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      Common cytokine receptor gamma chain (gammac)-deficient B cells persist in T cell-deficient gammac-mice and respond to a T-independent antigen.

      European Journal of Immunology
      Animals, Antigens, immunology, B-Lymphocytes, Female, Male, Mice, Mice, Inbred BALB C, Mice, Nude, Receptors, Antigen, T-Cell, alpha-beta, Receptors, Cytokine, T-Lymphocytes

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          Abstract

          Defects in the common cytokine receptor gamma chain (gammac) in man result in X-linked severe combined immunodeficiency disease (SCIDX1) characterized by an absence of alphabeta T cells, gammadelta T cells and NK cells, with the presence of circulating B cells. Mice made deficient for gammac lack gammadelta T cells and NK cells, but in contrast to SCIDX1 patients have appreciable numbers of alphabeta T cells, while B cells are reduced about tenfold in numbers and disappear with age. Here we show that when gammac- mice are rendered T cell deficient, B cell numbers are still reduced but the age-dependent loss of B cells does not occur. The peripheral B cells which persisted in gammac-/ nude and gammac-/TCRbeta-/- mice were able to respond to mitogen stimulation in vitro and to mount antigen-specific T-independent Ig responses in vivo. These results demonstrate that gammac- B cells are functionally competent and suggest that residual alphabeta T cells are implicated in the B cell loss in gammac mice. The gammac-/nude and gammac-/TCRbeta-/- mice provide new models to dissect the role of gammac-dependent receptors during murine B cell differentiation.

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