TGF-β Receptor Controls B Cell Responsiveness and Induction of IgA In Vivo
By B. B. Cazac, J. Roes. 2000
396 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/c32b7f38f4bca1ab1989dbc2ded997f62cb03b4a
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In Immunology
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In Pathology and Forensic Medicine
Citations in the corpus
- Tumor-infiltrating lymphocytes in the immunotherapy era (2020, background): “But even more when clustered together with T cells in well-organized TLSs, initiated by chemokine CXCL13.”
- The regulation of IgA class switching (2008, background): “Indeed, B-cell-conditional TGFβRII-deficient mice, SMAD2-deficient and SMAD3-deficient mice produce less IgA under steady-state and immunizing conditions in both systemic and mucosal sites, including the Peyer's patche”
- FOLLICULAR HELPER T CELLS: LINEAGE AND LOCATION (2009, background): “Antigen-specific inducible Treg cells producing TGF-b and IL-10 could direct IgA switch as Tfh10 cells (Cazac and Roes, 2000; Dullaers et al., 2009).”
- Cell Contact–Dependent Immunosuppression by Cd4+Cd25+Regulatory T Cells Is Mediated by Cell Surface–Bound Transforming Growth Factor β (2001, background): “In addition, mice with a conditioned knockout of TGF-� R type II gene, in which receptor signaling is inactivated in a B cell‐specific manner, develop anti-double stranded DNA autoantibodies because of the lack of ability to respond to suppressor T cells producing TGF-� ( 25 ).”