Tropical spastic paraparesis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
When infected by [[HTLV-1]] the host mounts an antigen specific immune response towards the [[HTLV-1]] antigen. [[Cytotoxic T-lymphocytes]] of the host’s immune response release [[cytokines]] in an effort to fight the infection. These [[cytokines]] facilitate the [[endothelium|transendothelial]] migration of [[lymphocytes]] across the blood-brain barrier. Once [[cytokines]] are within the central nervous system demyelination is brought as a result of bystander cell injury. The disease is [[chronic (medicine)|chronic]], progressing slowly, usually causing symptoms 20-30 years after infection. | |||
==References== | ==References== | ||
Revision as of 00:35, 11 December 2012
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Tropical spastic paraparesis Microchapters |
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Differentiating Tropical spastic paraparesis from other Diseases |
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Diagnosis |
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Treatment |
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Tropical spastic paraparesis pathophysiology On the Web |
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Directions to Hospitals Treating Tropical spastic paraparesis |
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Risk calculators and risk factors for Tropical spastic paraparesis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
When infected by HTLV-1 the host mounts an antigen specific immune response towards the HTLV-1 antigen. Cytotoxic T-lymphocytes of the host’s immune response release cytokines in an effort to fight the infection. These cytokines facilitate the transendothelial migration of lymphocytes across the blood-brain barrier. Once cytokines are within the central nervous system demyelination is brought as a result of bystander cell injury. The disease is chronic, progressing slowly, usually causing symptoms 20-30 years after infection.