![]() Moreover, a higher proportion of SARS-CoV-2 specific CD8 + T cells were detected in mild cases, and these CD8 + T cells have extensive and strong memory after the recovery period of COVID-19. However, these phenotypes between these two groups of CD4 + T cells of mild and moderate COVID-19 cases exhibit distinct functional signatures, distinct TCR sharing patterns, and may represent two divergent destinations for naive CD4 + T cells. Significant elevation and unusual phenotypes of CD4 + cells, which exhibit both a proliferative exhausted phenotype and a clonally expanded cytotoxic phenotype, were also observed in mild and moderate COVID-19 cases. It has been reported that the activated CD38 +HLA-DR +, CD8 + T cells, and CD38 +HLA-DR + CD4 + T cells that respond to virus infection are transiently increased in COVID-19 patients. The T cell response to SARS-CoV-2 peaks about one to two weeks after infection and can be detected during the months of recovery. Thus, T cells are an important target for assessing the degree of SARS-CoV-2 infection and disease progression. CD4 + T cells also promote the immune response of CD8 + T cells and the formation of long-term memory CD8 + T cells to exert antiviral capabilities effectively. The humoral immune response also includes CD4 + T cells that assist B cells in differentiating into plasma cells and subsequently producing antibodies specific to the viral antigen. The cellular immune response is mediated by T cells, which play a role in the direct killing of virus-infected cells via CD8 + cytotoxic T cells as well as helping to direct the overall immune response through CD4 + helper T cells. ![]() However, the specific T cell immune response against SARS-CoV-2, including the underlying mechanisms, remains unclear. A growing body of evidence suggests T cell responses are important for both early viral clearance as well as conferring protection through memory T cells for extended periods in COVID-19 patients. Many of the early studies on the immune response to SARS-CoV-2 have focused on neutralizing antibodies. The immune response to COVID-19 encompasses both B cell-mediated humoral responses through antibodies as well T cell activity. COVID-19 is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), which usually leads to respiratory infections, and severe cases develop into severe pneumonia or even death. Our study provides novel insights on TCR in COVID-19 with different convalescent phases, contributing to our understanding of the immune response induced by SARS-CoV-2.īeginning in December 2019, the coronavirus disease 2019 (COVID-19) outbreak has posed a serious threat to more than 200 countries worldwide and has caused more than 5.2 million deaths (. Finally, we found the dominant characteristic motifs of the CDR3 sequence between recovered COVID-19 and healthy control. More important, the TRBV6-5-TRBD2-TRBJ2-7 combination with high frequency was shared between CD4 + T and CD8 + T cells of different COVID-19 patients. ![]() We first identified CD4 + and CD8 + T cell clones with certain clonal expansion after infection, and then observed the preferential recombination usage of V(D) J gene segments in CD4 + and CD8 + T cells of COVID-19 patients with different convalescent stages. ![]() The TCR clustering and CDR3 annotation were exploited to discover groups of patient-specific TCR clonotypes with potential SARS-CoV-2 antigen specificities. ![]() In this study, using 5′RACE technology and PacBio sequencing, we analyzed the TCR repertoire of COVID-19 patients after recovery for 2 weeks and 6 months compared with the healthy donors. However, little has been known about the features of T cell response in convalescent COVID-19 patients. T cells play an essential role in the body’s fighting against the virus invasion, and the T cell receptor (TCR) is crucial in T cell-mediated virus recognition and clearance. Coronavirus disease 2019 (COVID-19) is a global infectious disease caused by the SARS-CoV-2 coronavirus. ![]()
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