Journal article
Murine B1 B Cells Require IL-5 for Optimal T Cell-Dependent Activation
The Journal of immunology (1950), Vol.166(3), pp.1531-1539
02/01/2001
DOI: 10.4049/jimmunol.166.3.1531
PMID: 11160193
Abstract
T helper cell-driven activation of murine B cells has been shown to depend upon CD40-CD40 ligand (CD40L) interactions and a defined set of cytokines. These observations are primarily based on the use of conventional B cells obtained from the spleen. Therefore, it is presently unclear whether all mature B cell subsets found in the mouse have an equal dependence upon CD40-CD40L interactions and use the same T cell-derived cytokines. The present study tested the response of splenic follicular and marginal zone as well as peritoneal B2 and B1 B cells to Th cell stimulation. Splenic and peritoneal B cell subsets were sort purified based on CD23 expression, and cultured with rCD40L and cytokines or Th2 cells. The results demonstrate that follicular, marginal zone, and peritoneal B2 B cells require CD40-CD40L interactions and preferentially use IL-4 for optimal proliferation, differentiation, and isotype switching. In contrast, peritoneal B1 B cells use IL-5 in conjunction with CD40-CD40L interactions for maximal Th cell-dependent responses. Furthermore, B1 B cells are capable of proliferating, differentiating, and isotype switching in the absence of CD40-CD40L interactions. B1 B cells are able to respond to Th2 clones in the presence of anti-CD40L mAb as well as to Th2 clones derived from CD40L(-/-) mice. The CD40-CD40L-independent response of B1 B cells is attributable to the presence of both IL-4 and IL-5, and may explain the residual Ab response to T cell-dependent Ags in CD40L- or CD40-deficient mice, and in X-linked hyper-IgM (X-HIM) patients.
Details
- Title: Subtitle
- Murine B1 B Cells Require IL-5 for Optimal T Cell-Dependent Activation
- Creators
- Loren D EricksonTeresa M FoyThomas J Waldschmidt
- Resource Type
- Journal article
- Publication Details
- The Journal of immunology (1950), Vol.166(3), pp.1531-1539
- DOI
- 10.4049/jimmunol.166.3.1531
- PMID
- 11160193
- NLM abbreviation
- J Immunol
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Language
- English
- Date published
- 02/01/2001
- Academic Unit
- Pathology
- Record Identifier
- 9984046824902771
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