| First Author | Barr TA | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 2 | Pages | 1005-12 |
| PubMed ID | 19542370 | Mgi Jnum | J:151505 |
| Mgi Id | MGI:4353959 | Doi | 10.4049/jimmunol.0803706 |
| Citation | Barr TA, et al. (2009) B cell intrinsic MyD88 signals drive IFN-gamma production from T cells and control switching to IgG2c. J Immunol 183(2):1005-12 |
| abstractText | The question of whether Ab responses to T-dependent Ags require B cell intrinsic signaling via the main TLR adaptor (MyD88) has become embroiled in confusion. In part this may be related to the methods used to analyze B cell intrinsic signaling. We have used a mixed bone marrow chimera model to generate mice in which the B cell compartment is completely deficient in MyD88 expression, while the other hematopoietic lineages are largely normal. These mice were immunized with T-dependent Ags or infected with Salmonella. We found that the Ag-specific IgG2c primary response was absolutely dependent on MyD88 signaling to B cells, while other Ig classes were not (IgG1 and IgG3) or much less so (IgG2b, IgA). The MyD88(B-/-) chimeric mice exhibited an impairment of development of IFN-gamma effector T cells, a likely contributory factor in the lack of IgG2c. We also found that B cell intrinsic MyD88 signals are required for the production of natural Abs. The data emphasize the nonredundant role of B cells as programmers of T cell differentiation in vivo. |
