Programmed cell death 1 positive lymphocytes at palate tonsils in the elder patients with chronic tonsillitis

Yuki Fujihara,Koji Yamanegi,Yasuyuki Nagasawa,Ayu Yoshida,Yukako Goto,Shunsuke Kumanishi,Hiroyuki Futani,Shigeo Fukunishi,Shinichi Yoshiya,Hiroshi Nishiura

doi:10.1016/j.bbrep.2020.100898

Abstract

Circulating lymphocytes infiltrate into local foci at the inflammatory phase of acute wound healing for activation of the immune system and express an immune checkpoint protein programmed cell death 1 (PD-1) at the resolution phase for inactivation of the immune system. Conversely, the PD-1 expression was still found even on circulating lymphocytes of the elder patients with chronic tonsillitis at the palliative stage. Recently, an adhesion G protein coupled receptor 56 (GPR56) was reported to at least work as a proliferation factor for infiltrated lymphocytes into local foci at the resolution phase of acute wound healing. To preliminary examine a similar role of PD-1 and GPR56 at local foci at chronic inflammation, palate tonsils were prepared from small amounts of patients with chronic tonsillitis and tonsillar hypertrophy. A positive relationship of RNA expression might be observed between PD-1 and GPR56 in the elder patients with chronic tonsillitis. In regard to immunohistopathological findings, there were huge and small amounts of PD-1 and GPR56 expression at the marginal zone of lymphoid follicles of palate tonsils with chronic tonsillitis. Moreover, the positive relationship of RNA expression between PD-1 and GPR56 confirmed in large numbers of the elder patients with chronic tonsillitis. Probably, GPR56 participates in a supplement of PD-1+ lymphocytes to circulating bloods of the elder patients with chronic tonsillitis through a lymphocyte cell maintenance system at the marginal zone of the lymphoid follicles of palate tonsils.

Highlights

Acute inflammation is often divided into three phases to explain the wound healing process for a short period: the initiation, the inflamma tion, and the resolution [1,2,3]
The STAT1/2 heterodimers bind to IRF9 to form IFN-stimulated gene factor 3, which binds to IFN-stimulated response elements in the pro moters of IFN-induced genes to initiate their transcription
It is likely that programmed cell death 1 (PD-1) expression is regulated via IFN receptors and TCR by both innate and acquired immune responses to antigens

Summary

Introduction

Acute inflammation is often divided into three phases to explain the wound healing process for a short period: the initiation, the inflamma tion, and the resolution [1,2,3]. Circulating lymphocytes are believed to infiltrate into local foci at the inflammation phase of acute wound healing for identifying foreign antigens on M1 macrophages activated by type II interferon (IFN gamma) in the mature immune system [4]. Type II IFN is produced in lymphocytes and natural killer cells for enhance ment of innate immunity at the inflammation phase of acute wound healing. Infiltrated lymphocytes express an immune checkpoint protein programmed cell death 1 (PD-1) for a short period through an induction of type I IFNs (IFN alpha and IFN beta) at the resolution phase of acute wound healing. Type I IFNs are produced in neutrophils and M2 macrophages for regulation of the mature immune system at the resolution phase of acute wound healing. PD-1 ligand 1/2 (PD-L1/L2) on M2 macrophages plays a key role in the lim itation of excessive activation of the mature immune system at the res olution phase of acute wound healing [5]

Methods

Results

Conclusion