Faculty Collaboration Database

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

09/05/2008

Pubmed ID

18768833

Pubmed Central ID

PMC2835404

DOI

10.4049/jimmunol.181.6.3804

Scopus ID

2-s2.0-56149110848   55 Citations

Abstract

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 LA

Author

Weiguo Cui PhD Associate Professor in the Microbiology and Immunology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Acute Disease
Adoptive 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