FCRL3 promotes TLR9-induced B-cell activation and suppresses plasma cell differentiation.
FCRL3 promotes TLR9-induced B-cell activation and suppresses plasma cell differentiation.
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DOI：
10.1002/eji.201243068
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发表时间：
2013-11
影响因子：
5.4
通讯作者：
Davis, Randall S.
中科院分区：
文献类型：
--
作者：
Li, Fu Jun;Schreeder, Daniel M.;Li, Ran;Wu, Jiongru;Davis, Randall S.
Fc receptor-like (FCRL) molecules are preferentially expressed by B lymphocytes and possess tyrosine-based immunoregulatory function. Although they generally inhibit B cell receptor (BCR) signaling, their influence on other activation pathways remains largely unexplored. In humans, FCRL3 encodes a type I transmembrane protein harboring both cytoplasmic ITAM and ITIM elements that can repress BCR activation. Despite this inhibitory property, mounting associations for FCRL3 with autoimmune and lymphoproliferative disorders imply a role for it in promoting B cell pathogenesis. Here we explore its influence on B cell responses to innate Toll-like receptor 9 (TLR9) stimulation. A detailed survey of blood B cell populations found that FCRL3 expression increased as a function of differentiation and was higher among memory subsets with innate-like features. FCRL3 ligation augmented CpG oligodeoxynucleotide TLR9-mediated B cell proliferation, activation, and survival, but surprisingly, abrogated plasma cell differentiation and antibody production. Although FCRL3 amplified the NF-κB and MAPK signaling cascades, it halted CpG triggered BLIMP1 induction in an ERK-dependent fashion. These findings indicate that FCRL3 differentially modulates innate signaling in B cells and provide new insight into the potential of this disease-associated receptor to counter-regulate adaptive and innate immunity.
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DOI：
10.1073/pnas.0703354104
发表时间：
2007-06-05
影响因子：
11.1
作者：
Haga, Christopher L.;Ehrhardt, Goetz R. A.;Cooper, Max D.
通讯作者：
Cooper, Max D.
影响因子：
32.4
作者：
Hatzivassiliou, G;Miller, I;Dalla-Favera, R
通讯作者：
Dalla-Favera, R
影响因子：
2.7
作者：
Chistiakov, Dimitry A.;Chistiakov, Alexander P.
通讯作者：
Chistiakov, Alexander P.
影响因子：
15.3
作者：
Moir, Susan;Ho, Jason;Fauci, Anthony S.
通讯作者：
Fauci, Anthony S.
DOI：
10.1038/nri1957
发表时间：
2006-11
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
Marshak-Rothstein A
通讯作者：
Marshak-Rothstein A