| First Author | Vosshenrich CA | Year | 2000 |
| Journal | Eur J Immunol | Volume | 30 |
| Issue | 6 | Pages | 1614-22 |
| PubMed ID | 10898497 | Mgi Jnum | J:62730 |
| Mgi Id | MGI:1859500 | Doi | 10.1002/1521-4141(200006)30:6<1614::AID-IMMU1614>3.0.CO;2-I |
| Citation | Vosshenrich CA, et al. (2000) Common cytokine receptor gamma chain (gammac)-deficient B cells persist in T cell-deficient gammac-mice and respond to a T-independent antigen. Eur J Immunol 30(6):1614-22 |
| abstractText | 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. |
