Three groups of black subjects (systemic lupus erythematosus patients, patients with nonrheumatic disease, and normal subjects) were screened for the expression of the T4 epitope, as recognized by the monoclonal antibody OKT4. We found that the T cell subsets within each group were similar, regardless of the T4 epitope phenotype (intact, intermediate, or deficient). In the subgroup of Jamaican subjects, there was an association between systemic lupus erythematosus and the T4 epitope-intermediate and T4 epitope-deficient phenotypes; this association was not detected in the nonJamaican population.The CD4 (T4) surface molecule is a T cell differentiation antigen expressed on T cells that exhibit helperhnducer function (1). Surface CD4 expresses many different determinants (epitopes) that can be individually recognized by different anti-CD4 monoclonal antibodies (MAb). A heterogeneity in expression of the epitope recognized by the MAb OKT4 (T4 epitope) has been described (2-6), and has given rise to 3 T4 epitope phenotypes (as detected by flow cytometry): T4 epitope-intact, T4 epitope-deficient, and T4 epitope-intermediate (3). This polymorphism is inherited in an autosomal codominant manner (3,4),
36527.with the T4 epitope-intermediate phenotype representing the heterozygous state. The T4 epitope-deficient and T4 epitope-intermediate phenotypes have been described in black subjects (2-6), but not in white subjects.We have previously described 3 black families whose members manifested systemic lupus erythematosus (SLE) in association with the T4 epitope-deficient phenotype (7). It is not known whether a correlation exists between T4 epitope phenotype and SLE in the general black population, or even within certain limited subpopulations. To address this question, the T4 epitope phenotype was determined in 3 groups of black subjects: those with SLE, those with nonrheumatic disorders, and those without apparent disease (normal subjects). We found that the T4 epitopedeficient and T4 epitopeintermediate phenotypes are more prevalent in black Jamaicans with SLE than in either black Jamaican control group. In nowJamaican black subjects, no such correlation between SLE and T4 epitope phenotype could be demonstrated.