TACI-Ig neutralizes molecules critical for B cell development and autoimmune disease. impaired B cell maturation in mice lacking BLyS.
By J. Gross, S. Dillon, S. Mudri, J. Johnston, A. Littau, R. Roque, M. Rixon, Ole Schou, K. Foley, H. Haugen and 8 more. Immunity, 2001
679 citations recorded by the source corpus.
Subfields: Immunology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/af6c69e4519b589f80e1d5986009da00d279528a
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In Immunology
Citations in the corpus
- Association of BAFF/BLyS overexpression and altered B cell differentiation with Sjögren's syndrome. (2002, background): “However, recent work has shown that a factor other than BAFF interacting with TACI might be responsible for B-1 cell development/survival (22).”
- 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): “ripheral B cell development occurs in mice deficient in BLyS (6)”
- NF-κB and the immune response (2006, background): “Indeed, BAFF knockout mice exhibit a complete failure of transitional B-cell maturation, which mirrors that seen in Bcl-XL knockout mice (Motoyama et al., 1995; Gross et al., 2001; Schiemann et al., 2001).”