B cell intrinsic myD88 signals drive IFN- production from T cells and control switching to IgG2c

Barr, T.A., Brown, S., Mastroeni, P. and Gray, D. (2009) B cell intrinsic myD88 signals drive IFN- production from T cells and control switching to IgG2c. Journal of Immunology, 183(2), pp. 1005-1012. (doi: 10.4049/jimmunol.0803706)

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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<sup>B−/−</sup> chimeric mice exhibited an impairment of development of IFN-γ 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.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Barr, Dr Tom
Authors: Barr, T.A., Brown, S., Mastroeni, P., and Gray, D.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
Journal Name:Journal of Immunology
Publisher:American Association of Immunologists

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