In:
Journal of Leukocyte Biology, Oxford University Press (OUP), Vol. 87, No. 3 ( 2009-12-09), p. 493-500
Abstract:
PI3K p85α subunit alters the superantigen presentation capacity of B cells and indirectly modulates the magnitude of the T cell response. PI3K plays crucial roles in the immune system. Mice deficient for p85α, a major regulatory subunit of class IA PI3K, show various defects and alterations in B cells, mast cells, macrophages, and DCs, and peripheral T cells are reportedly normal, at least in vitro. In normal mice, long-term exposure to a SAg, SEA, in vivo induced a high level of the protracted expansion of SEA-reactive Vβ3+CD4+ T cells, whereas the same treatment induced T cell expansion in p85α-deficient mice but to a much lesser extent than in normal mice. However, mixed bone marrow chimera mice, which have normal and p85α-deficient T and B cells, demonstrated equal responses of both T cells following stimulation with a SEA pump. In reciprocal cotransfer experiments of T and B cells from normal and p85α-deficient mice into Rag2-deficient mice, followed by SEA stimulation, p85α-deficient T cells revealed much higher proliferative capacity in the presence of normal B cells than did normal T cells with p85α-deficient B cells. Histologically, a marked B cell reduction was observed in the follicles and MZ of the spleen, and DCs accumulated in the MZ. In addition, p85α-deficient B cells had a low level of MHC class II expression. Collectively, these data suggested that the PI3K p85α subunit alters the SAg presentation capacity of B cells and indirectly modulates the magnitude of the T cell response, which may affect the protection against SEA-containing bacteria.
Type of Medium:
Online Resource
ISSN:
1938-3673
,
0741-5400
Language:
English
Publisher:
Oxford University Press (OUP)
Publication Date:
2009
detail.hit.zdb_id:
2026833-6
SSG:
12
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