| First Author | Schultz AB | Year | 2023 |
| Journal | Front Immunol | Volume | 14 |
| Pages | 1212190 | PubMed ID | 37559725 |
| Mgi Jnum | J:347968 | Mgi Id | MGI:7517457 |
| Doi | 10.3389/fimmu.2023.1212190 | Citation | Schultz AB, et al. (2023) T cell intrinsic STAT1 signaling prevents aberrant Th1 responses during acute toxoplasmosis. Front Immunol 14:1212190 |
| abstractText | Infection-induced T cell responses must be properly tempered and terminated to prevent immuno-pathology. Using transgenic mice, we demonstrate that T cell intrinsic STAT1 signaling is required to curb inflammation during acute infection with Toxoplasma gondii. Specifically, we report that mice lacking STAT1 selectively in T cells expel parasites but ultimately succumb to lethal immuno-pathology characterized by aberrant Th1-type responses with reduced IL-10 and increased IL-13 production. We also find that, unlike STAT1, STAT3 is not required for induction of IL-10 or suppression of IL-13 during acute toxoplasmosis. Each of these findings was confirmed in vitro and ChIP-seq data mining showed that STAT1 and STAT3 co-localize at the Il10 locus, as well as loci encoding other transcription factors that regulate IL-10 production, most notably Maf and Irf4. These data advance basic understanding of how infection-induced T cell responses are managed to prevent immuno-pathology and provide specific insights on the anti-inflammatory properties of STAT1, highlighting its role in shaping the character of Th1-type responses. |
