| First Author | Frentzel S | Year | 2019 |
| Journal | Eur J Immunol | Volume | 49 |
| Issue | 9 | Pages | 1391-1398 |
| PubMed ID | 31049948 | Mgi Jnum | J:280709 |
| Mgi Id | MGI:6369488 | Doi | 10.1002/eji.201847961 |
| Citation | Frentzel S, et al. (2019) Essential role of IkappaBNS for in vivo CD4(+) T-cell activation, proliferation, and Th1-cell differentiation during Listeria monocytogenes infection in mice. Eur J Immunol 49(9):1391-1398 |
| abstractText | Acquisition of effector functions in T cells is guided by transcription factors, including NF-kappaB, that itself is tightly controlled by inhibitory proteins. The atypical NF-kappaB inhibitor, IkappaBNS, is involved in the development of Th1, Th17, and regulatory T (Treg) cells. However, it remained unclear to which extend IkappaBNS contributed to the acquisition of effector function in T cells specifically responding to a pathogen during in vivo infection. Tracking of adoptively transferred T cells in Listeria monocytogenes infected mice antigen-specific activation of CD4(+) T cells following in vivo pathogen encounter to strongly rely on IkappaBNS . While IkappaBNS was largely dispensable for the acquisition of cytotoxic effector function in CD8(+) T cells, IkappaBNS -deficient Th1 effector cells exhibited significantly reduced proliferation, marked changes in the pattern of activation marker expression, and reduced production of the Th1-cell cytokines IFN-gamma, IL-2, and TNF-alpha. Complementary in vitro analyses using cells from novel reporter and inducible knockout mice revealed that IkappaBNS predominantly affects the early phase of Th1-cell differentiation while its function in terminally differentiated cells appears to be negligible. Our data suggest IkappaBNS as a potential target to modulate specifically CD4(+) T-cell responses. |
