MIP-2 Recruits NKT Cells to the Spleen During Tolerance Induction

Peripheral tolerance occurs after intraocular administration of Ag and is dependent on an increase in splenic NKT cells. New data here show that macrophage inflammatory protein-2 (MIP-2) is selectively up-regulated in tolerance-conferring APCs and serves to recruit NKT cells to the splenic marginal...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2001-01, Vol.166 (1), p.313-321
Main Authors: Faunce, Douglas E, Sonoda, Koh-Hei, Stein-Streilein, Joan
Format: Article
Language:English
Subjects:
Animals
Anterior Chamber - immunology
Antigens - administration & dosage
Antigens, Differentiation - biosynthesis
CD3 Complex - biosynthesis
Chemokine CXCL2
Chemokines - biosynthesis
Chemokines - physiology
Chemotaxis, Leukocyte - genetics
Chemotaxis, Leukocyte - immunology
Female
Immune Tolerance - genetics
Killer Cells, Natural - cytology
Killer Cells, Natural - immunology
Lymphocyte Activation - genetics
macrophage inflammatory protein 2
Macrophages - immunology
Macrophages - metabolism
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
MIP-2 protein
NK antigen
Ovalbumin - administration & dosage
Ovalbumin - immunology
Spleen - cytology
Spleen - immunology
T-Lymphocyte Subsets - cytology
T-Lymphocyte Subsets - immunology
T-Lymphocyte Subsets - metabolism
Up-Regulation - genetics
Up-Regulation - immunology
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Summary:Peripheral tolerance occurs after intraocular administration of Ag and is dependent on an increase in splenic NKT cells. New data here show that macrophage inflammatory protein-2 (MIP-2) is selectively up-regulated in tolerance-conferring APCs and serves to recruit NKT cells to the splenic marginal zone, where they form clusters with APCs and T cells. In the absence of the high-affinity receptor for MIP-2 (as in CXCR2-deficient mice) or in the presence of a blocking Ab to MIP-2, peripheral tolerance is prevented, and Ag-specific T regulatory cells are not generated. Understanding the regulation of lymphocyte traffic during tolerance induction may lead to novel therapies for autoimmunity, graft acceptance, and tumor rejection.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.166.1.313