| First Author | Ozga AJ | Year | 2022 |
| Journal | Immunity | Volume | 55 |
| Issue | 1 | Pages | 82-97.e8 |
| PubMed ID | 34847356 | Mgi Jnum | J:321765 |
| Mgi Id | MGI:6874621 | Doi | 10.1016/j.immuni.2021.11.002 |
| Citation | Ozga AJ, et al. (2022) CXCL10 chemokine regulates heterogeneity of the CD8(+) T cell response and viral set point during chronic infection. Immunity 55(1):82-97.e8 |
| abstractText | CD8(+) T cells responding to chronic infection adapt an altered differentiation program that provides some restraint on pathogen replication yet limits immunopathology. This adaptation is imprinted in stem-like cells and propagated to their progeny. Understanding the molecular control of CD8(+) T cell differentiation in chronic infection has important therapeutic implications. Here, we find that the chemokine receptor CXCR3 is highly expressed on viral-specific stem-like CD8(+) T cells and that one of its ligands, CXCL10, regulates the persistence and heterogeneity of responding CD8(+) T cells in spleens of mice chronically infected with lymphocytic choriomeningitis virus. CXCL10 is produced by inflammatory monocytes and fibroblasts of the splenic red pulp, where it grants stem-like cells access to signals promoting differentiation and limits their exposure to pro-survival niches in the white pulp. Consequently, functional CD8(+) T cell responses are greater in Cxcl10(-/-) mice and are associated with a lower viral set point. |
