In vitro and in vivo activation of murine γ/δ T cells induces the expression of IgA, IgM, and IgG Fc receptors

Abstract

The present studies examined resting and activated murine γ/δ T lymphocytes, in vitro and in vivo, for surface expression of FcR. Polyclonal γ/δ TCR+ lymphocytes selectively grown from the spleen and intestine of normal mice did not express FcR when the cells were in a resting state, but when cells were activated with anti-CD3 antibody virtually all of the splenic γ/δ lymphocytes and a large subpopulation of the intestinal γ/δ lymphocytes expressed IgA and IgM FcR. This was confirmed by using transgenic mice. Resting γ/δ TCR+ lymphocytes from the spleen, thymus, lymph node, and blood of γ/δ TCR transgenic mice did not express FcR for any of the five major classes of Ig H chains. Activation of the γ/δ TCR+ cells via the CD3/TCR complex induced high levels of IgM and IgA FcR and low levels of IgG FcR. Finally, in hepatic granulomas of schistosome-infected mice, activated γ/δ TCR+ cells are present and express high levels of IgA and IgM FcR and low levels of IgG FcR. These investigations establish that transition of γ/δ TCR+ lymphocytes from a resting to an activated state (triggered via the T3Ti TCR complex) is accompanied by the induction of surface membrane receptors specific for Ig H chain isotypes. The activation-linked expression of FcR on γ/δ TCR+ lymphocytes provides potential mechanisms for coupling the functional activities of γ/δ T lymphocytes with immune mechanisms that involve Ig molecules, such as antibody-dependent cellular cytotoxicity.