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(American Journal of Pathology. 2006;169:189-199.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.051225

Role of Neuronal Interferon-{gamma} in the Development of Myelopathy in Rats Infected with Human T-Cell Leukemia Virus Type 1

Yukiko Miyatake, Hitoshi Ikeda, Akihiro Ishizu, Tomohisa Baba, Toru Ichihashi, Akira Suzuki, Utano Tomaru, Masanori Kasahara and Takashi Yoshiki

From the Department of Pathology/Pathophysiology, Division of Pathophysiological Science, Hokkaido University Graduate School of Medicine, Sapporo, Japan

Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of not only adult T-cell leukemia but also HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Among the rat strains infected with HTLV-1, chronic progressive myelopathy, named HAM rat disease, occurs exclusively in WKAH rats. In the present study, we found that HTLV-1 infection induces interferon (IFN)-{gamma} production in the spinal cords of HAM-resistant strains but not in those of WKAH rats. Neurons were the major cells that produced IFN-{gamma} in HTLV-1-infected, HAM-resistant strains. Administration of IFN-{gamma} suppressed expression of pX, the gene critically involved in the onset of HAM rat disease, in an HTLV-1-immortalized rat T-cell line, indicating that IFN-{gamma} protects against the development of HAM rat disease. The inability of WKAH spinal cord neurons to produce IFN-{gamma} after infection appeared to stem from defects in signaling through the interleukin (IL)-12 receptor. Specifically, WKAH-derived spinal cord cells were unable to up-regulate the IL-12 receptor ß2 gene in response to IL-12 stimulation. We suggest that the failure of spinal cord neurons to produce IFN-{gamma} through the IL-12 pathway is involved in the development of HAM rat disease.




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