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Results for “Immunity, Innate”

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At least 811 records · Page 45Linked to original sources
PubMed2004

The role of innate immune cells in the response of heat-treated Mycobacterium tuberculosis (M.tb) antigens stimulating PBMCs.

The proliferation response of gammadelta T cells to the antigen from heat-treated Mycobacterium tuberculosis H37Ra (M.tb Ag) was used as a good model in gammadeltaT cell research. From preliminary research it is found that activated NK cells positively elevated gammadeltaT cells proliferation after simulating PBMCs with M.tb Ag. To investigate different behaviors of NK cells, gammadeltaNKT cells, gammadeltaT cells and relationships between these cell subsets, activation and proliferation of different cell subsets of PBMCs in response to M.tb Ag were analyzed. We demonstrated that NK cells, gammadeltaNKT cells and gammadeltaT cells could be activated after stimulation with M.tb Ag. gammadeltaNKT cells and gammadelta T cells proliferated while the number of NK cells decreased after 11 day-simulation with M.tb Ag. Meanwhile, at the early time of stimulation the cytotoxicity of PBMCs was enhanced.

Antigens, Bacterial↗
PubMed2005

[Innate immunity, receptors for exogenous and endogenous danger patterns in immunopathogenesis of atherosclerosis--part II: TLR receptors, significance of genetic polymorphism of danger signals receptors].

The most important set of receptors for danger patterns are TLR receptors. Together ten different TLR receptors were identified so far. Majority of TLR receptors is expressed on the cell surface to identify extracellulary localized danger signals. Some TLR receptors are also expressed in the intracellular compartment to identify intracellular danger signals. Receptors for danger signals display individual differences delineated by genetic polymorphism. The individual immune reactivity is developed in the context of genetic predisposition and the exposition to variable environmental factors. The differences in an individual immune reactivity are probably responsible for individual susceptibility or resistance to the development of immunopathological reactivity, which is involved in the immunopathogenesis of atherosclerosis.

Animals↗
PubMed2006

Effect of tick saliva on mechanisms of innate immune response against Borrelia afzelii.

The effect of salivary gland extract (SGE) and saliva from the tick Ixodes ricinus (L.) on the interaction of Borrelia afzelii spirochetes with mouse macrophages as well as on the borreli-acidal effect of calf serum was studied. SGE reduced both the number of phagocytosing cells and phagocytosed bacteria. An inhibitory effect of SGE on the killing of spirochetes by the alternative pathway of complement activation also was observed. Both SGE and saliva down-regulated production of proinflammatory cytokine tumor necrosis factor-alpha by macrophages stimulated with interferon-gamma and live B. afzelii spirochetes. The production of another macrophage cytokine, interleukin-6, remained unchanged. SGE and saliva exerted a different effect on the production of nitric oxide by stimulated macrophages. Whereas SGE up-regulated NO production, saliva decreased it. The significance of immunosuppressive effects of tick saliva for the transmission of Borrelia spirochetes is discussed.

Animals↗
PubMed1989

Mechanism of innate immunity to amoebic infection in guineapigs.

The direct lymphocyte cytotoxicity and antibody dependent cell mediated cytotoxicity against Entamoeba histolytica was studied in 3-4 wk old and 8-10 wk old guineapigs. Both these parameters were significantly increased in splenic cells in the older animals. This might be due to maturation of the immune system or to natural infection by related parasite, leading to immunity.

Aging↗
PubMedDate not supplied

Innate immunity.

Explore the source record for details and available documents.

Animals↗
PubMed1998

Impaired mast cell development and innate immunity in Mac-1 (CD11b/CD18, CR3)-deficient mice.

Mac-1 (CD11b/CD18, CR3), a beta2 integrin expressed on leukocytes, is important in leukocyte migration. We demonstrate that Mac-1 is also expressed on peritoneal mast cells and LPS stimulated bone marrow-derived cultured mast cells, and that Mac-1-deficient mice, which lack this receptor, have significant reductions in the numbers of mast cells resident in the peritoneal cavity, peritoneal wall, and dorsal skin. The reduced numbers of mast cells in Mac-1-deficient mice may have important functional consequences, in that Mac-1-deficient mice exhibit significantly increased mortality after cecal ligation and puncture, a model of acute septic peritonitis in which host resistance has been shown to be dependent on both mast cells and complement. These findings demonstrate that Mac-1 is required for the expression of normal levels of mast cells in the peritoneal cavity, peritoneal wall, and certain areas of the skin, as well as for maintaining adequate mast cell-dependent host defense against bacterial infection.

Acute Disease↗