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Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65.

Abstract：

:During signal transduction through the B cell antigen receptor (BCR), several signaling elements are brought together by the adaptor protein SLP-65. We have investigated the role of SLP-65 in B cell maturation and function in mice deficient for SLP-65. While the mice are viable, B cell development is affected at several stages. SLP-65-deficient mice show increased proportions of pre-B cells in the bone marrow and immature B cells in peripheral lymphoid organs. B1 B cells are lacking. The mice show lower IgM and IgG3 serum titers and poor IgM but normal IgG immune responses. Mutant B cells show reduced Ca2+ mobilization and reduced proliferative responses to B cell mitogens. We conclude that while playing an important role, SLP-65 is not always required for signaling from the BCR.

journal_name

Immunity

journal_title

Immunity

authors

Jumaa H,Wollscheid B,Mitterer M,Wienands J,Reth M,Nielsen PJ

doi

10.1016/s1074-7613(00)80130-2

keywords:

subject

Has Abstract

pub_date

1999-11-01 00:00:00

pages

547-54

issue

5

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(00)80130-2

journal_volume

11

pub_type

杂志文章

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