Role of Chemokines in Endocrine Autoimmune Diseases

Abstract

Chemokines are a group of peptides of low molecular weight that induce the chemotaxis of different leukocyte subtypes. The major function of chemokines is the recruitment of leukocytes to inflammation sites, but they also play a role in tumoral growth, angiogenesis, and organ sclerosis.

IL-17A increases the expression of proinflammatory chemokines in human pancreatic islets

“…Chemokines play an important role in the recruitment of leucocytes, monocytes and activated T cells to areas of inflammation in autoimmune diseases [43,44]. CXCL1 is important in the recruitment of neutrophils, which infiltrate the pancreas and are present in low numbers in the periphery in diabetic patients [45].…”

Negative feedback regulation of cellular antiviral signaling by RBCK1-mediated degradation of IRF3

“…These observations suggest that RBCK1 viral replication in infected and neighboring uninfected cells. However, uncontrolled excessive production of type I IFNs significantly contributes to chronic inflammation and autoimmune diseases, underscoring the importance of negative regulation of type I IFN [35][36][37][38]. The host innate immune system has developed distinct strategies to ensure proper production of type I IFNs following viral infection [ [18][19][20][21][22][23][24][25][26].…”

Anti-coreceptor therapy drives selective T cell egress by suppressing inflammation-dependent chemotactic cues

“…Islet T cell recruitment is regulated in part by expression of chemokine receptors (CKRs) and corresponding ligands, especially CXCR3 (and CXCL9/10), CCR5 (and CCL3/4/5), and CCR7 (and CCL19/21) (11)(12)(13)(14). Once islet T cell residency is established, T cell receptor (TCR) signaling drives expression of proinflammatory cytokines, which further stimulates local production of chemotactic ligands (15)(16)(17)(18)(19).…”

“…T cell-derived IFN-γ for instance, upregulates CXCL9 and CXCL10 production by islet-resident cells, including β cells, resulting in further recruitment of pathogenic CXCR3 + T H 1 cells, and innate effectors (20)(21)(22). Such feed-forward circuits are thought to be common among autoimmune diseases (11,15,18).…”