| First Author | Huang Y | Year | 2015 |
| Journal | Proc Natl Acad Sci U S A | Volume | 112 |
| Issue | 1 | Pages | E39-48 |
| PubMed ID | 25535377 | Mgi Jnum | J:218241 |
| Mgi Id | MGI:5617071 | Doi | 10.1073/pnas.1415107111 |
| Citation | Huang Y, et al. (2015) gammadelta T cells affect IL-4 production and B-cell tolerance. Proc Natl Acad Sci U S A 112(1):E39-48 |
| abstractText | gammadelta T cells can influence specific antibody responses. Here, we report that mice deficient in individual gammadelta T-cell subsets have altered levels of serum antibodies, including all major subclasses, sometimes regardless of the presence of alphabeta T cells. One strain with a partial gammadelta deficiency that increases IgE antibodies also displayed increases in IL-4-producing T cells (both residual gammadelta T cells and alphabeta T cells) and in systemic IL-4 levels. Its B cells expressed IL-4-regulated inhibitory receptors (CD5, CD22, and CD32) at diminished levels, whereas IL-4-inducible IL-4 receptor alpha and MHCII were increased. They also showed signs of activation and spontaneously formed germinal centers. These mice displayed IgE-dependent features found in hyper-IgE syndrome and developed antichromatin, antinuclear, and anticytoplasmic autoantibodies. In contrast, mice deficient in all gammadelta T cells had nearly unchanged Ig levels and did not develop autoantibodies. Removing IL-4 abrogated the increases in IgE, antichromatin antibodies, and autoantibodies in the partially gammadelta-deficient mice. Our data suggest that gammadelta T cells, controlled by their own cross-talk, affect IL-4 production, B-cell activation, and B-cell tolerance. |
