4.7 Article

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

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NATURE IMMUNOLOGY
卷 21, 期 10, 页码 1267-+

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NATURE PORTFOLIO
DOI: 10.1038/s41590-020-0765-7

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资金

  1. NIAID [5T32AI007334-28]
  2. NIAMS [R01AR069520]
  3. Rheumatology Research Foundation Innovative Research Award
  4. Uehara Memorial Foundation Research Fellowship
  5. Burroughs Wellcome Fund
  6. Cancer Research Institute Lloyd J. Old STAR grant
  7. Innovative Genomics Institute
  8. Parker Institute for Cancer Immunotherapy
  9. HHMI Medical Research Fellows program

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Antigen stimulation (signal 1) triggers B cell proliferation and primes B cells to recruit, engage and respond to T cell help (signal 2). Failure to receive signal 2 within a defined time window results in B cell apoptosis, yet the mechanisms that enforce dependence on co-stimulation are incompletely understood. Nr4a1-3 encode a small family of orphan nuclear receptors that are rapidly induced by B cell antigen receptor stimulation. Here, we show that Nr4a1 and Nr4a3 play partially redundant roles to restrain B cell responses to antigen in the absence of co-stimulation and do so, in part, by repressing the expression of BATF and, consequently, MYC. The NR4A family also restrains B cell access to T cell help by repressing expression of the T cell chemokines CCL3 and CCL4, as well as CD86 and ICAM1. Such NR4A-mediated regulation plays a role specifically under conditions of competition for limiting T cell help.

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