| First Author | Symonds AL | Year | 2020 |
| Journal | Life Sci Alliance | Volume | 3 |
| Issue | 9 | PubMed ID | 32709717 |
| Mgi Jnum | J:341791 | Mgi Id | MGI:6729563 |
| Doi | 10.26508/lsa.202000766 | Citation | Symonds AL, et al. (2020) Egr2 and 3 control inflammation, but maintain homeostasis, of PD-1(high) memory phenotype CD4 T cells. Life Sci Alliance 3(9) |
| abstractText | The transcription factors Egr2 and 3 are essential for controlling inflammatory autoimmune responses of memory phenotype (MP) CD4 T cells. However, the mechanism is still unclear. We have now found that the Egr2(+) subset (PD-1(high) MP) of MP CD4 T cells expresses high levels of checkpoint molecules (PD-1 and Lag3) and also markers of effector T cells (CXCR3 and ICAM-1). Egr2/3 are not required for PD-1(high) MP CD4 cell development but mediate a unique transcriptional programme that effectively controls their inflammatory responses, while promoting homeostatic proliferation and adaptive responses. Egr2 negative PD-1(high) MP CD4 T cells are impaired in homeostatic proliferation and adaptive responses against viral infection but display inflammatory responses to innate stimulation such as IL-12. PD-1(high) MP CD4 T cells have recently been implicated in rheumatoid arthritis pathogenesis, and we have now found that Egr2 expression is reduced in PD-1(high) MP CD4 T cells from patients with active rheumatoid arthritis compared with healthy controls. These findings demonstrate that Egr2/3 control the inflammatory responses of PD-1(high) MP CD4 T cells and maintain their adaptive immune fitness. |
