Activation and accumulation of B cells in TACI-deficient mice

Yan, Minhong; Wang, Hua; Chan, Betty; Roose-Girma, Meron; Erickson, Sharon; Baker, Thad; Tumas, Daniel B.; Grewal, Iqbal S.; Dixit, Vishva M.

doi:10.1038/89790

Cited by 376 publications

(244 citation statements)

References 28 publications

Supporting

Mentioning

227

Contrasting

Unclassified

Order By: Relevance

“…The finding that B cell development is normal in APRIL Ϫ/Ϫ mice is consistent with the observation that neither TACI nor BCMA are important for the development of mature B cells (36)(37)(38). However, TACI has been shown to play an important role in B cell homeostasis, because TACI Ϫ/Ϫ mice have increased numbers of B cells and develop a B cell lymphoproliferative disorder (38,39). Because the B cell compartment was normal in size and distribution in APRIL However, APRIL Ϫ/Ϫ mice exhibit significantly increased serum IgG antibody responses and have increased numbers of germinal centers in their spleens after immunization with TD antigen.…”

Section: Discussionsupporting

confidence: 77%

“…Further investigations are needed to examine T cell function in APRIL Ϫ/Ϫ mice. Because TACI is indispensable for TI-2 antibody responses (37,38), the normal response of APRIL Ϫ/Ϫ mice to the TI-2 antigen NP-Ficoll suggests that APRIL and BAFF are redundant in delivering signals that are essential for antibody responses to TI-2 antigens via TACI.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Impaired IgA class switching in APRIL-deficient mice

Castigli

Scott

Dedeoğlu

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

402

314

View full text Add to dashboard Cite

The tumor necrosis factor (TNF) family member APRIL binds to the receptors BCMA on B cells and TACI on B and T cells. To investigate the role of APRIL in immunity, we generated APRIL-deficient mice. APRIL ؊/؊ mice have normal T and B lymphocyte development, normal T and B cell proliferation in vitro, but increased numbers of CD44 hi CD62L lo CD4 ؉ effector͞memory T cells and increased IgG responses to T-dependent antigens. Serum IgA levels were significantly decreased, and serum IgA antibody responses to mucosal immunization with TD antigens and to type 1 T-independent antigens were impaired in APRIL ؊/؊ mice. APRIL by itself induced IgA as well as IgG1 isotype switching in CD40-deficient IgM ؉ IgD ؉ sorted B cells. These results suggest that APRIL down-regulates T cell-dependent antibody responses and promotes IgA class switching.

show abstract

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Impaired IgA class switching in APRIL-deficient mice

Castigli

Scott

Dedeoğlu

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

402

314

View full text Add to dashboard Cite

show abstract

“…2A and B), they were severely impaired in responding to NP-Ficoll (Fig. 2C), as shown previously (33,42). Similarly, while BAFF Ϫ/Ϫ mice possessed a B1b compartment, they were severely impaired in responding to NP-Ficoll (Fig.…”

Section: Resultssupporting

confidence: 55%

“…While studies have demonstrated that TACI is required for efficient TI responses to polysaccharide antigens (32,33,42), we find that TACI is dispensable for TI humoral responses to B. hermsii (Fig. 3).…”

Section: Discussionmentioning

confidence: 65%

Efficient B Cell Responses to Borrelia hermsii Infection Depend on BAFF and BAFFR but Not TACI

et al. 2014

View full text Add to dashboard Cite

bT cell-independent antibody responses develop rapidly, within 3 to 4 days, and are critical for preventing blood-borne pathogens from evolving into life-threatening infections. The interaction of BAFF, also known as BLyS, with its receptors BAFFR and TACI on B cells is critical for B cell homeostasis and function. Using a synthetic polysaccharide antigen, it has previously been shown that TACI is critical for T cell-independent antibody responses. To examine the role of BAFFR and TACI in T cell-independent antibody responses to an active infection, we utilized the Borrelia hermsii infection system. In this infection system, T cell-independent responses mediated by the B1b cell subset are critical for controlling bacteremia. We found that B1b cells express BAFFR and TACI and that the surface expression of both receptors is upregulated on B1b cells following exposure to whole B. hermsii cells. Surprisingly, we found that TACI ؊/؊ mice are not impaired either in specific antibody responses to B. hermsii or in controlling B. hermsii bacteremia. In contrast, TACI-deficient mice immunized with heat-killed type 3 serotype pneumococcus cells are impaired in generating pneumococcal polysaccharide-specific responses and succumb to challenge with live type 3 serotype pneumococcus, indicating that TACI is required for T cell-independent antibody responses to bacterial-associated polysaccharides. Although we have found that TACI is dispensable for controlling B. hermsii infection, mice deficient in BAFFR or BAFF exhibit impairment in B. hermsii-specific IgM responses and clearance of bacteremia. Collectively, these data indicate a disparity in the roles for TACI and BAFFR in primary T cell-independent antibody responses to bacterial pathogens.

show abstract

“…In contrast, the TACI knockout is defective in responses to T cell-independent antigens but not in B cell survival. On the contrary, B cell numbers are increased 2-fold in mice lacking TACI (24), and these mice develop autoimmunity and lymphomas with age (25). The role of the BAFF/BCMA interaction is less well understood, as mouse BAFF binds mouse BCMA poorly and mice deficient in BCMA have no obvious phenotype (23,26).…”

mentioning

confidence: 99%