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The Journal of Immunology, 2000, 164: 2759-2768.
Copyright © 2000 by The American Association of Immunologists

IFN-{gamma} Shapes Immune Invasion of the Central Nervous System Via Regulation of Chemokines1

Elise H. Tran, Esther N. Prince and Trevor Owens2

Neuroimmunology Unit, Montreal Neurological Institute, and Department of Microbiology and Immunology, McGill University, Montreal, Quebec, Canada

Dynamic interplay between cytokines and chemokines directs trafficking of leukocyte subpopulations to tissues in autoimmune inflammation. We have examined the role of IFN-{gamma} in directing chemokine production and leukocyte infiltration to the CNS in experimental autoimmune encephalomyelitis (EAE). BALB/c and C57BL/6 mice are resistant to induction of EAE by immunization with myelin basic protein. However, IFN-{gamma}-deficient (BALB/c) and IFN-{gamma}R-deficient (C57BL/6) mice developed rapidly progressing lethal disease. Widespread demyelination and disseminated leukocytic infiltration of spinal cord were seen, unlike the focal perivascular infiltrates in SJL/J mice. Gr-1+ neutrophils predominated in CNS, and CD4+ T cells with an activated (CD69+, CD25+) phenotype and eosinophils were also present. RANTES and macrophage chemoattractant protein-1, normally up-regulated in EAE, were undetectable in IFN-{gamma}- and IFN-{gamma}R-deficient mice. Macrophage inflammatory protein-2 and T cell activation gene-3, both neutrophil-attracting chemokines, were strongly up-regulated. There was no induction of the Th2 cytokines, IL-4, IL-10, or IL-13. RNase protection assays and RT-PCR showed the prevalence of IL-2, IL-3, and IL-15, but no increase in IL-12p40 mRNA levels in IFN-{gamma}- or IFN-{gamma}R-deficient mice with EAE. Lymph node cells from IFN-{gamma}-deficient mice proliferated in response to myelin basic protein, whereas BALB/c lymph node cells did not. These findings show a regulatory role for IFN-{gamma} in EAE, acting on T cell proliferation and directing chemokine production, with profound implications for the onset and progression of disease.




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O. S. Targoni, J. Baus, H. H. Hofstetter, M. D. Hesse, A. Y. Karulin, B. O. Boehm, T. G. Forsthuber, and P. V. Lehmann
Frequencies of Neuroantigen-Specific T Cells in the Central Nervous System Versus the Immune Periphery During the Course of Experimental Allergic Encephalomyelitis
J. Immunol., April 1, 2001; 166(7): 4757 - 4764.
[Abstract] [Full Text] [PDF]

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 J. Leukoc. Biol.Home page
P. Matthys, K. Vermeire, H. Heremans, and A. Billiau
The protective effect of IFN-{gamma} in experimental autoimmune diseases: a central role of mycobacterial adjuvant-induced myelopoiesis
J. Leukoc. Biol., October 1, 2000; 68(4): 447 - 454.
[Abstract] [Full Text]

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 J. Immunol.Home page
Y. Luo, F. R. Fischer, W. W. Hancock, and M. E. Dorf
Macrophage Inflammatory Protein-2 and KC Induce Chemokine Production by Mouse Astrocytes
J. Immunol., October 1, 2000; 165(7): 4015 - 4023.
[Abstract] [Full Text] [PDF]

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 JEMHome page
C.-Q. Chu, S. Wittmer, and D. K. Dalton
Failure to Suppress the Expansion of the Activated CD4 T Cell Population in Interferon {gamma}-deficient Mice Leads to Exacerbation of Experimental Autoimmune Encephalomyelitis
J. Exp. Med., July 3, 2000; 192(1): 123 - 128.
[Abstract] [Full Text] [PDF]


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