Abstract We have recently demonstrated that atopic T lymphocytes have decreased sensitivity to prostaglandin E 2 (PGE 2). In order to determine whether this decreased sensitivity was reflected at the receptor level, we have employed a radioligand binding assay utilizing [ 3H]PGE 2. We have demonstrated a single specific reversible binding site for [ 3H]PGE 2 on normal T cells ( N = 10) with a mean K D (± SD) of 32.2 (± 25.0) n M, a binding capacity of 20.2 (± 13.0) p M, and a mean of 1004 (± 118) receptors per cell. Atopic T cells ( N = 10) were also found to have a single specific binding site for [ 3H]PGE 2 with a mean K D of 24.9 (± 17.8) n M, a binding capacity of 7.1 (± 10.1) p M, and a mean of 372 (± 61) receptors per cell. These radioligand binding studies were correlated with functional studies in the same subjects. Phytohemagglutinin-stimulated protein synthesis ([ 3H]leucine uptake) was suppressed in a dose-dependent fashion by PGE 2 (10 −6−10 −12 M). The maximal effect of PGE 2 on normal T cells was 10 −6 M PGE 2 with an IC 50 of 10 −12 M. Atopic T cells responded quantitatively less than normal T cells to PGE 2. Further, the maximum suppression of protein synthesis by PGE 2 occurred at 10 −6 M with an IC 50, of 10 −10 to 10 −11 M. These studies suggest that part of the decreased sensitivity of atopic T cells to PGE 2 may result from a reduction in PGE 2 binding sites.