γδ T cells affect IL-4 production and B-cell tolerance.

Huang Y., Heiser R. A., Detanico T. O., Getahun A., Kirchenbaum G. A., Casper T. L., Aydintug M. K., Carding S. R., Ikuta K., Huang H., Cambier J. C., Wysocki L. J., O'Brien R. L., Born W. K.. (2015)

Proceedings of the National Academy of Sciences of the United States of America, 112, E39-48

γδ T cells can influence specific antibody responses. Here, we report that mice deficient in individual γδ T-cell subsets have altered levels of serum antibodies, including all major subclasses, sometimes regardless of the presence of aß T cells. One strain with a partial γδ deficiency that increases IgE antibodies also displayed increases in IL-4-producing T cells (both residual γδ T cells and aß 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 a 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 γδ 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 γδ-deficient mice. Our data suggest that γδ T cells, controlled by their own cross-talk, affect IL-4 production, B-cell activation, and B-cell tolerance.

Proceedings of the National Academy of Sciences of the United States of America, 112, E39-48

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