Synapse - Impaired humoral immunity is associated with prolonged COVID-19 despite robust CD8 T cell responses

Impaired humoral immunity is associated with prolonged COVID-19 despite robust CD8 T cell responses Journal Article

Authors:	Lyudovyk, O.; Kim, J. Y.; Qualls, D.; Hwee, M. A.; Lin, Y. H.; Boutemine, S. R.; Elhanati, Y.; Solovyov, A.; Douglas, M.; Chen, E.; Babady, N. E.; Ramanathan, L.; Vedantam, P.; Bandlamudi, C.; Gouma, S.; Wong, P.; Hensley, S. E.; Greenbaum, B.; Huang, A. C.; Vardhana, S. A.
Article Title:	Impaired humoral immunity is associated with prolonged COVID-19 despite robust CD8 T cell responses
Abstract:	How immune dysregulation affects recovery from COVID-19 infection in patients with cancer remains unclear We analyzed cellular and humoral immune responses in 103 patients with prior COVID-19 infection, more than 20% of whom had delayed viral clearance. Delayed clearance was associated with loss of antibodies to nucleocapsid and spike proteins with a compensatory increase in functional T cell responses. High-dimensional analysis of peripheral blood samples demonstrated increased CD8(+) effector T cell differentiation and a broad but poorly converged COVID-specific T cell receptor (TCR) repertoire in patients with prolonged disease. Conversely, patients with a CD4(+) dominant immunophenotype had a lower incidence of prolonged disease and exhibited a deep and highly select COVID-associated TCR repertoire, consistent with effective viral clearance and development of T cell memory. These results highlight the importance of B cells and CD4(+) T cells in promoting durable SARS-CoV-2 clearance and the significance of coordinated cellular and humoral immunity for long-term disease control.
Keywords:	virus; cd4(+)
Journal Title:	Cancer Cell
Volume:	40
Issue:	7
ISSN:	1535-6108
Publisher:	Cell Press
Date Published:	2022-07-11
Start Page:	738
End Page:	753.e5
Language:	English
ACCESSION:	WOS:000827824400010
DOI:	10.1016/j.ccell.2022.05.013
PROVIDER:	wos
PMCID:	PMC9149241
PUBMED:	35679859
Notes:	Article -- Source: Wos