MRI Contributes to the Differentiation Between MS and HTLV-I Associated Myelopathy in British Columbian Coastal Natives

Howard, Andrew; Li, David K.B.; Oger, Joél

doi:10.1017/s0317167100002420

Cited by 31 publications

(29 citation statements)

References 29 publications

(47 reference statements)

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“…3). Increased (3)(4)(5)(6)(7)(8)(15)(16)(17). In particular, thoracic cord atrophy without signal intensity changes on MRI is accepted to be characteristic of HAM/TSP, but its incidence was varied, ranging from 20% to 74% (6)(7)(8).…”

Section: F I G U R E 1 T H O R a C I C C O R D Mr I Ma G E S I N T mentioning

confidence: 99%

Incidence and Clinical Significances of Human T-cell Lymphotropic Virus Type I-Associated Myelopathy with T2 Hyperintensity on Spinal Magnetic Resonance Images

et al. 2008

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Section: F I G U R E 1 T H O R a C I C C O R D Mr I Ma G E S I N T mentioning

confidence: 99%

Incidence and Clinical Significances of Human T-cell Lymphotropic Virus Type I-Associated Myelopathy with T2 Hyperintensity on Spinal Magnetic Resonance Images

et al. 2008

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“…11,13 No studies have examined HTLV-I carriers without indications for MRI. Moreover, no studies have tried to correlate immunological measures with WM lesions.…”

Section: Introductionmentioning

confidence: 99%

Brain Magnetic Resonance Imaging White Matter Lesions Are Frequent in HTLV-I Carriers and Do Not Discriminate from HAM/TSP

Morgan

Caskey

Abbehusen³

et al. 2007

AIDS Research and Human Retroviruses

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Human T lymphotropic virus (HTLV)-I is known to cause HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and other pronounced disease in less than 4% of those infected. However, evidence is accumulating that a proportion of HTLV-I carriers have neurological and urological symptoms without fulfilling criteria for HAM/TSP. Brain white matter (WM) lesions on magnetic resonance imaging (MRI) are frequently seen in HAM/TSP. HTLV-I carriers with MRI scans for other neurological diagnoses have WM lesions more frequently than expected. We studied 10 patients with HAM/TSP and 20 HTLV-I carriers without overt neurological disease and evaluated clinical characteristics, viral load, total, small, large, confluent WM lesion number, and lesion volume on MRI. Cerebral WM lesions were found in of 85% of HTLV-I carriers and 80% of HAM/TSP patients. Lesion number, size or location was no different between carriers and HAM/TSP. Cognitive function was lower in HAM/TSP (p = 0.045) but did not correlate with WM lesion number. Viral load and peripheral blood mononuclear cell interferon-γ production correlated positively (p = 0.001) but did not correlate with lesion number or volume. Conventional brain MRI frequently shows WM lesions in HTLV-I-infected individuals suggesting potential early central nervous system inflammation with rare development of progressive disease.

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“…The persistent demyelination in these diseases and the reported sensibility of neural progenitors to inflammatory mediators suggest the dysfunction or death of the precursors or myelinating oligodendrocytes required for remyelination (26 -28). Axonal loss, detected early in the disease by magnetic resonance spectroscopy (29,30), could result from defects in remyelination (31) and abnormal levels of molecular signals that regulate axon extension such as semaphorins (32). Assuming that immune semaphorins produced by infiltrating T lymphocytes may have a deleterious effect on neural cells, we investigated the in vitro effect of activated T cells releasing sCD100-SEMA-4D and rsCD100 protein on human pluripotent neural precursors and on rat oligodendrocytes.…”

mentioning

confidence: 99%

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

Giraudon¹,

Vincent²,

Vuaillat³

et al. 2004

The Journal of Immunology

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An inappropriate cross talk between activated T lymphocytes infiltrating the CNS and neural cells can sustain the onset and progression of demyelination and axonal degeneration in neuroinflammatory diseases. To mimic this deleterious cross talk, we designed an experimental paradigm consisting of transient cocultures of T lymphocytes chronically activated by retrovirus infection (not virus productive) with human multipotent neural precursors or primary oligodendrocytes from rat brain. We showed that activated T lymphocytes induced apoptotic death of multipotent neural progenitors and immature oligodendrocytes after a progressive collapse of their process extensions. These effects were reminiscent of those induced by brain semaphorin on neural cells. Blockade by specific Abs of soluble CD100 (sCD100)/semaphorin 4D released by activated T cells, or treatment with rsCD100, demonstrated that this immune semaphorin has the ability to collapse oligodendrocyte process extensions and to trigger neural cell apoptosis, most likely through receptors of the plexin family. The specific presence of sCD100 in the cerebrospinal fluid and of CD100-expressing T lymphocytes in the spinal cord of patients suffering with neuroinflammatory demyelination pointed to the potential pathological effect of sCD100 in the CNS. Thus, our results show that CD100 is a new important element in the deleterious T cell-neural cell cross talk during neuroinflammation and suggest its role in demyelination or absence of remyelination in neuroinflammatory diseases including multiple sclerosis and human T lymphotropic virus type 1-associated myelopathy.

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MRI Contributes to the Differentiation Between MS and HTLV-I Associated Myelopathy in British Columbian Coastal Natives

Cited by 31 publications

References 29 publications

Incidence and Clinical Significances of Human T-cell Lymphotropic Virus Type I-Associated Myelopathy with T2 Hyperintensity on Spinal Magnetic Resonance Images

Incidence and Clinical Significances of Human T-cell Lymphotropic Virus Type I-Associated Myelopathy with T2 Hyperintensity on Spinal Magnetic Resonance Images

Brain Magnetic Resonance Imaging White Matter Lesions Are Frequent in HTLV-I Carriers and Do Not Discriminate from HAM/TSP

Semaphorin CD100 from Activated T Lymphocytes Induces Process Extension Collapse in Oligodendrocytes and Death of Immature Neural Cells

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