Inhibitory immune checkpoint molecules and exhaustion of T cells in COVID-19

Title:

Inhibitory immune checkpoint molecules and exhaustion of T cells in COVID-19

Creator:

Barnova, Martina, Bobcakova, Anna, Urdova, Veronika, Kosturiak, Radovan, Kapustova, Lenka, Dobrota, Dusan, and Jesenak, Milos

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:67283f06-af20-4e50-a9da-6fe359a11829
uuid:67283f06-af20-4e50-a9da-6fe359a11829
doi:10.33549/physiolres.934757

Subject:

inhibitory checkpoint molecules, T cell exhaustion, COVID-19, and SARS-CoV-2

Type:

model:article and TEXT

Format:

počítač and online zdroj

Description:

COVID-19 (Coronavirus Disease) is an infectious disease caused by the coronavirus SARS-CoV-2 (Severe acute respiratory syndrome Coronavirus 2), which belongs to the genus Betacoronavirus. It was first identified in patients with severe respiratory disease in December 2019 in Wuhan, China. It mainly affects the respiratory system, and in severe cases causes serious lung infection or pneumonia, which can lead to the death of the patient. Clinical studies show that SARS-CoV-2 infection in critical cases causes acute tissue damage due to a pathological immune response. The immune response to a new coronavirus is complex and involves many processes of specific and non-specific immunity. Analysis of available studies has shown various changes, especially in the area of specific cellular immunity, including lymphopenia, decreased T cells (CD3+, CD4+ and CD8+), changes in the T cell compartment associated with symptom progression, deterioration of the condition and development of lung damage. We provide a detailed review of the analyses of immune checkpoint molecules PD-1, TIM-3, LAG-3 CTLA-4, TIGIT, BTLA, CD223, IDO-1 and VISTA on exhausted T cells in patients with asymptomatic to symptomatic stages of COVID-19 infection. Furthermore, this review may help to better understand the pathological T cell immune response and improve the design of therapeutic strategies for patients with SARS-CoV-2 infection.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Coverage:

S227-S247

Source:

Physiological research | 2021 Volume:70 | Number:Supplement 2

Harvested from:

CDK

Metadata only:

false