| First Author | Tan C | Year | 2020 |
| Journal | Nat Immunol | Volume | 21 |
| Issue | 10 | Pages | 1267-1279 |
| PubMed ID | 32868928 | Mgi Jnum | J:306652 |
| Mgi Id | MGI:6706691 | Doi | 10.1038/s41590-020-0765-7 |
| Citation | Tan C, et al. (2020) NR4A nuclear receptors restrain B cell responses to antigen when second signals are absent or limiting. Nat Immunol 21(10):1267-1279 |
| abstractText | 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. |
