PD-L1 correlates with chemokines and cytokines in gingival crevicular fluid from healthy and diseased sites in subjects
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BMC Research Notes Open Access
RESEARCH NOTE
PD‑L1 correlates with chemokines and cytokines in gingival crevicular fluid from healthy and diseased sites in subjects with periodontitis Andrew Shelby1, Chandler Pendleton2, Emma Thayer3, Georgia K. Johnson1, Xian Jin Xie2,3 and Kim A. Brogden1,3*
Abstract Objective: PD-L1 is an immune checkpoint molecule that regulates immune and inflammatory responses. While cells of periodontal tissues express PD-L1, its presence in GCF is not known. The purpose of this study was to measure the PD-L1 values in GCF and correlate values with the presence of chemokine and cytokine values from periodontally diseased subjects and periodontally healthy subjects. Results: PD-L1 values (pg/30 s), determined in triplicate using a fluorescent microparticle-based immunoassay ranged from 0.04–31.65 pg/30 s. PD-L1 correlated with 15 out of 22 chemokine and cytokine responses. In 85 healthy sites in 31 subjects, PD-L1 values were negatively correlated with IL6, CXCL8, IL10, and CCL3 values. In 53 diseased sites in 20 subjects, PD-L1 values were positively correlated with CCL11, CSF2, IFNG, IL1A, IL1B, IL2, IL7, IL15, and CCL5 values and negatively correlated with IL12A and IL5 values. Gene ontology (GO) annotations identified roles of PD-L1 in Th1 and Th2 activation and T-cell exhaustion signaling canonical pathways. PD-L1 values were correlated with the expression of chemokines and cytokines, which likely regulates immune cell trafficking and protects the periodontium from uncontrolled immune responses to pathogens and inflammation-induced tissue damage. Keyword: PD-1, PD-L1, Cytokine, Periodontal disease, Periodontitis Introduction PD-L1 is a 33.28 kDa type I transmembrane protein expressed on the surface of immune and non-immune cells [1–3]. It is a co-inhibitory and immune checkpoint protein that binds to receptor PD-1 on T-cells [4]. The PD-L1/PD-1 interaction regulates the balance between co-stimulatory and co-inhibitory immune signals and maintains the breadth and magnitude of immune responses. Increased expression of PD-L1 inhibits T-cell *Correspondence: kim‑[email protected] 1 Department of Periodontics, College of Dentistry, University of Iowa, Iowa City, IA, USA Full list of author information is available at the end of the article
proliferation, reduces T-cell survival, inhibits cytokine release, promotes T-cell apoptosis, and leads to T-cell exhaustion and immunosuppression [5, 6]. Although this mechanism is thought to occur in periodontal disease to protect against inflammation-induced tissue damage [7], there are no known reports of PD-L1 detected in GCF or no known correlations of PD-L1 with the presence of chemokines and cytokines in GCF. Periodontal patients often demonstrate a reduced immune response that allows periodontopathogens to exert an exaggerated suppressive mechanism on T-cell function [8–15]. Demonstrating the presence of PD-L1 in GCF would support its role in protecting tissue against
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