Only: item control page
