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NR4A nuclear receptors restrain B cell responses to antigen when second signals are absent or limiting

Authors
  • Tan, Corey1, 1
  • Hiwa, Ryosuke1
  • Mueller, James L.1
  • Vykunta, Vivasvan1
  • Hibiya, Kenta1
  • Noviski, Mark1, 1
  • Huizar, John1
  • Brooks, Jeremy F.1
  • Garcia, Jose1
  • Heyn, Cheryl1
  • Li, Zhongmei2, 1, 1, 3, 4, 5
  • Marson, Alexander2, 1, 1, 3, 4, 5
  • Zikherman, Julie1
  • 1 University of California, San Francisco, CA, USA , San Francisco (United States)
  • 2 J. David Gladstone Institutes, San Francisco, CA, USA , San Francisco (United States)
  • 3 University of California, Berkeley, CA, USA , Berkeley (United States)
  • 4 Parker Institute for Cancer Immunotherapy, San Francisco, CA, USA , San Francisco (United States)
  • 5 Chan Zuckerberg Biohub, San Francisco, CA, USA , San Francisco (United States)
Type
Published Article
Journal
Nature Immunology
Publisher
Springer Nature
Publication Date
Aug 31, 2020
Volume
21
Issue
10
Pages
1267–1279
Identifiers
DOI: 10.1038/s41590-020-0765-7
Source
Springer Nature
License
Yellow

Abstract

Antigen-activated B cells are short lived in the absence of a second signal provided by CD4+ T cells or cytokines. Zikherman and colleagues report that the NR4A family of nuclear receptors (NUR77 and NOR-1) are responsible for enforcing this ‘tolerance’ to self-antigen (signal 1 only) and explain, in part, why B cells are dependent upon a second signal.

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