Physical exercise, mental stress, or infusion of beta-adrenergic agonists result in an increase in the number of natural killer (NK) cells in the peripheral circulation. In view of the specific migration pattern of NK cells in vivo, it has been suggested that these cells may be released from the marginating pool in blood vessels. In the present report, the in vitro effect of catecholamines on the adhesion of NK cells to unstimulated human endothelial cells (EC) was characterized. Peripheral blood mononuclear cells were allowed to adhere to monolayers of EC, after which the adherent lymphocyte fraction was analyzed phenotypically by flow cytometry. NK cells were found to adhere preferentially to EC, a process that was reversed by the addition of various adrenergic agonists. Catecholamines selectively affected adhesion of NK cells and had no effect on T cell adhesion to EC, as was determined by the use of purified cell populations. Detachment of NK cells from EC could be achieved by short incubations (5 min) with epinephrine (EPI) and was concentration-dependent, with an ED50 of 2 x 10(-10)M. Using a panel of alpha- and beta-adrenergic agonists and antagonists, we show that the detachment of NK cells is mediated via beta 2-adrenergic receptors. In line with the lower affinity for beta 2-adrenergic receptors, norepinephrine was less effective than EPI in inducing detachment of NK cells from EC. Direct activation of adenylate-cyclase with forskolin gave similar results as observed with EPI, indicating that signaling through cAMP is necessary to induce detachment of NK cells from EC. The results of the present study lend support to the hypothesis that catecholamines, via beta 2-adrenergic receptors, can induce recruitment of NK cells from the marginating pool to the circulating pool, by changing the adhesive interactions between NK cells and EC.

Abstract-In a previous study it was shown that antibody formation after vaccination with a low-dose recombinant DNA (rDNA) hepatitis B vaccine was negatively influenced by psychological stress. The present study was designed to assess whether the same inverse relation between HBs-antibody levels and psychological stress could be observed, while administering the standard, and thus higher, dose of vaccine. Volunteers (n = 68) scoring extremely low or high on a combination of questionnaires measuring daily problems and psychoneurotic symptoms were selected for participation. Antibody levels were determined 2, 6, and 7 months after the first vaccination. Questionnaires were completed before entering the study and at month 6. In contrast to the previous study, psychological stress was not found to be related to the antibody levels at any timepoint. These results suggest that, under certain conditions, stress-induced immunomodulation in vivo might be dependent on antigen dose.

In this study, a respiration-deficient Chinese hamster cell line with a defect in succinate dehydrogenase activity is shown to result from a single base change in a codon in the coding sequence for the membrane anchor protein C II-3 (also referred to as QPs-1). A premature translation stop results in the truncation of 33 amino acids from the C terminus. Bovine cDNA encoding this peptide complements the mutation. There is about 82% identity between these two mammalian proteins. The gene for C II-3 was mapped on human chromosome 1, and because it is also found on minichromosomes characterized by our laboratory, we can localize it on the short arm within 1-2 megabases from the centromere.A series of respiration-deficient Chinese hamster cell mutants isolated by our laboratory can grow normally in tissue culture as long as an adequate supply of glucose is available for glycolysis (1-3). Depletion of glucose leads to rapid cessation of growth and cell death. The mutants were grouped into seven complementation groups by somatic cell fusions (1), and one, represented by mutant CCL16-B9, was characterized to be almost completely deficient in succinate dehydrogenase activity (SDH) 1 (4,5). This enzyme, which links the reactions of the Krebs cycle to the electron transport chain, is part of a complex of four polypeptides (complex II) in the inner mitochondrial membrane. The active site for the substrate is on the flavoprotein (Fp, 70 kDa), while the iron-sulfur protein (Ip, 27 kDa) is believed to link it to two small integral membrane proteins (C II-3 and C II-4 , 15 and 7-9 kDa, respectively). A b-type heme group is associated with the membrane proteins. Electrons from the oxidation of the substrate in the mitochondrial matrix pass from the Fp via three non-heme iron-sulfur centers in the Ip , , ) to the integral membrane proteins and from there to ubiquinone. The function of the heme group associated with the membrane proteins is not completely clear (see Refs. 6 -9 for reviews).All four peptides are encoded by nuclear genes in eukaryotic organisms. Thus, the precursor polypeptides are synthesized in the cytosol and subsequently or concurrently imported into mitochondria. Following processing to their mature forms, the biogenesis of a functional complex II requires covalent attachment of flavin to the largest subunit (Fp) (10), formation of the three non-heme iron-sulfur clusters in the Ip subunit, and assembly of the heme with the membrane anchor proteins. Although this complex is the smallest and least intricate of the electron transport complexes in the inner mitochondrial membrane, much remains to be learned about the mechanism or pathway of its assembly.With the Fp-Ip complex dissociated from the membrane by chaotropic ions, SDH activity can be assayed with artificial electron acceptors such as tetrazolium ions, phenazine methosulfate and dichlorophenol-indophenol, or ferricyanide. Based on the absence of activity in the mutant CCL16-B9, we hypothesized that the defective protein was either the Ip or the Fp subun...

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Two studies are presented on the influence of psychological factors on immunoregulation of latent Epstein‐Barr virus (EBV) infection. In the first study, 121 students completed questionnaires on daily hassles, psychoneurotic symptoms, coping styles and loneliness. No significant association between these psychological measures and levels of antibodies to EBV was found. It was reasoned that this might be explained by the fact that the psychological stress levels were generally low. Therefore, in a second study, from a larger population of 390 students, 95 subjects were selected based on low or high scores on a daily hassles and a psychoneurotic symptom checklist. No significant relationship was found between psychological variables and EBV antibody titres or specific cytotoxic activity against autologous EBV‐transformed B cells. It is concluded that in the cross‐sectional studies presented, the psychological factors measured are not related to immune control of latent EBV. © 1998 John Wiley & Sons, Ltd.