MyD88 plays a critical T cell-intrinsic role in supporting CD8 T cell expansion during acute lymphocytic choriomeningitis virus infection. J Immunol 2008 Sep 15;181(6):3804-10
Date
09/05/2008Pubmed ID
18768833Pubmed Central ID
PMC2835404DOI
10.4049/jimmunol.181.6.3804Scopus ID
2-s2.0-56149110848 (requires institutional sign-in at Scopus site) 63 CitationsAbstract
During acute lymphocytic choriomeningitis virus (LCMV) infection, CD8 T cells rapidly expand and differentiate into effectors that are required for viral clearance. The accumulation of activated T cells is greatly reduced in mice lacking the adaptor molecule MyD88. Although MyD88 has generally been considered to indirectly regulate adaptive immune responses by controlling inflammatory cytokine production and Ag presentation in innate immune cells, in this study, we identify an unappreciated cell-intrinsic role for MyD88 in LCMV-specific CD8 T cells. Using reciprocal adoptive transfer models and bone marrow chimeras, we show that Myd88(-/-) CD8 T cells are defective in their clonal expansion in response to LCMV infection, independent of their environment. Furthermore, we show that while MyD88 is dispensable for initial activation and division of LCMV-specific CD8 T cells during the early stages of viral infection, MyD88-dependent signals are critical for supporting their survival and sustained accumulation.
Author List
Rahman AH, Cui W, Larosa DF, Taylor DK, Zhang J, Goldstein DR, Wherry EJ, Kaech SM, Turka LAMESH terms used to index this publication - Major topics in bold
Acute DiseaseAdoptive Transfer
Animals
CD8-Positive T-Lymphocytes
Cell Proliferation
Cell Survival
Cells, Cultured
Clone Cells
Epitopes, T-Lymphocyte
Immunologic Memory
Lymphocytic Choriomeningitis
Lymphocytic choriomeningitis virus
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
Myeloid Differentiation Factor 88
Signal Transduction
