Clinical and laboratory evidence of @entity792 in acute XXXX .

@entity1 @entity8990 @entity146 @entity161 @entity792
A number of assays were performed to assess immunologic function in 28 @entity1 with clinically well-defined @entity161 . Our data provide laboratory evidence that @entity1 with @entity161 have characteristics consistent with an autoimmune process, directed to components of the brain, which may participate in either the pathogenesis or etiology of @entity161 . One-third of our @entity1 had a clinically evident @entity792 unrelated to their @entity146 . Of the nine @entity1 with an @entity792 , two had one autoantibody in their serum and five had more than one autoantibodies. Twelve of eighteen @entity1 without clinical evidence of @entity792 had no detectable autoantibodies. Mitogenic responses to @entity8990 and PWM were significantly reduced in the @entity1 population when compared to controls. Fifty percent of the @entity1 had an increased percentage (greater than 5%) of blood-borne HLA-DR (+) OKT4 (+) T-helper lymphocytes. Immune reactivity toward brain antigens was sought by measuring lymphocyte transformation to a saline extract of frontal lobe, and by immunoblotting of antigens extracted from frontal lobe, cingulate gyrus, interventricular septum, and hippocampus. Lymphocyte transformation did not reveal differences between @entity1 and control groups. Normal sera were found to contain antibody to some of these brain antigens. However, @entity1 with @entity161 had antibody to antigens of the hippocampus, septal region and cingulate gyrus which were not encountered during analysis of normal sera.
