Lymphocyte Antigens in Neuropsychiatric Systemic Lupus Erythematosus
Article first published online: 9 DEC 2005
Copyright © 1994 American College of Rheumatology
Arthritis & Rheumatism
Volume 37, Issue 3, pages 369–375, March 1994
How to Cite
Denburg, S. D., Behmann, S. A., Carbotte, R. M. and Denburg, J. A. (1994), Lymphocyte Antigens in Neuropsychiatric Systemic Lupus Erythematosus. Arthritis & Rheumatism, 37: 369–375. doi: 10.1002/art.1780370310
- Issue published online: 9 DEC 2005
- Article first published online: 9 DEC 2005
- Manuscript Accepted: 12 AUG 1993
- Manuscript Received: 1 SEP 1992
- Arthritis Society of Canada
- Lupus Society of Hamilton
- Ontario Lupus Association
- Ontario Mental Health Foundation.
Objective. To examine the relationships among specific lymphocyte antigenic reactivities of lupus sera and central nervous system complications of systemic lupus erythematosus (SLE), lymphocytotoxic antibody (LCA) positivity, and specific cognitive impairment.
Methods. Sera from 115 patients with SLE were examined for the presence of IgM- and IgG-class auto-antibodies binding to surface target antigens on lymphocytes, by immunoblotting and microdroplet lymphocytotoxicity studies. Seventy-three of these patients also underwent detailed neuropsychological testing within the same time period.
Results. Significant associations were found between reactivities to several lymphocyte antigenic moieties and neuropsychiatric SLE (NPSLE) or cognitive impairment. Specifically, immunoblot reactivities to 31–32-kd, 50–52-kd, 54–56-kd, and 97–98-kd targets were associated with clinical NPSLE; there was a significant association between reactivity to the 50–52-kd moiety in particular and cognitive impairment. There were also associations between LCA and immunoblot reactivity. Furthermore, the previously reported association between LCA positivity and specific visuospatial cognitive impairment was confirmed with data obtained from 2 different batteries of neuropsychological tests.
Conclusion. In some cases, specific antigenic targets of LCA-containing sera may be implicated in the pathogenesis of NPSLE.