Roles of CCR10 in regulation of IgA responses to SARS-CoV-2 infection

NIH RePORTER · NIH · R21 · $232,500 · view on reporter.nih.gov ↗

Abstract

Summary The novel coronavirus SARS-CoV-2 causes the COVID-19 pandemic. The virus infects through the respiratory tracts. While most COVID-19 patients display no or mild clinical symptoms, a small percentage develop severe immune-mediated pathological complications, which could lead to injury and failure of the lung and various important organs and account for the majority of COVID-19 deaths. Understanding how different components of the immune system are involved in the viral control and pathological development is crucial for our understanding of pathogenesis of the disease and developing preventative and therapeutic strategies. In this grant application, we propose to dissect involvement of CCR10-regulated mucosal IgA antibody responses in SARS-CoV-2 infection clearance versus immune-pathological development using mouse models in two specific aims. In the Aim 1, we will determine the role of CCR10-regulated primary mucosal IgA responses in SARS-CoV-2-infection clearance and immunopathological development. In the Aim 2, we will determine the role of CCR10- regulated memory mucosal IgA responses in SARS-CoV-2 infection and immune-pathological development. The findings of our proposed study will not only help our understanding of involvement of mucosal IgA responses in clearance of the viral infection and pathogenesis of COVID-19 but also provide a guide on future development of vaccination strategies to induce proper IgA response for the disease prevention.

Key facts

NIH application ID
10442019
Project number
1R21AI169430-01
Recipient
UNIVERSITY OF TEXAS HLTH SCIENCE CENTER
Principal Investigator
YAN XIANG
Activity code
R21
Funding institute
NIH
Fiscal year
2022
Award amount
$232,500
Award type
1
Project period
2022-05-16 → 2024-04-30