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Pathomechanism of HTLV-I-associated myelopathy (HAM). Takeshi TABIRA 1 , Junichi INOBE 1 1National Institute of Neuroscience, NCNP pp.774-784
Published Date 1991/10/10
DOI https://doi.org/10.11477/mf.1431900174
  • Abstract
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Genetic, viral, immunological and pathologic studies of HTLV-I-associated myelopathy (HAM) were reviewed and a hypothetical pathomechanism was postulated. 1) HTLV-I infection is a prerequisit in HAM. 2) Those who have susceptibility gene develop HAM. 3) Chronic continuous inflammatory process by lymphocytes, macrophages and microglias takes place in the thoracic cord, which mimics parainfections myelitis. 4) Viral antigens and genomes are absent or hardly detectable in the lesion. 5) T-cells and B-cells are markedly activated polyclonally by transactivation of IL-2 and IL-2R, viral antigens, alloantigens, cytokines and other mechanism. 6) HAM patients and HTLV-I carriers are frequently associated with autoimmune-like diseases such as SLE, polymyositis, Sjogren syndrome, uveitis, arthritis, bronchopneumonitis and others, and transgenic mice of the HTLV-I PX gene developed Sjogren-like syndrome. From these findings, the authors speculate that generation of autoagressive T-cells towards the spinal cord is the key mechanism in HAM. However, the antigen, effector mechanism and homing mechanism are remained to be studied.


Copyright © 1991, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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