Neil E. Kay

Enhancement of human lymphocyte natural killing function by non-opioid fragments of β-endorphin

Opioid peptides have been shown to enhance peripheral blood lymphocyte natural killer (NK) cell function. In this study, we report that certain non-opioid fragments of beta-endorphin (2-16, 2-17, and 6-17) enhance NK activity with peak dose responses seen at 10(-12) to 10(-15) concentrations. This effect can be inhibited by naloxone. We conclude that non-opioid fragments of beta-endorphin are more potent than either beta- or gamma-endorphin in enhancing human lymphocyte NK activity.

Defective expression of T cell antigens in chronic lymphocytic leukaemia: relationship to T cell dysfunction.

Summary. In chronic lymphocytic leukaemia (CLL) peripheral blood T cells have a variety of functional abnormalities. To explore more extensively the T cell status of B‐CLL patients, surface immunoglobulin‐negative cells were isolated by sheep erythrocyte rosetting (ER) and the membrane phenotypes of the ER + cells defined by immunofluorescence utilizing monoclonal antibodies (MAb). In 11 of 18 CLL patients (CLL group I) there was excellent correlation between ER + and T3 (mature T cell marker) positivity. In the remaining patients (CLL group II), only 5–45% of ER+ cells were T3 positive, suggesting that many rosetting cells were non‐T, However, the ER+, T3 negative cells were nonreactive with OKM‐1 (MAb which detects monocytes and ‘null’ lymphocytes) or with OKT11, 9.6, and 35.1, MAb against the T cell E receptor. Moreover ER +, T3 negative cells were not stained with OKT4, OKT8, OKT6, OKT9, or OKT10. Treatment of group II ER + cells with neuraminidase increased (from 27% to 74%) the mean percentages of T3 positive cells detected, but not other membrane antigens. ER+ cells from group II patients, compared with normal and group I patients, exhibited diminished proliferative responses to PHA and Con‐A (P<0.01) and supported poorly pokeweed mitogeninduced proliferation of normal allogeneic B cells (P<0.01). Thus, in approximately one‐third of the CLL patients studied, many ER+ cells poorly express a number of membrane antigens characteristic of normal mature T cells, one of which (T3) is unmasked by neuraminidase treatment. This phenotypic abnormality appears to be associated with significant T cell dysfunction in vitro and may, at least in part, contribute to the commonly encountered immunological defects present in these patients.

A New Marker of T Lymphocyte Activation in Type I Diabetes

Biological changes underlying T lymphocyte activation, are known to be complex and are still poorly understood (1). Prominent in the early activation-related phenomena (minutes to a few hours after the activation signal) are the elevation of cytoplasmic calcium and changes in transmembrane electrical potential (TMP) (2–4). Resting T lymphocytes possess a relatively constant TMP. However, following mitogen or antigen challenge, T cell TMP changes over several minutes to hours with consecutive periods of depolarization, repolarization and hyperpolarization (2). Selective membrane NA, K-ATP-ase, and the K and Na permeable channels, abrogate both the TMP changes and T cell activation indicating a relationship between them and suggesting that cell membrance depolarization is an integral part of cell activation (2).