tetano
Editor, Senior Moderator
Cell Commun Signal
. 2022 Jun 2;20(1):79.
doi: 10.1186/s12964-022-00856-w.
A comprehensive review about immune responses and exhaustion during coronavirus disease (COVID-19)
Rebar N Mohammed[SUP] 1 2 [/SUP], Rozita Tamjidifar[SUP] 3 [/SUP], Heshu Sulaiman Rahman[SUP] 4 5 [/SUP], Ali Adili[SUP] 6 [/SUP], Shadi Ghoreishizadeh[SUP] 3 [/SUP], Hossein Saeedi[SUP] 3 [/SUP], Lakshmi Thangavelu[SUP] 7 [/SUP], Navid Shomali[SUP] 3 [/SUP], Ramin Aslaminabad[SUP] 8 [/SUP], Faroogh Marofi[SUP] 3 [/SUP], Mina Tahavvori[SUP] 3 [/SUP], Svetlana Danishna[SUP] 9 [/SUP], Morteza Akbari[SUP] 10 [/SUP], Gülinnaz Ercan[SUP] 11 12 [/SUP]
Affiliations
Abstract
Coronavirus disease (COVID-19) is a viral infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. The infection was reported in Wuhan, China, in late December 2019 and has become a major global concern due to severe respiratory infections and high transmission rates. Evidence suggests that the strong interaction between SARS-CoV-2 and patients' immune systems leads to various clinical symptoms of COVID-19. Although the adaptive immune responses are essential for eliminating SARS-CoV-2, the innate immune system may, in some cases, cause the infection to progress. The cytotoxic CD8[SUP]+[/SUP] T cells in adaptive immune responses demonstrated functional exhaustion through upregulation of exhaustion markers. In this regard, humoral immune responses play an essential role in combat SARS-CoV-2 because SARS-CoV-2 restricts antigen presentation through downregulation of MHC class I and II molecules that lead to the inhibition of T cell-mediated immune response responses. This review summarizes the exact pathogenesis of SARS-CoV-2 and the alteration of the immune response during SARS-CoV-2 infection. In addition, we've explained the exhaustion of the immune system during SARS-CoV-2 and the potential immunomodulation approach to overcome this phenomenon. Video Abstract.
Keywords: COVID-19; Immune system exhaustion; SARS-CoV-2; T cells.
. 2022 Jun 2;20(1):79.
doi: 10.1186/s12964-022-00856-w.
A comprehensive review about immune responses and exhaustion during coronavirus disease (COVID-19)
Rebar N Mohammed[SUP] 1 2 [/SUP], Rozita Tamjidifar[SUP] 3 [/SUP], Heshu Sulaiman Rahman[SUP] 4 5 [/SUP], Ali Adili[SUP] 6 [/SUP], Shadi Ghoreishizadeh[SUP] 3 [/SUP], Hossein Saeedi[SUP] 3 [/SUP], Lakshmi Thangavelu[SUP] 7 [/SUP], Navid Shomali[SUP] 3 [/SUP], Ramin Aslaminabad[SUP] 8 [/SUP], Faroogh Marofi[SUP] 3 [/SUP], Mina Tahavvori[SUP] 3 [/SUP], Svetlana Danishna[SUP] 9 [/SUP], Morteza Akbari[SUP] 10 [/SUP], Gülinnaz Ercan[SUP] 11 12 [/SUP]
Affiliations
- PMID: 35655192
- DOI: 10.1186/s12964-022-00856-w
Abstract
Coronavirus disease (COVID-19) is a viral infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. The infection was reported in Wuhan, China, in late December 2019 and has become a major global concern due to severe respiratory infections and high transmission rates. Evidence suggests that the strong interaction between SARS-CoV-2 and patients' immune systems leads to various clinical symptoms of COVID-19. Although the adaptive immune responses are essential for eliminating SARS-CoV-2, the innate immune system may, in some cases, cause the infection to progress. The cytotoxic CD8[SUP]+[/SUP] T cells in adaptive immune responses demonstrated functional exhaustion through upregulation of exhaustion markers. In this regard, humoral immune responses play an essential role in combat SARS-CoV-2 because SARS-CoV-2 restricts antigen presentation through downregulation of MHC class I and II molecules that lead to the inhibition of T cell-mediated immune response responses. This review summarizes the exact pathogenesis of SARS-CoV-2 and the alteration of the immune response during SARS-CoV-2 infection. In addition, we've explained the exhaustion of the immune system during SARS-CoV-2 and the potential immunomodulation approach to overcome this phenomenon. Video Abstract.
Keywords: COVID-19; Immune system exhaustion; SARS-CoV-2; T cells.