Activation Of Lymphocyte Subpopulations Research Articles

Requirement of contact for direct antibacterial activity of lymphocyte subpopulations in ginbuna crucian carp

Requirement of contact for direct antibacterial activity of lymphocyte subpopulations in ginbuna crucian carp

Is loaded breathing an inflammatory stimulus?

To summarize recent data indicating that loaded breathing generates an inflammatory response. Loaded breathing initiates an inflammatory response consisting of elevation of plasma cytokines and recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes but are instead produced within the diaphragm secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction secondary to loaded breathing. The production of cytokines within the diaphragm may mediate the diaphragm muscle fiber injury that occurs with strenuous contractions, or contribute to the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute to the development of muscle cachexia. They may also have systemic effects, mobilizing glucose from the liver and free fatty acids from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to the production of adrenocorticotropic hormone and beta-endorphins. The adrenocorticotropic hormone response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles through the production of glucocorticoids and the induction of the acute-phase response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles. Loaded breathing is an immune challenge for the body, initiating an inflammatory response. Further studies are needed to elucidate the role of this response in the development of ventilatory failure.

The immune response to resistive breathing

Resistive breathing is an "immune challenge" for the body, initiating an inflammatory response consisting of an elevation of plasma cytokines, and the recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes, but are, instead, produced within the diaphragm, secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction, secondary to resistive breathing. The production of cytokines within the diaphragm may be mediating the diaphragm muscle fibre injury that occurs with strenuous contractions, or contributing towards the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute towards the development of muscle cachexia. They may also have systemic effects, mobilising glucose from the liver and free fatty acid from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to production of adrenocorticotropin and beta-endorphins. The adrenocorticotropin response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles via the production of glucocorticoids and the induction of the acute phase-response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles.

The immune response to resistive breathing: Implications for respiratory failure

Resistive breathing is an “immune challenge” for the body, initiating an inflammatory response consisting of elevation of plasma cytokines and recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes, but are instead produced within the diaphragm secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction secondary to resistive breathing. The production of cytokines within the diaphragm may be mediating the diaphragm muscle fiber injury that occurs with strenuous contractions, or contribute to the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute to the development of muscle cachexia. They may also have systemic effects, mobilizing glucose from the liver and free fatty acid from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal (HPA) axis leading to production of adrenocort...

Allergic and nonallergic asthmatics have distinct patterns of T-cell activation and cytokine production in peripheral blood and bronchoalveolar lavage.

Activation of lymphocyte subpopulations was determined in conjunction with levels of cytokines in peripheral blood and bronchoalveolar lavage (BAL) of asthmatics. Allergic asthmatics had increased numbers of CD4+ IL-2R+ T cells in peripheral blood and BAL, and T-cell activation closely correlated with numbers of low-affinity IgE receptor (CD23) bearing B cells. In contrast, in nonallergic asthmatics both CD4+ and CD8+ T cells from blood and BAL had increased expression of IL-2R, HLA-DR, and VLA-1. Furthermore, in the nonallergic asthmatics CD8+ T cells were decreased in blood but increased in BAL. Cytokine levels were determined in BAL fluid and supernatants from purified peripheral blood T cells and enriched BAL lymphocyte preparations. Allergic asthmatics were characterized by increased levels of IL-4 and IL-5, and this elevated IL-4 contributed to the elevated IgE levels found in these allergic subjects. In contrast, nonallergic asthmatics had elevated levels of IL-2 and IL-5, with IL-2 contributing to T-cell activation. In both types of asthma, the close correlation of IL-5 levels with eosinophilia suggests that IL-5 is responsible for the characteristic eosinophilia of asthma. Thus, we provide evidence of distinct T-cell activation resulting in different spectra of cytokines in allergic and nonallergic asthma.

Activation of Lymphocyte Subpopulations in Patients with Chronic Lymphocytic Leukemia

T lymphocytes from the peripheral blood of normal donors and patients with CLL were isolated by nylon wool filtration or E-rosette separation and tested for functional activities.Unseparated CLL lymphocytes showed a poor response to phytomitogens and to allogeneic cells. Subpopulations enriched in E-RFC showed an increased PHA- and a normal MLC-reactivity ; the Con A responses, however, were markedly reduced in all experiments. Subpopulations which were T cell depleted showed no reactivity to all mitogens.Purified T cells from normal donors showed a decreased reactivity to PHA, Con A and PWM. The Con A responses were completely abolished in almost all experiments. These diminished responses could be restored by unseparated cells or by small numbers of syngeneic, mitomycin-treated monocytes. The data suggest that mitogen-induced T lymphocyte stimulation in vitro in general depends on the presence of monocytes.