To determine whether a defect in the T cell response to adenosine exists at the level of the adenosine receptor in systemic lupus erythematosus (SLE) we measured the binding affinity and maximum binding of T cell membranes from both normal and SLE T cells by utilizing radiolabeled adenosine ligands. Normal T lymphocyte membranes possess a single class of [3H]5‐N‐ethylcarboxamide adenosine binding sites with aKdof 0.61 μM, aBmaxof 23.5 pmol/mg protein, and a Hill coefficient of 0.98, which indicates the presence of noncooperative sites. In contrast, T cell membranes do not bind significant amounts of either [3H]cyclohexyladenosine or [3H]phenylisopropyladeno‐sine. These data indicate that T lymphocyte membranes have only A2, and notA1, adenosine receptors. Similarly, T cells from both active and inactive SLE subjects also express only A2receptors with aKdof 0.93 μM, aBmaxof 20.4 pmol/mg protein, and a Hill coefficient of 0.85, which is consistent with the presence of noncooperative sites. There is no difference in the on‐rate, affinity, or density of T cell A2receptors from active SLE patients, inactive SLE patients, or healthy controls. We conclude that T lymphocytes from both healthy and SLE subjects express A2, but not A1, receptors. Thus, the inability of SLE T cells to respond to adenosine does not reflect a decreased density of A2(stimulatory) receptors, diminished A2receptor binding, or an increased affinity or number of A1(inhibitory) adenosine receptors. These observations support the conclusion that the defect in the T cell cAMP‐dependent pathway may occur at a point distal to the adenosine receptor.—Schultz, L. A.; Kammer, G. M.; Rudolph, S. A. Characterization of the human T lymphocyte adenosine receptor: comparison of normal and systemic lupus erythematosus cells.FASEB J.2: 244‐250; 1988.