Effects of long duration spaceflight on human T lymphocyte and monocyte activity.
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Experiments were performed on blood samples from 5 cosmonauts in order to investigate the effects of long duration spaceflight (26 to 166 days) on immune activity. The experiments were performed on cultured mononuclear cells purified from blood samples collected during the preflight period and 24 h after landing. The production of interleukin 2, which is the major cytokine involved in T lymphocyte proliferation, was found to be enhanced after flight in some individuals, whereas the ability of mitogen-stimulated cells to express interleukin 2 receptor was impaired 24 h after flight for two cosmonauts out of five. Normal interleukin 2 receptor expression was obtained in all cases when lymphocytes were directly activated by a protein kinase C activating phorbol ester. On the other hand, no significant changes were observed in interleukin 1 production by cultured peripheral blood mononuclear cells. Lastly, the distribution of T lymphocytes subsets was examined in peripheral blood sampled 24 h after landing and was found to be within normal values.Keywords:
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HIV infection ultimately leads to AIDS, despite the immune responses elicited soon after infection. In addition to the observed changes in lymphoid cell subsets, alteration of the cytokine network most likely accompanies and/or contributes to the lack of protective immune responses. In an attempt to delineate the early events in the immune response to lentivirus infection, we have sequentially monitored levels of proinflammatory (IL-1β, IL-6, and TNF-α) and antiinflammatory (IL-10) cytokine mRNAs in PBMCs of cynomolgus macaques during primary SIVmac infection. Eight monkeys were infected i.v. with 4 AID50 of cell-free SIVmac251. All monkeys seroconverted between days 16 and 21 postinfection (p.i.), and had detectable peripheral viremia. The viral load peaked between days 12 and 16 p.i., and fell sharply thereafter. A marked increase in the expression of IL-6 mRNA was observed in all macaques during the first weeks following infection. An increase in the levels of expression of IL-1β, TNF-α, and IL-10 mRNA was also determined in six, six, and five of the eight monkeys, respectively. While IL-6, TNF-α, and IL-10 increased transiently, increased levels of IL-1β mRNA expression were sustained over 44 days in most monkeys.
Interleukin 15
Interleukin 19
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We investigated cellular immune responses at baseline in peripheral blood mononuclear cells (PBMC) of patients with multiple sclerosis (MS) treated with interferon (IFN)-β and classified into responders and non-responders according to clinical response criteria. Levels for IFN-γ, interleukin (IL)-17A, IL-17F, IL-10 and IL-4 were determined in activated PBMC of 10 responders, 10 non-responders and 10 healthy controls by cytometric bead arrays. Cytokine levels in cell culture supernatants were similar between responders and non-responders, and comparable to those obtained in healthy controls. These findings do not support differential cellular immune responses in PBMC at baseline between IFN-β responders and non-responders.
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The blastogenic response to mitogens of peripheral blood mononuclear cells (PBMC) obtained from healthy volunteers and patients with chronic or acute tuberculosis (TB) was evaluated. Cells derived from TB patients showed a reduced proliferative capacity compared to that of healthy individuals. Three possible causes of such an impairment were investigated, namely: 1) a change in the proportion of lymphocyte subpopulations; 2) an altered ratio between monocytes and lymphocytes and 3) a reduction in the state of monocyte-macrophage activation, with an impaired production of interleukin-1 (IL-1). We observed no significant modification of lymphocyte subsets from TB patients and normal individuals. However, the relative number of monocytes in the patients was always higher than the controls. Furthermore, circulating monocytes from the patients with TB exhibited a decreased phagocytosis of latex beads, a normal expression of DR antigens, and an increased spontaneous production of IL-1. The possibility that the hyperactivation of macrophages may be responsible for the observed low blastogenic response is discussed.
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Experiments were performed on blood samples from 5 cosmonauts in order to investigate the effects of long duration spaceflight (26 to 166 days) on immune activity. The experiments were performed on cultured mononuclear cells purified from blood samples collected during the preflight period and 24 h after landing. The production of interleukin 2, which is the major cytokine involved in T lymphocyte proliferation, was found to be enhanced after flight in some individuals, whereas the ability of mitogen-stimulated cells to express interleukin 2 receptor was impaired 24 h after flight for two cosmonauts out of five. Normal interleukin 2 receptor expression was obtained in all cases when lymphocytes were directly activated by a protein kinase C activating phorbol ester. On the other hand, no significant changes were observed in interleukin 1 production by cultured peripheral blood mononuclear cells. Lastly, the distribution of T lymphocytes subsets was examined in peripheral blood sampled 24 h after landing and was found to be within normal values.
Monocyte
Spaceflight
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The production and mRNA expression of the cytokines interferon-gamma (IFN-gamma) and interleukin (IL)-4, -10, and -12 by peripheral blood mononuclear cells (PBMC) after incubation with the coccidioidal antigen toluene spherule lysate (TSL) from various subjects were measured. The IFN-gamma concentration in PBMC supernatants incubated for 72 h from 8 subjects with disseminated coccidioidomycosis was significantly less than that from 7 healthy, coccidioidal-immune subjects (P = .015). No differences were seen among the subject groups in the concentrations of IL-4, -10, or -12. By use of competitive polymerase chain reaction, PBMC from subjects with disseminated coccidioidomycosis also expressed less mRNA for IFN-gamma and IL-12 than did cells from healthy, immune subjects. These data suggest that patients with disseminated coccidioidomycosis have a diminished T helper lymphocyte type 1 response.
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Polyclonal B cell activation is the most visible biological manifestation of systemic lupus erythematosus (SLE) autoimmunity. Murine models and in vitro lymphocyte studies are the most important tools used to improve our comprehension of the disease. It was successively demonstrated that there is an intrinsic B lymphocyte hyperreactivity in human and murine lupus; that the B lymphocytes overreact to stimulating factors produced by T lymphocytes; and that these stimulating factors could be over-produced. This last feature contrasts with decreased interleukin 2 production and lymphocyte response to this cytokine. A more precise study of the interleukins involved in the control of the humoral response shows the importance of interleukins 4, 5, 6 and of gamma-interferon. Further investigations are needed to improve our understanding of B cell hyperreactivity during SLE. These studies will benefit from better molecular characterization of many interleukins and their receptors.
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Impaired immune regulation is considered to be involved in the pathogenesis of primary Sjögren's syndrome (primary SS). A qualitative T lymphocyte defect is suggested by previous reports of impaired lymphocyte proliferation, impairment of interleukin-2 (IL-2) production, and a decreased number of IL-2 receptors, whereas the capacity of monocytes to produce IL-1 is normal in most patients. We here report on the IL-1 sensitivity of monocyte-depleted mononuclear cells (MDC) from patients with primary SS. IL-1 responsiveness, evaluated by measuring the enhancing effect of an IL-1 standard on the proliferative response of the patient's MDC, was decreased compared to that of the control group, and there was a positive correlation between patients' IL-1 production and IL-1 sensitivity. The results confirm the notion of impaired T lymphocyte function in primary SS, and suggest a pathogenetic mechanism that involves both monocytes and T lymphocytes.
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