Cellular signaling pathways of T cells in giant cell arteritis.

Abstract

Giant cell arteritis (GCA) is a commonly occurring large vacuities characterized by angiopathy of medium and large-sized vessels. GCA granulomatous formation plays an important role in the pathogenesis of GCA. Analysis of T cell lineages and signaling pathways in GCA have revealed the essential role of T cells in the pathology of GCA. T cells are the dominant population present in GCA lesions. CD4+ T cell subtypes that are present include Th1, Th2, Th9, Th17, follicular helper T (Tfh) cells, and regulatory T (Treg) cells. CD8 T cells can primarily differentiate into cytotoxic CD8+ T lymphocytes and Treg cells. The instrumental part of GCA is the interplay between dendritic cells, macrophages and endothelial cells, which can result in the vascular injury and the characteristics granulomatous infiltrates formation. During the inflammatory loop of GCA, several signaling pathways have been reported to play an essential role in recruiting, activating and differentiating T cells, including T-cell receptor (TCR) signaling, vascular endothelial growth factor (VEGF)-Jagged-Notch signaling and the Janus kinase and signal transducer and activator of transcription (STAT) pathway (JAK-STAT) pathway. In this review, we have focused on the role of T cells and their potential signaling mechanism (s) that are involved in the pathogenesis of GCA. A better understanding of the role of T cells mediated complicated orchestration during the homeostasis and the changes could possibly favor developments of novel treatment strategies against immunological disorders associated with GCA.