| First Author | Morsy DE | Year | 2013 |
| Journal | J Immunol | Volume | 191 |
| Issue | 6 | Pages | 3112-8 |
| PubMed ID | 23966626 | Mgi Jnum | J:205857 |
| Mgi Id | MGI:5546542 | Doi | 10.4049/jimmunol.1202098 |
| Citation | Morsy DE, et al. (2013) Reduced T-dependent humoral immunity in CD20-deficient mice. J Immunol 191(6):3112-8 |
| abstractText | CD20 is a tetraspanning membrane protein expressed on B lymphocytes. CD20 deficiency in both mice and humans has recently been shown to have deleterious effects on Ab responses to T-independent Ags; however, no effect on T-dependent immunity has been reported. In this study, we used a Cd20(-)/(-) mouse line to evaluate Ab responses to adeno-associated virus and SRBCs. The neutralizing Ab response to adeno-associated virus was significantly reduced by CD20 deficiency; both primary (IgM) and secondary (IgG1 and IgG2b) responses to SRBC were also reduced in Cd20(-)/(-) mice, and this was associated with a reduction in the number of germinal center B cells. A successful humoral response requires the integration of intracellular signaling networks that critically rely on calcium mobilization. In this article, we confirm that BCR-mediated calcium mobilization is reduced in Cd20(-)/(-) murine B cells after BCR stimulation in vitro, and further show that the reduction is due to an effect on calcium influx rather than calcium release from intracellular stores. Calcium-dependent upregulation of CD69 was impaired in CD20-deficient B cells, as was upregulation of CD86. Altogether, this study demonstrates a role for CD20 in B cell activation and T-dependent humoral immunity. |
