| First Author | Gulbranson-Judge A | Year | 1999 |
| Journal | Eur J Immunol | Volume | 29 |
| Issue | 2 | Pages | 477-87 |
| PubMed ID | 10064063 | Mgi Jnum | J:53743 |
| Mgi Id | MGI:1333361 | Doi | 10.1002/(SICI)1521-4141(199902)29:02<477::AID-IMMU477>3.0.CO;2-V |
| Citation | Gulbranson-Judge A, et al. (1999) Defective immunoglobulin class switching in Vav-deficient mice is attributable to compromised T cell help. Eur J Immunol 29(2):477-87 |
| abstractText | Vav, a guanine nucleotide exchange factor for members of the Rho family of small GTPases, is activated through engagement of B and T lymphocyte antigen receptors. It is important for establishing the signaling threshold of the TCR, as mice lacking Vav display defective thymocyte selection. Here, conventional B cells are shown to develop normally in Vav-deficient mice but these mice have few B-1 B cells. The threshold for inducing B cell proliferation through BCR engagement in vitro is greater in Vav-deficient B cells. Nevertheless, in vivo the mutant mice have normal antibody responses to haptenated Ficoll. In contrast, Vav-/- mice show defective class switching to IgG and germinal center formation when immunized with haptenated protein. Interestingly, this defect is reversed in chimeras where normal T cells are present. Antigen-specific proliferation of T cells in the T zone was found to be similar in wild-type and Vav-/- mice but the induction of IL-4 mRNA and switch transcripts was specifically impaired. These results suggest that defective immunoglobulin class switching in Vav-deficient mice is attributable to compromised T cell help. |
