# Manipulating alpha(v) integrins on B cells to promote lung-resident B cell responses

> **NIH AI R01** · SEATTLE CHILDREN'S HOSPITAL · 2026 · $767,781

## Abstract

Project Summary/Abstract
Current vaccines against mucosal respiratory viruses, although effective at reducing disease severity, do not
provide protection at the respiratory tract, the site of infection, cannot effectively protect against multiple variants
of the viruses and do not induce long-lived immune response. Therefore, there is a need to design more effective
vaccines that can trigger durable and protective immunity against mucosal respiratory viruses, directly at
respiratory sites. However, a major barrier for progress in this area is that the signals that regulate immune
responses at respiratory sites remain unclear. Viral infection can induce B cell mediated immune response in
the lungs, that result in mucosal antibodies capable of targeting multiple antigenic variants on viruses and long-
lived memory B cells. Therefore, our objective in this renewal application is to understand how viral infection
elicits long-lived and protective B cell responses in the lungs and design strategies to mimic these therapeutically.
 Our R01 studies revealed a new mechanism regulating B cell responses in the lungs during viral infection. In
previous work, we showed that a family of integrins, αv integrins, expressed on B cells, restrain toll-like receptor
(TLR) signaling response of B cells to TLR ligands. TLR ligands are integral components of viral products and
mice with deletion of αv from B cells, showed increase in B cell TLR signaling and increase in long-lived
protective B cell responses after immunization with viral antigens. In recent R01 studies, we found that this
function of αv also regulates long-lived B cell responses locally in the lungs after viral infection. Deletion of B cell
αv integrin, in mice (αv-CD19 mice), promoted sustained increase in lung-resident GC and memory B cells, after
influenza infection. These B cells can target multiple influenza antigens. Moreover, we find that αv antagonists
can also improve B cell responses in mice and in human B cell

## Key facts

- **NIH application ID:** 11295936
- **Project number:** 2R01AI151167-05A1
- **Recipient organization:** SEATTLE CHILDREN'S HOSPITAL
- **Principal Investigator:** Mridu  Acharya
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** AI
- **Fiscal year:** 2026
- **Award amount:** $767,781
- **Award type:** 2
- **Project period:** 2020-08-01T00:00:00 → 2031-03-31T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11295936

## Citation

> US National Institutes of Health, RePORTER application 11295936, Manipulating alpha(v) integrins on B cells to promote lung-resident B cell responses (2R01AI151167-05A1). Retrieved via AI Analytics 2026-06-05 from https://api.ai-analytics.org/grant/nih/11295936. Licensed CC0.

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