Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions

Krzysztof Selmaj, Cedric S. Raine, Barbara Cannella, Celia F. Brosnan

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636 Citations (Scopus)

Abstract

Multiple sclerosis (MS) brain tissue, spleen, and PBMC were studied using immunocytochemistry and FACS® for immunoreactivity for lymphotoxin (LT) and TNF. Both cytokines were identified in acute and chronic active MS lesions but were absent from chronic silent lesions. LT was associated with CD3+ lymphocytes and Leu-M5+ microglia cells at the lesion edge and to a lesser extent, in adjacent white matter. TNF was associated with astrocytes in all areas of the lesion, and with foamy macrophages in the center of the active lesion. In acute lesions, immunoreactivity for TNF in endothelial cells was noted at the lesion edge. No LT or TNF reactivity was detected in Alzheimer's or Parkinson's disease brain tissues but was present at lower levels in central nervous system (CNS) tissue from other inflammatory conditions, except for adrenoleucodystrophy which displayed high levels of LT in microglia. No increase in LT and TNF reactivity was detected in spleen and PBMC of MS patients suggesting specific reactivity within the CNS. These results indicate that LT and TNF may be involved in the immunopathogenesis of MS, and can be detected in both inflammatory cells and cells endogenous to the CNS.

Original languageEnglish (US)
Pages (from-to)949-954
Number of pages6
JournalJournal of Clinical Investigation
Volume87
Issue number3
StatePublished - 1991

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Lymphotoxin-alpha
Multiple Sclerosis
Tumor Necrosis Factor-alpha
Central Nervous System
Microglia
Spleen
Adrenoleukodystrophy
Nerve Tissue
Brain
Astrocytes
Parkinson Disease
Alzheimer Disease
Endothelial Cells
Immunohistochemistry
Macrophages
Lymphocytes
Cytokines

Keywords

  • Central nervous system
  • Cytokines
  • Demyelination
  • Glial cells
  • Lymphocytes

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Selmaj, K., Raine, C. S., Cannella, B., & Brosnan, C. F. (1991). Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions. Journal of Clinical Investigation, 87(3), 949-954.

Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions. / Selmaj, Krzysztof; Raine, Cedric S.; Cannella, Barbara; Brosnan, Celia F.

In: Journal of Clinical Investigation, Vol. 87, No. 3, 1991, p. 949-954.

Research output: Contribution to journalArticle

Selmaj, K, Raine, CS, Cannella, B & Brosnan, CF 1991, 'Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions', Journal of Clinical Investigation, vol. 87, no. 3, pp. 949-954.
Selmaj, Krzysztof ; Raine, Cedric S. ; Cannella, Barbara ; Brosnan, Celia F. / Identification of lymphotoxin and tumor necrosis factor in multiple sclerosis lesions. In: Journal of Clinical Investigation. 1991 ; Vol. 87, No. 3. pp. 949-954.
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N2 - Multiple sclerosis (MS) brain tissue, spleen, and PBMC were studied using immunocytochemistry and FACS® for immunoreactivity for lymphotoxin (LT) and TNF. Both cytokines were identified in acute and chronic active MS lesions but were absent from chronic silent lesions. LT was associated with CD3+ lymphocytes and Leu-M5+ microglia cells at the lesion edge and to a lesser extent, in adjacent white matter. TNF was associated with astrocytes in all areas of the lesion, and with foamy macrophages in the center of the active lesion. In acute lesions, immunoreactivity for TNF in endothelial cells was noted at the lesion edge. No LT or TNF reactivity was detected in Alzheimer's or Parkinson's disease brain tissues but was present at lower levels in central nervous system (CNS) tissue from other inflammatory conditions, except for adrenoleucodystrophy which displayed high levels of LT in microglia. No increase in LT and TNF reactivity was detected in spleen and PBMC of MS patients suggesting specific reactivity within the CNS. These results indicate that LT and TNF may be involved in the immunopathogenesis of MS, and can be detected in both inflammatory cells and cells endogenous to the CNS.

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