Unknown

Dataset Information

0

Cutting Edge: BAFF Promotes Autoantibody Production via TACI-Dependent Activation of Transitional B Cells.


ABSTRACT: Mice overexpressing B cell activating factor of the TNF family (BAFF) develop systemic autoimmunity characterized by class-switched anti-nuclear Abs. Transmembrane activator and CAML interactor (TACI) signals are critical for BAFF-mediated autoimmunity, but the B cell developmental subsets undergoing TACI-dependent activation in settings of excess BAFF remain unclear. We report that, although surface TACI expression is usually limited to mature B cells, excess BAFF promotes the expansion of TACI-expressing transitional B cells. TACI(+) transitional cells from BAFF-transgenic mice are characterized by an activated, cycling phenotype, and the TACI(+) cell subset is specifically enriched for autoreactivity, expresses activation-induced cytidine deaminase and T-bet, and exhibits evidence of somatic hypermutation. Consistent with a potential contribution to BAFF-mediated humoral autoimmunity, TACI(+) transitional B cells from BAFF-transgenic mice spontaneously produce class-switched autoantibodies ex vivo. These combined findings highlight a novel mechanism through which BAFF promotes humoral autoimmunity via direct, TACI-dependent activation of transitional B cells.

SUBMITTER: Jacobs HM 

PROVIDER: S-EPMC4868625 | biostudies-literature | 2016 May

REPOSITORIES: biostudies-literature

altmetric image

Publications

Cutting Edge: BAFF Promotes Autoantibody Production via TACI-Dependent Activation of Transitional B Cells.

Jacobs Holly M HM   Thouvenel Christopher D CD   Leach Sarah S   Arkatkar Tanvi T   Metzler Genita G   Scharping Nicole E NE   Kolhatkar Nikita S NS   Rawlings David J DJ   Jackson Shaun W SW  

Journal of immunology (Baltimore, Md. : 1950) 20160328 9


Mice overexpressing B cell activating factor of the TNF family (BAFF) develop systemic autoimmunity characterized by class-switched anti-nuclear Abs. Transmembrane activator and CAML interactor (TACI) signals are critical for BAFF-mediated autoimmunity, but the B cell developmental subsets undergoing TACI-dependent activation in settings of excess BAFF remain unclear. We report that, although surface TACI expression is usually limited to mature B cells, excess BAFF promotes the expansion of TACI  ...[more]

Similar Datasets

| S-EPMC6779322 | biostudies-literature
| S-EPMC3669680 | biostudies-literature
| S-EPMC9780177 | biostudies-literature
| S-EPMC4299698 | biostudies-literature
| S-EPMC3832927 | biostudies-literature
| S-EPMC5636672 | biostudies-literature
| S-EPMC4505955 | biostudies-literature
| S-EPMC4606984 | biostudies-literature
| S-EPMC4490998 | biostudies-literature
| S-EPMC5366357 | biostudies-literature