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Short Communication Activation of NF- k B and c- jun Transcription Factors in Multiple Sclerosis Lesions Implications for Oligodendrocyte Pathology

Oligodendrocytes are a major target of the purported autoimmune response in multiple sclerosis (MS) lesions, but little is known about the mechanisms un-derlying their demise. Despite the expression of proapoptotic receptors, these cells are rarely seen to undergo apoptosis in situ . On the other hand, cytotoxic mediators present in MS lesions, such as tumor necrosis factor- a , are known to generate survival signals through the activation of the transcription factors NF- k B and c- jun . The aim of this study was to investigate in chronic active and silent MS lesions and control white matter the expression of c- jun , its activating molecule, JNK, as well as NF- k B complex and its inhibitor, I k B. By immunohistochemistry we found negligible reactivity for these molecules in control white matter and silent MS plaques. In active MS lesions, double-label immunohistochemistry with oligodendrocyte markers showed up-regulation of the nuclear staining for both NF- k B and JNK on a large proportion of oligodendrocytes located at the edge of active lesions and on microglia/macrophages throughout plaques. Oligodendrocytes showed no reactivity for I k B, which was predominantly confined to the cytoplasm of microglia/macrophages. We hypothesize that activation of these transcriptional pathways may be one mechanism accounting