Journal
NATURE IMMUNOLOGY
Volume 21, Issue 10, Pages 1267-+Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41590-020-0765-7
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Funding
- NIAID [5T32AI007334-28]
- NIAMS [R01AR069520]
- Rheumatology Research Foundation Innovative Research Award
- Uehara Memorial Foundation Research Fellowship
- Burroughs Wellcome Fund
- Cancer Research Institute Lloyd J. Old STAR grant
- Innovative Genomics Institute
- Parker Institute for Cancer Immunotherapy
- 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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