The effect of environmental pollution on immune evasion checkpoints of SARS-CoV-2

ENGİN A. B., ENGİN E. D., ENGİN A.

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, cilt.81, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 81
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1016/j.etap.2020.103520
  • Dergi Adı: ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Environment Index, Greenfile, MEDLINE, Pollution Abstracts, Veterinary Science Database
  • Anahtar Kelimeler: Aryl hydrocarbon receptor, Environmental pollution, Indoleamine 2,3-dioxygenase, Severe acute respiratory syndrome coronavirus 2, Angiotensin-converting enzyme 2, Interferons, ARYL-HYDROCARBON RECEPTOR, POLYCYCLIC AROMATIC-HYDROCARBONS, SUBCELLULAR-LOCALIZATION, AH RECEPTOR, IN-VITRO, ACTIVATION, KYNURENINE, TRYPTOPHAN, INDUCTION, SEVERITY
  • Gazi Üniversitesi Adresli: Evet

Özet

Many diverse strategies allow and facilitate severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to evade antiviral innate immune mechanisms. Although the type I interferon (IFN) system has a critical role in restricting the dissemination of viral infection, suppression of IFN receptor signals by SARS-CoV-2 constitutes a checkpoint that plays an important role in the immune escape of the virus. Environmental pollution not only facilitates SARS-CoV-2 infection but also increases infection-associated fatality risk, which arises due to Systemic Aryl hydrocarbon Receptor (AhR) Activation Syndrome. The intracellular accumulation of endogenous kynurenic acid due to overexpression of the indoleamine 2,3-dioxygenase (IDO) by AhR activation induces AhRinterleukin-6 (IL-6)-signal transducers and activators of the transcription 3 (STAT3) signaling pathway. The AhR-IDO1-Kynurenine pathway is an important checkpoint, which leads to fatal consequences in SARS-CoV-2 infection and immune evasion in the context of Treg/Th17 imbalance and cytokine storm.