Decreased plasma glutamine level and CD4+ T cell number in response to 8 wk of anaerobic training.

The purpose of the present study was to investigate the role of plasma amino acids and glutathione (GSH) on the absolute number of leukocyte and lymphocyte subpopulations in response to different training programs. Healthy untrained subjects were randomly assigned to an 8-wk aerobic (AET) or anaerobic (ANT) exercise training program. Absolute number of cell counts did not significantly change in AET, whereas a decrease of CD4+ T cell counts (P < 0.

Elevated venous glutamate levels in (pre)catabolic conditions result at least partly from a decreased glutamate transport activity.

Abnormally high postabsorptive venous plasma glutamate levels have been reported for several diseases that are associated with a loss of body cell mass including cancer, human/simian immunodeficiency virus infection, and amyotrophic lateral sclerosis. Studies on exchange rates in well-nourished cancer patients now show that high venous plasma glutamate levels may serve as a bona fide indicator for a decreased uptake of glutamate by the peripheral muscle tissue in the postabsorptive period and may be indicative for a precachectic state. High glutamate levels are also moderately correlated with a decreased uptake of glucose and ketone bodies.

Interleukin-2 receptor gene expression by bronchoalveolar lavage lymphocytes in pulmonary sarcoidosis.

Current concepts of the immunopathogenesis of sarcoidosis favor a central role of activated, interleukin-2 (IL-2) producing helper T-cells at sites of inflammation. Normally, activated T-cells release IL-2 and express IL-2 receptors (IL-2R). IL-2R+ cells, however, are not uniformly found in patients with clinically active disease.

Definition of discrete signals involved in human T-cell activation.

Mitogenic activities of monoclonal antibodies directed at defined receptor structures expressed on the surface of mature human T lymphocytes were employed to study, in detail, signals involved in primary T-cell activation. Based on differential requirements for stimulation, two discrete pathways of human T-cell activation can be defined: the antigen-induced mode of activation initiated through the Ti-T3 antigen-receptor complex and an alternative pathway which can be triggered by monoclonal antibodies directed at the T11 glycoprotein. Perhaps more importantly, the approach taken here allows the definition of stable intermediate cellular stages within the activation cascade and, thus, to analyze the signalling capabilities of individual receptor molecules.