Cxcl17−/− mice develop exacerbated disease in a T cell‐dependent autoimmune model.

Autor: Hernández‐Ruiz, Marcela, Othy, Shivashankar, Herrera, Carolina, Nguyen, Hong‐Tam, Arrevillaga‐Boni, Gerardo, Catalan‐Dibene, Jovani, Cahalan, Michael D., Zlotnik, Albert
Předmět:
Zdroj: Journal of Leukocyte Biology; May2019, Vol. 105 Issue 5, p1027-1039, 13p
Abstrakt: CXCL17 is a homeostatic chemokine in the mucosa known to chemoattract dendritic cells and macrophages but can also be expressed elsewhere under inflammatory conditions. Cxcl17−/− mice have lower numbers of macrophages or dendritic cells in mucosal tissues. CXCL17 is also able to chemoattract suppressor myeloid cells that can recruit regulatory T cells. To explore a possible role of Cxcl17 in T cells, we studied T cell populations from Cxcl17−/− or wild‐type (WT) littermate mice. Cxcl17−/− mice have higher numbers of CD4+ and CD8+ T cells in spleen and lymph nodes (LNs). Upon activation, they produce higher levels of several proinflammatory cytokines and chemokines. Furthermore, a Cxcl17−/− mouse developed exacerbated disease in a T cell‐dependent model of experimental autoimmune encephalomyelitis (EAE). By 18 days after immunization with myelin oligodendrocyte peptide, only 44% of Cxcl17−/− mice were still alive vs. 90% for WT mice. During EAE, Cxcl17−/− mice exhibited higher numbers of lymphoid and myeloid cells in spleen and LNs, whereas they had less myeloid cell infiltration in the CNS. Cxcl17−/− mice also had higher levels of some inflammatory cytokines in serum, suggesting that they may be involved in the poor survival of these mice. Abnormal T cell function may reflect altered myeloid cell migration, or it could be due to altered T cell development in the thymus. We conclude that CXCL17 is a novel factor regulating T cell homeostasis and function. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index