An Essential Role for BAFF in the Normal Development of B Cells Through a BCMA-Independent Pathway

By Barbara J. Schiemann, J. Gommerman, K. Vora, T. Cachero, Svetlana Shulga-Morskaya, Max Dobles, E. Frew, M. Scott. Science, 2001

1,170 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/b8bf3b0a11a0438efac44937daf9fb2abd047f96

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In Immunology

1. S. Ghosh
2. M. Hayden
3. A. West
4. F. Mackay
5. A. Cerutti
6. J. Tschopp
7. C. Mackay
8. Shizuo Akira

Citations in the corpus

• Mutations in TNFRSF13B encoding TACI are associated with common variable immunodeficiency in humans (2005, background): “BAFF-deficient mice have fewer peripheral B cells and impaired T cell–dependent and –independent antibody response”
• To be, or not to be: NF-κB is the answer – role of Rel/NF-κB in the regulation of apoptosis (2003, background): “NF-kB has also been implicated in attenuating apoptosis in response to the cytokine BAFF (also known as BlyS), which is necessary for peripheral B-cell development, as illustrated by the phenotype of mice expressing nonfunctional BAFF receptor (BAFF-R) or lacking BAFF (Schiemann et al., 2001).”
• Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome. (2002, background): “Moreover, B cell maturation in BAFF-deficient mice is arrested at the transitional type I (T1) immature B cell stage, which precedes the T2 B cell stage (21, 22).”
• NF-κB and the immune response (2006, background): “Although both canonical and noncanonical NF-kB pathways are functional during B-cell development, recent work (Batten et al., 2000; Schiemann et al., 2001; Claudio et al., 2002) has underscored the importance of BAFF ligation in selectively activating the non-canonical NF-kB pathway and the…”
• TACI is mutant in common variable immunodeficiency and IgA deficiency (2005, background): “Mice deficient in BAFF and BAFF-R have severe failure of B-cell differentiation and very low levels of serum Ig”
• DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL (2002, background): “, BLyS deficiency impairs both TD and TI IgG and IgA productio”
• NF-κB1 p50 Is Required for BLyS Attenuation of Apoptosis but Dispensable for Processing of NF-κB2 p100 to p52 in Quiescent Mature B Cells1 (2003, background): “It is possible that BR3 mediates the BLyS signals for p100 processing in mature B cells, given its essential role in peripheral B cell development (5, 6) and in the activation of p100 processing in immature T1 B cells (17, 18).”