Cytokines interleukin types

T-lymphocyte activation leads to release of cytokines from type 2 T-helper (TH2) cells that mediate allergic inflammation (interleukin [IL] -4, IL-5, and IL-13). Conversely, type 1 T-helper (THj) cells produce IL-2 and interferon-y that are essential for cellular defense mechanisms. Allergic asthmatic inflammation may result from an imbalance between THj and TH2 cells. 

The pathophysiology of VKC is derived from a combination of type I and IV hypersensitivity reactions.This allergic response involves IgE,Th-2 lymphocytes, eosinophils, mast cells, basophils, neutrophils, macrophages, proin-flammatory cytokines, interleukins, histamine, and other associated mediators. Also involved in this immune response are hormonal and neuroendocrine influences. This immune response results in the clinical manifestations of photophobia, itching, redness, tearing, papillae, corneal vascularization, mucous discharge, and plaque formation. 

Yanagida M, Fukamachi H, Ohgami K, et al. Effects of T-helper 2-type cytokines, interleukin-3 (IL-3), IL-4, IL-5, and IL-6 on the survival of cultured human mast cells. Blood 1995 86 3705-14. 

A straightforward approach to in vivo hypothesis testing is to generate a knockout mouse for the gene of interest, inoculate with prions and look at the effect on incubation time as compared to wild type controls. Experiments of this nature have been carried out for the anti-inflammatory cytokines interleukin-4 (114), 1110 and 1113 and the chemokine, monocyte chemoattractant protein-1 (Mcpl) [82, 83]. Following intracerebral inoculation with the RML strain of mouse adapted scrapie, no significant differences were seen for mice deficient in either 114,1113 or both. However, for mice... 

Ultrastmctural studies suggest that endothelial and/or epithelial injury precedes inflammation and fibrosis in early SSc-ILD (51). Thereafter, both proliferation of myofibroblasts and the overdevelopment of capillary microvessels seem to be involved in progressive lung fibrosis (66). T lymphocytes may play a fundamental role. T-cell responses to epitopes of DNA topoisomerase I are restricted, both in healthy subjects and in those with SSc (67-69). Thus, the anti-topoisomerase antibody may provoke a pathogenetic immune response in individuals with responsive T-cell clones. Lung tissue of patients with SSc-ILD displays lymphoid follicles with germinal centers and CD4 T cells of both THl and TH2 subsets that express the hallmark profile of cytokines [interleukin-4 (EL-4), EL-5, and y-interferon (INF-y)] in balanced numbers at the mRNA level (10), as well as accumulation of memory type lymphocytes (70). In BAL, patients with SSc-ELD show a predominance of CD8 T cells that produce Th2 cytokines, most notably EL-4, in contrast to those with no ILD (71). 

The inflammatory response in UC is propagated by atypical type 2 helper T cells that produce proinflammatory cytokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor (TNF).7 As discussed previously, a genetic predisposition to UC may partially explain the development of excessive colonic and rectal inflammation. The finding of positive perinuclear antineutrophil cytoplasmic antibodies (pANCA) in association with the human leukocyte antigen (HLA)-DR2 allele in a large percentage of patients with UC supports this theory.4,12... 

The term cytokine was first introduced in the mid 1970s. It was applied to polypeptide growth factors controlling the differentiation and regulation of cells of the immune system. The interferons and interleukins represented the major polypeptide families classified as cytokines at that time. Additional classification terms were also introduced, including lymphokines (cytokines such as IL-2 and IFN-y, produced by lymphocytes) and monokines (cytokines such as TNF-a, produced by monocytes). However, classification on the basis of producing cell types also proved inappropriate, as most cytokines are produced by a range of cell types (e.g. both lymphocytes and monocytes produce IFN-a). 

Many cell types can produce more than one cytokine. Lymphocytes, for example, produce a wide range of interleukins, CSFs, TNF, IFN-as and IFN-y. Fibroblasts can produce IL-1, -6, -8, and -11, CSFs, IFN-0 and TNF. 

Table 9.1 Many cell types are capable of producing a whole range of interleukins. T-lymphocytes are capable of producing all the interleukins, with the possible exception of IL-7 and IL-15. Many cell types producing multiple interleukins can also produce additional cytokines. For example, both macrophages and fibroblasts are capable of producing several interleukins, CSFs and PDGF...

Some growth factors may be classified as cytokines (e.g. interleukins, TGF-P and CSFs). Others (e.g. IGFs) are not members of this family. Each growth factor has a mitogenic (promotes cell division) effect on a characteristic range of cells. Whereas some such factors affect only a few cell types, most stimulate growth of a wide range of cells. 

The initiation and maintenance of IgE antibody responses are regulated by, and dependent upon, the generation of T lymphocyte responses of the correct (Th2-type) phenotype. These cells produce type 2 cytokines (including interleukins (IL) 4, 5, and 13) that collectively facilitate IgE antibody production, and that participate importantly in the elicitation of IgE-mediated allergic reactions [34-36],... 

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