Expression of alphaB-crystallin in glia cells during lesional development in multiple sclerosis.

The small heat shock protein alphaB-crystallin was recently identified as a dominant human T-cell antigen in myelin derived from multiple sclerosis (MS) patients. Using immunohistochemical techniques, oligodendrocytes as well as astrocytes in MS lesions were shown to express alphaB-crystallin. In the present study we examined the expression of alphaB-crystallin, human natural killer cell marker (HNK-1; as a marker for immature oligodendrocytes) and heat shock protein 60 (hsp60) in glia cells at different stages of MS lesion development i.e. in early active lesions, late active lesions and inactive lesions. The results demonstrate that already at the earliest stages of lesional development a subpopulation of oligodendrocytes express detectable levels of alphaB-crystallin. In active lesions about 5-10% of all oligodendrocytes were found to express alphaB-crystallin, whereas in inactive lesions the relative number of alphaB-crystallin-expressing oligodendrocytes was approximately tenfold less. For astrocytes the relative number of alphaB-crystallin-expressing cells was 40-50% for all three types of lesions. Also, alphaB-crystallin-expressing oligodendrocytes and astrocytes displayed different patterns of distribution in lesional areas. These data suggest different regulatory pathways for alphaB-crystallin expression in either type of glia cell. No correlation was found between expression patterns of HNK-1 and alphaB-crystallin indicating that the subpopulation of alphaB-crystallin-expressing oligodendrocytes consisted of both mature and immature oligodendrocytes. In addition, no correlation was found between expression of hsp60 and alphaB-crystallin in MS lesions suggesting different regulatory pathways for either hsp.