MOUSE GAMMA-DELTA-TCR(-4, ARE MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-I INDEPENDENT, AND ARE DEVELOPMENTALLY RELATED TO ALPHA-BETA-TCR(+)NK1.1(+) THYMOCYTES()NK1.1(+) THYMOCYTES SPECIFICALLY PRODUCE INTERLEUKIN)

Mouse T cells co-expressing an alpha beta T cell receptor (TCR) and th e NK1.1 antigen have been shown to be major interleukin (IL)-4-produci ng cells and could therefore regulate cell-mediated immune responses. We have identified a related subset of thymocytes co-expressing a gamm a delta TCR and NK1.1 which also produce IL-4. Unlike alpha beta(+)NK1 .1(+) thymocytes, the selection of gamma delta(+)NK1.1(+) thymocytes i s not dependent upon beta 2-microglobulin (beta 2m)-associated class I molecule expression because these cells are present in beta 2m-defici ent mice. This suggests that gamma delta(+)NK1.1(+) T cells may regula te immune responses to a different variety of antigens. However, the d evelopment of alpha beta(+)NK1.1(+) and gamma delta(+)NK1.1(+) thymocy tes appears to be related. Analysis of different mutant mice lacking a lpha beta(+)NK1.1(+) thymocytes revealed a specific increase in gamma delta(+)NK1.1(+) thymocyte production when the block in alpha beta(+)N K1.1(+) thymocyte differentiation occurs after beta TCR rearrangement.