NDLI: Invariant NKT cells preferentially modulate the function of CD8 alpha+ dendritic cell subset in inducing type 1 immunity against infection.

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Invariant NKT cells preferentially modulate the function of CD8 alpha+ dendritic cell subset in inducing type 1 immunity against infection.

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Invariant NKT cells preferentially modulate the function of CD8 alpha+ dendritic cell subset in inducing type 1 immunity against infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Joyee, Antony George Yang, Xi Uzonna, Jude
Description	Country affiliation: Canada Author Affiliation: Joyee AG ( Department of Medical Microbiology, Laboratory for Infection and Immunity, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.)
Abstract	Although studies suggest that NKT cell (NKT) activation modulates the function of dendritic cells (DCs) in inducing T cell responses, it is unknown whether this modulating effect is biased to a DC subset. We previously reported that NKT activation could modulate DC function in inducing protective T cell immunity to Chlamydia pneumoniae, an intracellular bacterial infection. In this study, we investigated the effect of NKT activation on DC subsets, using multiple approaches, including gene knockout mice, alpha- galactosylceramide stimulation, adoptive transfer of invariant NKT (iNKT), and functional analysis of DC subsets in both in vitro and in vivo settings. We found a preferential modulating effect of iNKTs on the CD8alpha(+) DC subset. Specifically, we found that iNKT-deficient mice, compared with wild-type (WT) mice, showed reduced CD8alpha(+) DC expansion with lower CD40 expression and IL-12 production, whereas enhancing iNKT activation in WT mice or adoptive transfer of iNKTs to Jalpha18(-/-) mice resulted in increased function of CD8alpha(+) DCs in inducing type 1 immune responses. Further, DC-iNKT coculture experiments showed a direct CD40L-dependent enhancing effect of iNKTs on IL-12p70 production by CD8alpha(+) DCs. More importantly, CD8alpha(+) DCs from Jalpha18(-/-) mice, compared with those from WT mice, showed significantly reduced ability to activate IFN-gamma-producing T cells in vitro and to induce type 1 immunity and protection in vivo. Moreover, a similar CD8alpha(+) DC subset alteration was found in the Jalpha18(-/-) mice following Leishmania major infection. Our data provide the first direct evidence that iNKTs preferentially promote the functional development of a subset of DC to generate protective immunity against infections.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	4
Volume Number	184
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2010-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd8 Biosynthesis Dendritic Cells Immunology Natural Killer T-cells Th1 Cells Adoptive Transfer Animals Cells, Cultured Chlamydophila Pneumoniae Coculture Techniques Microbiology Transplantation Immunity, Cellular Leishmania Major Leishmaniasis, Cutaneous Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Parasitology Pneumonia, Bacterial Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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The mechanism of splenic invariant NKT cell activation dictates localization in vivo.

T cells from Leishmania major-susceptible BALB/c mice have a defect in efficiently up-regulating CXCR3 upon activation.

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Invariant NKT cells preferentially modulate the function of CD8 alpha+ dendritic cell subset in inducing type 1 immunity against infection.

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Invariant NKT cells preferentially modulate the function of CD8 alpha+ dendritic cell subset in inducing type 1 immunity against infection.