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Results for “Immune function”

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At least 1,585 records · Page 88Linked to original sources
PubMed2005

Releasing signals, secretory pathways, and immune function of endogenous extracellular heat shock protein 72.

Heat shock proteins (Hsp) were first characterized as intracellular proteins, which function to limit protein aggregation, facilitate protein refolding, and chaperone proteins. During times of cellular stress, intracellular Hsp levels increase to provide cellular protection. Recently, it has been recognized that Hsp, particularly Hsp72, are also found extracellularly (eHsp72), where they exhibit potent immunomodulatory effects on innate and acquired immunity. Circulating eHsp72 levels also greatly increase during times of stress (i.e., when an organism is exposed to a physical/psychological stressor or suffers from various pathological conditions). It has been proposed that elevated eHsp72 serves a protective role by facilitating immunological responses during times of increased risk of pathogenic challenge and/or tissue damage. This review focuses on the in vivo releasing signals and immunomodulatory function(s) of endogenous eHsp72. In addition, we present data that emphasize the importance of caution when conducting in vitro immunological tests of Hsp72 function.

Animals↗
PubMed2004

ST64B is a defective bacteriophage in Salmonella enterica serovar Typhimurium DT64 that encodes a functional immunity region capable of mediating phage-type conversion.

The Salmonella enterica subsp. enterica serovar Typhimurium (S. Typhimurium) defective bacteriophage ST64B has a putative immunity (immC) region consisting of cI, cro and cII-like genes. Since ST64B is widespread in S. Typhimurium, studies were undertaken to determine whether this region might be functional and influence phage typing results. Cloning of ST64B immC-like genes and their subsequent expression in S. Typhimurium DTs showed that this region is able to mediate phage-type conversion in DTs 41 and 44. This confirms the functionality of the immC region and the patterns of lysis produced by phage typing are consistent with the predicted mechanism of action of the encoded protein products.

Bacteriophage Typing↗
PubMed1978

Cellular immune function in marasmic and underweight infants with prolonged diarrhoea.

Lymphocytes from 10 marasmic and underweight infants with prolonged diarrhoea responded normally to phytohaemagglutinin stimulation. There was no gross deficiency in the total number of lymphocytes, serum immunoglobulins, or serum C3. Defective cellular immunity does not appear to play a major role in the pathogenesis of diarrhoea in these children.

Blood Proteins↗
PubMed1979

Immune function in systemic lupus erythematosus. Impairment of in vitro T-cell proliferation and in vivo antibody response to exogenous antigen.

Peripheral blood mononuclear cells from 46 systemic lupus erythematosus (SLE) patients showed reduced ability to proliferate in vitro in response to the soluble antigen, tetanus toxoid, as compared with 96 normal controls. Special studies of 27 untreated SLE patients also revealed significantly decreased blastogenic responses to tetanus toxoid. In both the total and untreated SLE populations, decreased mean tetanus antibody titers also were found as compared with the control population. However, the reduction in antibody titer and blastogenic response was not strictly parallel. A limited immunization program was initiated in low-responding volunteers from the SLE and normal populations. Three out of four SLE patients did not develop a significant blastogenic response despite increases in anti-tetanus titers after immunization, whereas all normals showed significant increases in both blastogenic and antibody responses. The accumulated evidence indicated that the unresponsiveness was the result of a defect in T-cell function. Monocyte reactivity was demonstrated to be normal, and no evidence was found for the presence of suppressor cells, inhibition by immune complexes, or increased prostaglandins to explain the defect.

Antibodies, Bacterial↗
PubMed1993

Immune function in alcoholism: a controlled study.

Several studies have shown an increased risk for infection and cancer in alcoholic patients. The mechanisms for such observations remain largely unknown. In an effort to investigate the possibility of immunological dysfunction in alcoholism, we studied three immune parameters in 47 hospitalized chronic alcoholic patients and 47 age- and sex-matched normal controls. The immune measures were: (1) lymphocyte phenotyping, with estimates of percentages of T cells, B cells, T helpers, T suppressors, natural killer (NK) cells, and cells carrying the activation markers IL2R1 and I2; (2) NK cell activity; and (3) lymphokine-activated killer cell activity. Results indicate a significant increase in the IL2R and I2 lymphocyte markers in alcoholic patients compared with matched controls. We also found a nonsignificant trend for a decrease in the percentage of suppressor T cells in the alcoholic group, as well as a trend for a negative correlation between the percentage of T suppressor cells and age. There were no significant differences in either NK or lymphokine-activated killer cell activities between the two groups. Furthermore, there were no significant associations between duration and intensity of alcohol consumption and any of the immune measures. These results suggest subtle alterations in immune regulation in alcoholic patients that cannot be explained solely on the basis of duration and/or amount of alcohol consumed.

Adult↗