NK T cells contribute to expansion of CD8(+) T cells and amplification of antiviral immune responses to respiratory syncytial virus.

Johnson TR, Hong S, Van Kaer L, Koezuka Y, Graham BS
J Virol. 2002 76 (9): 4294-303

PMID: 11932395 · PMCID: PMC155085 · DOI:10.1128/jvi.76.9.4294-4303.2002

CD1d-deficient mice have normal numbers of T lymphocytes and natural killer cells but lack Valpha14(+) natural killer T cells. Respiratory syncytial virus (RSV) immunopathogenesis was evaluated in 129xC57BL/6, C57BL/6, and BALB/c CD1d(-/-) mice. CD8(+) T lymphocytes were reduced in CD1d(-/-) mice of all strains, as shown by cell surface staining and major histocompatibility complex class I tetramer analysis, and resulted in strain-specific alterations in illness, viral clearance, and gamma interferon (IFN-gamma) production. Transient activation of NK T cells in CD1d(+/+) mice by alpha-GalCer resulted in reduced illness and delayed viral clearance. These data suggest that early IFN-gamma production and efficient induction of CD8(+)-T-cell responses during primary RSV infection require CD1d-dependent events. We also tested the ability of alpha-GalCer as an adjuvant to modulate the type 2 immune responses induced by RSV glycoprotein G or formalin-inactivated RSV immunization. However, immunized CD1-deficient or alpha-GalCer-treated wild-type mice did not exhibit diminished disease following RSV challenge. Rather, some disease parameters, including cytokine production, eosinophilia, and viral clearance, were increased. These findings indicate that CD1d-dependent NK T cells play a role in expansion of CD8(+) T cells and amplification of antiviral responses to RSV.

MeSH Terms (17)

Animals Antigen Presentation Antigens, CD1 Antigens, CD1d Galactosylceramides Immunization Killer Cells, Natural Ligands Lymphocyte Activation Mice Mice, Inbred BALB C Mice, Inbred C57BL Respiratory Syncytial Viruses Respiratory Syncytial Virus Infections Respiratory Syncytial Virus Vaccines T-Lymphocytes, Cytotoxic Viral Proteins

Connections (1)

This publication is referenced by other Labnodes entities:

Links