ICAM-1 expression is required for regulatory T cell localization in the lungs of M. tuberculosis infected mice (97.2)

Abstract

Abstract Mycobacterium tuberculosis (Mtb) is a widespread human pathogen that persists in the lung of latently infected individuals. Control over Mtb infection relies upon migration of leukocytes into the granuloma. We hypothesized that the adhesion molecule ICAM-1 plays a role in the migration, retention and interaction of leukocytes during Mtb infection. While previous studies in ICAM-1−/− mice have indicated that ICAM-1 is required for long-term control over Mtb infection, the mechanism remains unclear. In this study, ICAM-1−/− mice infected with Mtb survived over 10 months post-infection and controlled bacterial burden. Although granuloma formation appeared normal, higher overall cell numbers were observed by H&E staining and flow cytometry. We observed inhibited T cell contraction in the absence of ICAM-1 following primary Mtb infection. T regulatory cells were significantly reduced in ICAM-1−/− mice, which could play a role on T cell contraction. We conclude that ICAM-1 expression helps to control lung pathology by supporting T regulatory cells. Future studies will attempt to elucidate the mechanism by which ICAM-1 affects T regulatory cell recruitment to or retention in the lungs.