Abstract
V-domain Ig suppressor of T cell activation (VISTA) is a novel coinhibitory immune checkpoint molecule that maintains immune homeostasis. The present study explored the role of VISTA in human and murine inflammatory tissues of apical periodontitis (AP). VISTA was upregulated in inflammatory tissues of human AP. In mice, the expression of VISTA gradually increased with the development of mouse experimental apical periodontitis (MAP), the CD3+ T cells, CD11b+ myeloid cells, and FOXP3+ regulatory T cells also gradually accumulated. Moreover, a blockade of VISTA using a mouse in vivo anti-VISTA antibody aggravated periapical bone loss and enhanced the infiltration of immune cells in an experimental mouse periapical periodontitis model. The collective results suggest that VISTA serves as a negative regulator of the development and bone loss of apical periodontitis.
Highlights
Apical periodontitis (AP) is characterized by sustained local inflammation around the root apex, which results in periapical alveolar bone loss [1]
Immunostaining indicated that the number of V-domain Ig suppressor of T cell activation (VISTA)-positive cells sharply rose in inflamed periapical tissues compared with that of healthy oral mucosa (Figure 1C)
We first demonstrated that VISTA is involved in the development of periapical periodontitis (AP)
Summary
Apical periodontitis (AP) is characterized by sustained local inflammation around the root apex, which results in periapical alveolar bone loss [1]. Exogenous bacteria activate the host immune system, leading to the recruitment of immune cells such as neutrophils, macrophages and T cells around the root apex [2]. These immune cells secrete inflammatory chemokines and cytokines to modulate the inflammatory process [3]. The infection is not completely obliterated by the host defense; a sustained chronic inflammatory immune microenvironment involving bacterial virulence, immune cells, chemokines and cytokines is established (Figure 1A) [4]. The innate immunoregulatory response against inflammation is mediated by other subsets of immune cells such as regulatory T cells (Tregs), which lead to the dampening of inflammatory and osteoclastogenic pathways [7]. Many studies have successfully altered inflammatory bone loss by modulating the reaction of immune cells [8, 9]
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