EXPRESSION OF ALPHA-B-CRYSTALLIN IN GLIA CELLS DURING LESIONAL DEVELOPMENT IN MULTIPLE-SCLEROSIS

The small heat shock protein alpha B-crystallin was recently identifie d as a dominant human T-cell antigen in myelin derived from multiple s clerosis (MS) patients. Using immunohistochemical techniques, oligoden drocytes as well as astrocytes in MS lesions were shown to express alp ha B-crystallin. In the present study we examined the expression of al pha B-crystallin, human natural killer cell marker (HNK-1; as a marker for immature oligodendrocytes) and heat shock protein 60 (hsp60) in g lia cells at different stages of MS lesion development i.e. in early a ctive lesions, late active lesions and inactive lesions. The results d emonstrate that already at the earliest stages of lesional development a subpopulation of oligodendrocytes express detectable levels of alph a B-crystallin. In active lesions about 5-10% of all oligodendrocytes were found to express alpha B-crystallin, whereas in inactive lesions the relative number of alpha B-crystallin-expressing oligodendrocytes was approximately tenfold less. For astrocytes the relative number of alpha B-crystallin-expressing cells was 40-50% for all three types of lesions. Also, alpha B-crystallin-expressing oligodendrocytes and astr ocytes displayed different patterns of distribution in lesional areas. These data suggest different regulatory pathways for alpha B-crystall in expression in either type of glia cell. No correlation was found be tween expression patterns of HNK-1 and alpha B-crystallin indicating t hat the subpopulation of alpha B-crystallin-expressing oligodendrocyte s consisted of both mature and immature oligodendrocytes. In addition, no correlation was found between expression of hsp60 and alpha B-crys tallin in MS lesions suggesting different regulatory pathways for eith er hsp. (C) 1997 Elsevier Science B.V.