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Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
It is presumed that the abnormal uptake of synthetic chemicals such as phenol, which has an extreme affinity for the vessel wall, triggers either the complement or other mediator systems. Complement activation would, in turn, lead to swelling, inflammation, and finally fibrosis. Certainly, complement changes after chemical challenge occurred in some patients with this entity. C-reactive protein also could be a factor in triggering the patients. T lymphocyte abnormality may also be important in this type patient. T lymphocyte changes occurred with ambient-dose incitant challenge in some patients. Abnormality could lead to lymphokine triggering with resultant blood vessel inflammation. All T-lymphocytes measured in these patients were depressed, suggesting a suppressor deficiency or helper-function depression causing overuse of this system. However, too few patients were studied for valid statistical analysis.
Bioartificial organs
Published in Ronald L. Fournier, Basic Transport Phenomena in Biomedical Engineering, 2017
This binding of the CD4+ T cell and the antigen/MHC class II complex constitutes the first signal for the activation of the CD4+ T cell. This is then followed by the release of a second signal by the APC of a soluble substance called interleukin-1 (IL-1) that is also essential for T cell activation. IL-1 is a small protein with a molecular weight of 15,000 g mol−1 that belongs to a class of substances called lymphokines. Lymphokines are cellular messengers that have an effect on other lymphocytes and are a subcategory of a broader class of intercellular messengers called cytokines. The CD4+ T cell then becomes activated and begins to secrete its own interleukins, specifically IL-2, IL-4, and IL-5. IL-2 induces the CD4+ T cell to proliferate, rapidly forming a clone of CD4+ T cells that are reactive to the specific antigen presented by the APC. IL-4 then activates the B cells, and IL-5 induces the activated B cells to proliferate in number, forming a clone of B cells.
Liposomal Nanomedicines
Published in Vladimir Torchilin, Mansoor M Amiji, Handbook of Materials for Nanomedicine, 2011
Liposomes have long ago been shown to be effective immunological adjuvants for protein and peptide antigens (see nice summary of numerous studies in Refs. 424 and 425) They are capable of inducing both humoral and cellular immune responses towards the liposomal antigens. Liposomes with encapsulated protein or peptide antigen are phagocytosed by macrophages and eventually end in lysosomes. There, proteins and peptides are degraded by the lysosomal enzymes, and their fragments are then presented on the macrophage surface being associated with the MHCII complex. This results in the stimulation of specific T-helper cells, and, via the lymphokine secretion and interaction of T cells with B cells that captured free antigen, stimulation of specific B cells and subsequent secretion of antibodies.425 In some cases, however, the fraction of the liposomal antigen can escape from endosomes into the cytoplasm (for example, when pH-sensitive liposomes are used) and in this case the liberated antigen is processed and presented being associated with the MHCI complex, inducing thus cytotoxic T lymphocytes (CTL response). The ability to induce the CTL response provides liposomes with certain benefits when compared to traditional adjuvants (such as Freund’s adjuvant) that do not induce any significant CTL response.
Lung tissue inflammatory response and pneumonocyte apoptosis of Sprague-Dawley rats after a 30-day exposure in methyl mercaptan vapor
Published in Journal of the Air & Waste Management Association, 2021
Lu Jiang, Jingjing Fang, Kexian Li, Xinhong Xu, Jiangbo Qiao
Altogether, two complements and 10 cytokines were tested in the study, as shown in Table 4. These parameters are involved in autocrine signaling, paracrine signaling, and endocrine signaling as immunomodulating agents. Cytokines include chemokines, interferons, interleukins, lymphokines, and tumor necrosis factors. Cytokines are produced by a broad range of cells, including immune cells, endothelial cells, fibroblasts, and various stromal cells; a given cytokine may be produced by more than one type of cell. Most parameters showed obvious changes in serum and lung tissue at different phrases except C3, C4, and IGE. The levels of IL4, IL8, IGM, IGG, IGA, TNF-α and TNF-β were significantly different in the exposure group compared with the control groups in various phrases. TNF-α in serum in the female exposure groups was significantly increased compared with the control groups after 10 days (P < .01), but with the extent of the exposure, it was significantly decreased after 20 days (P < .01). TNF-α in lung tissue in the female exposure groups was significantly decreased after 10 days and 20 days (P < .01). The levels of TNF-β showed significantly increased in serum and decreased in lung tissue for each sex compared with the control group in each endpoint. While the levels of these cytokines in the lung tissue showed no statistical difference, there was a decreasing trend among these groups. IGM mostly showed a significant higher value in lung tissue and serum, except in the female exposure groups after 10 days (P < .05). Changes of these cytokine levels in serum and lung tissue indicated activation of the immune system.