Abstract
γδ (gamma–delta) T cells, a small population of unconventional T cells, have been found in central nervous system lesions of multiple sclerosis (MS) patients, but their function in disease activity is not clearly understood. Previous studies in experimental autoimmune encephalomyelitis (EAE) were inconsistent in identifying their specific roles in suppressing or promoting disease pathogenesis. Emerging advancements in the biology of γδ T cells especially in the context of their being the major initial producers of IL-17, suggested their crucial role in pathogenesis of EAE. In addition, γδ T cells express high levels of IL-23R and IL-1R, which further enhance their effector functions in the pathogenesis of EAE. Nonetheless, activated heterogeneous γδ T cells display functional dichotomy, which is crucial in determining the outcomes of tissue inflammation in EAE. In this review, we discussed recent advances in understanding the biology of γδ T cells in tissue inflammation as well as their roles in suppressing or promoting the development of EAE.
Highlights
Γδ T cells comprise a small fraction (~1–5%) of the total blood lymphocytes of mice and humans and are more commonly localized in mucosal tissue and skin where they constitute a major population of lymphocytes [1]
A number of studies have demonstrated a potential role of γδ T cells in the induction and maintenance of demyelinating central nervous system (CNS) inflammation. γδ T cells are multifaceted cells, which are equipped with variety of functions to potentially influence all levels of inflammation by recognizing diverse array of antigens, rapid production of inflammatory mediators, and influencing the differentiation of their αβ counterparts
The identification of IL-17-producing inflammatory γδ T cells suggested their pathogenic role in EAE
Summary
Previous studies in experimental autoimmune encephalomyelitis (EAE) were inconsistent in identifying their specific roles in suppressing or promoting disease pathogenesis. Emerging advancements in the biology of γδ T cells especially in the context of their being the major initial producers of IL-17, suggested their crucial role in pathogenesis of EAE. Γδ T cells express high levels of IL-23R and IL-1R, which further enhance their effector functions in the pathogenesis of EAE. Activated heterogeneous γδ T cells display functional dichotomy, which is crucial in determining the outcomes of tissue inflammation in EAE.
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