[gamma][delta] T cells affect IL-4 production and B-cell tolerance

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Publisher: National Academy of Sciences
Document Type: Report
Length: 7,909 words
Lexile Measure: 1520L

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Abstract :

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

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Source Citation   

Gale Document Number: GALE|A431966117