Yonsei Med J.  2009 Feb;50(1):12-21. 10.3349/ymj.2009.50.1.12.

Intracellular Bacterial Infection and Invariant NKT Cells

Affiliations
  • 1Laboratory of Immunology, Department of Laboratory Sciences, Gunma University School of Health Sciences, Maebashi, Gunma, Japan. memoto@health.gunma-u.ac.jp

Abstract

The invariant (i) natural killer (NK)T cells represent a unique subset of T lymphocytes which express the V alpha14 chain of the T cell receptor (TCR), that recognizes glycolipid antigens presented by the nonpolymorphic major histocompatibility complex (MHC) class I-like antigen presentation molecule CD1d, and they participate in protection against some microbial pathogens. Although iNKT cells have originally been regarded as T cells co-expressing NKR-P1B/C (NK1.1: CD 161), they do not seem to consistently express this marker, since NK1.1 surface expression on iNKT cells undergoes dramatic changes following facultative intracellular bacterial infection, which is correlated with functional changes of this cell population. Accumulating evidence suggests that NK1.1 allows recognition of "missing-self", thus controling activation/inhibition of NK1.1-expressing cells. Therefore, it is tempting to suggest that iNKT cells participate in the regulation of host immune responses during facultative intracellular bacterial infection by controlling NK1.1 surface expression. These findings shed light not only on the unique role of iNKT cells in microbial infection, but also provide evidence for new aspects of the NK1.1 as a regulatory molecule on these cells.

Keyword

Natural killer T cell; natural killer 1.1; NKR-P1; intracellular bacteria; liver; Listeria monocytogenes

MeSH Terms

Animals
Humans
Listeria Infections/*immunology
Listeria monocytogenes/*immunology
Natural Killer T-Cells/*immunology/*microbiology

Figure

  • Fig. 1 Course of intracellular bacteria following systemic infection.

  • Fig. 2 Course of iNKT cells following α-GalCer stimulation or L. monocytogenes infection (A) α-GalCer stimulation; (B) L. monocytogenes infection.

  • Fig. 3 Accumulation of iNKT cells under physiological and inflammatory conditions.

  • Fig. 4 Cytokine profile of CD4+ and DN iNKT cells following L. monocytogenes infection.

  • Fig. 5 NKR-P1 as a "missing-self" recognition molecule.


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