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1 Secretion In Vivo1
*
Neurological Diseases and
Cellular Immunology Sections, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892;
Institute of Experimental Internal Medicine, Department of Internal Medicine, Otto-von-Guericke University, Magdeburg, Germany;
Office of the Clinical Director, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; and
¶ Institute of Biochemistry, Department of Biochemistry and Biotechnology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany
CD26 or dipeptidyl peptidase IV (DP IV) is expressed on various
cell types, including T cells. Although T cells can receive activating
signals via CD26, the physiological role of CD26/DP IV is largely
unknown. We used the reversible DP IV inhibitor
Lys[Z(NO2)]-pyrrolidide (I40) to dissect the role of DP
IV in experimental autoimmune encephalomyelitis (EAE) and to explore
the therapeutic potential of DP IV inhibition for autoimmunity. I40
administration in vivo decreased and delayed clinical and
neuropathological signs of adoptive transfer EAE. I40 blocked DP IV
activity in vivo and increased the secretion of the immunosuppressive
cytokine TGF-
1 in spinal cord tissue and plasma during acute EAE. In
vitro, while suppressing autoreactive T cell proliferation and TNF-
production, I40 consistently up-regulated TGF-1 secretion. A
neutralizing anti-TGF-1 Ab blocked the inhibitory effect of I40
on T cell proliferation to myelin Ag. DP IV inhibition in vivo was not
generally immunosuppressive, neither eliminating encephalitogenic T
cells nor inhibiting T cell priming. These data suggest that DP IV
inhibition represents a novel and specific therapeutic approach
protecting from autoimmune disease by a mechanism that includes an
active TGF-1-mediated antiinflammatory effect at the site of
pathology.
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