Galectin-1 is required for the regulatory function of B cells.
Galectin-1 is required for the regulatory function of B cells.
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DOI：
10.1038/s41598-018-19965-z
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发表时间：
2018-02-09
影响因子：
4.6
通讯作者：
Lombardi G
中科院分区：
文献类型：
--
作者：
Alhabbab R;Blair P;Smyth LA;Ratnasothy K;Peng Q;Moreau A;Lechler R;Elgueta R;Lombardi G
Galectin-1 (Gal-1) is required for the development of B cells in the bone marrow (BM), however very little is known about the contribution of Gal-1 to the development of B cell regulatory function. Here, we report an important role for Gal-1 in the induction of B cells regulatory function. Mice deficient of Gal-1 (Gal-1−/−) showed significant loss of Transitional-2 (T2) B cells, previously reported to include IL-10+ regulatory B cells. Gal-1−/− B cells stimulated in vitro via CD40 molecules have impaired IL-10 and Tim-1 expression, the latter reported to be required for IL-10 production in regulatory B cells, and increased TNF-α expression compared to wild type (WT) B cells. Unlike their WT counterparts, T2 and T1 Gal-1−/− B cells did not suppress TNF-α expression by CD4+ T cells activated in vitro with allogenic DCs (allo-DCs), nor were they suppressive in vivo, being unable to delay MHC-class I mismatched skin allograft rejection following adoptive transfer. Moreover, T cells stimulated with allo-DCs show an increase in their survival when co-cultured with Gal-1−/− T2 and MZ B cells compared to WT T2 and MZ B cells. Collectively, these data suggest that Gal-1 contributes to the induction of B cells regulatory function.
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影响因子：
15.9
作者：
Matsushita, Takashi;Yanaba, Koichi;Tedder, Thomas F.
通讯作者：
Tedder, Thomas F.
DOI：
10.1084/jem.186.10.1749
发表时间：
1997-11-17
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Mizoguchi A;Mizoguchi E;Smith RN;Preffer FI;Bhan AK
通讯作者：
Bhan AK
影响因子：
4.4
作者：
Evans, Jamie G.;Chavez-Rueda, Karina A.;Mauri, Claudia
通讯作者：
Mauri, Claudia
影响因子：
20.3
作者：
Espeli, Marion;Mancini, Stephane J. C.;Schiff, Claudine
通讯作者：
Schiff, Claudine
影响因子：
20.3
作者：
Garin, Marina I.;Chu, Chung-Ching;Lechler, Robert I.
通讯作者：
Lechler, Robert I.