Rapid development of a gamma interferon-secreting glycolipid/CD1d-specific Valpha14+ NK1.1- T-cell subset after bacterial infection.

Abstract:

:The phenotypic and functional changes of glycolipid presented by CD1d(glycolipid/CD1d) specific Valpha14+ T cells in the liver of mice at early stages of bacterial infection were investigated. After Listeria monocytogenes infection or interleukin-12 (IL-12) treatment, alpha-galactosylceramide/CD1d tetramer-reactive (alpha-GalCer/CD1d+) T cells coexpressing natural killer (NK) 1.1 marker became undetectable and, concomitantly, cells lacking NK1.1 emerged in both euthymic and thymectomized animals. Depletion of the NK1.1+ subpopulation prevented the emergence of alpha-GalCer/CD1d+ NK1.1- T cells. Before infection, NK1.1+, rather than NK1.1-, alpha-GalCer/CD1d+ T cells coexpressing CD4 were responsible for IL-4 production, whereas gamma interferon (IFN-gamma) was produced by cells regardless of NK1.1 or CD4 expression. After infection, IL-4-secreting cells became undetectable among alpha-GalCer/CD1d+ T cells, but considerable numbers of IFN-gamma-secreting cells were found among NK1.1-, but not NK1.1+, cells lacking CD4. Thus, NK1.1 surface expression and functional activities of Valpha14+ T cells underwent dramatic changes at early stages of listeriosis, and these alterations progressed in a thymus-independent manner. In mutant mice lacking all alpha-GalCer/CD1d+ T cells listeriosis was ameliorated, suggesting that the subtle contribution of the NK1.1- T-cell subset to antibacterial protection is covered by more profound detrimental effects of the NK1.1+ T-cell subset.

journal_name

Infect Immun

journal_title

Infection and immunity

authors

Emoto M,Yoshizawa I,Emoto Y,Miamoto M,Hurwitz R,Kaufmann SH

doi

10.1128/IAI.00311-06

subject

Has Abstract

pub_date

2006-10-01 00:00:00

pages

5903-13

issue

10

eissn

0019-9567

issn

1098-5522

pii

74/10/5903

journal_volume

74

pub_type

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