Immune response gene effect

Steinman, L., Rosenbaum, J., Sriram, S., and McDevitt, H. O., In vivo effects of antibodies to immune response gene products. Prevention of experimental allergic encephalomyelitis, Proc. Natl. Acad. Sci. U.S.A., 78, 7111, 1981. 

Ideally, the most effective prevention of HIV infection would be a vaccine that blocks virus infection in individuals. Indeed, effective vaccines have been developed against most human viruses that cause serious diseases. While several different possible vaccines against HIV are under development, there are some theoretical reasons why it may be difficult to develop an effective one. First, HIV has the unique ability to evade the immune system in an infected individual. Briefly, this results from (1) the high mutation rate of the virus, particularly in the env gene (2) the ability of the virus to establish a latent state in some cells and (3) the ability of the virus to spread by cell-to-cell contact. The object of the vaccine is to raise a protective immune response to the infectious agent. Since HIV evades the immune system so efficiently, it may be difficult for a vaccine to prevent HIV infection in an individual, even if it can induce production of neutralizing antibodies or cell-mediated immunity. 

The acute toxicity and oxidative effects of nano-scale Ti02 depend on the size of the nanoparticle (bulk Ti02 is positively nontoxic) and increase notably through illumination, as this leads to the formation of hydroxyl radicals [74], further indicating oxidative stress as a major candidate for the mechanism of action of NP toxicity. However, a recent microarray analysis of the transcriptome of zebrafish embryos treated with Ti02 NP showed no major increase of transcripts related to oxidative stress. Instead, significant effects were observed on expression of genes involved in circadian rhythm, kinase activity, vesicular transport, and immune response [75]. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

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