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Th2 Differentiation (th2 + differentiation)

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Medical Sciences100%

Selected Abstracts

Signaling pathways in Th2 development

IMMUNOLOGICAL REVIEWS, Issue 1 2004
Kerri A. Mowen
Summary:, In order for an immune response to be successful, it must be of the appropriate type and magnitude. Intracellular residing pathogens require a cell-mediated immune response, whereas extracellular pathogens evoke a humoral immune response. T-helper (Th) cells orchestrate the immune response and are divided into two subsets, Th1 and Th2 cells. Here, we discuss the mechanisms of Th2 development with a focus on signal transduction pathways that influence Th2 differentiation. [source]

The immunobiology of Th1 polarization in high-pathology schistosomiasis

IMMUNOLOGICAL REVIEWS, Issue 1 2004
Miguel J. Stadecker
Summary:, Schistosomiasis is a serious global helminthic disease, in which the main immunopathology consists of a granulomatous and fibrosing reaction against tissue-trapped parasite eggs. The severity of this inflammatory process, the product of a CD4+ T-cell-mediated immune response against parasite egg antigens, is, however, markedly uneven, both in human patients and among mouse strains in an experimental model. Severe schistosomiasis is associated with persistently elevated pro-inflammatory T-helper-1 (Th1)-type cytokines, whereas milder pathology is present when Th2 cytokines dominate. This scenario is supported by the pronounced pathology resulting from the obliteration of pathways that facilitate Th2 differentiation and by the development of more intense lesions in mouse strains that fail to downregulate the Th1 response. Genetically prone high-pathology mice have a higher proportion of CD4+ T cells in lymph nodes and granulomas, in which the Th1 phenotype is driven by interleukin-12; they also develop a dominant repertoire against peptide 234,246 of the major Sm-p40 egg antigen, utilizing a strikingly restricted T-cell receptor structure that involves V,11.3,8. In turn, low-pathology mice exhibit enhanced CD4+ T-cell apoptosis, which contributes to limit pathology. The definition of distinctive immune profiles associated with polar forms of schistosomiasis opens opportunities for targeted immuno-intervention in individuals suffering from or at risk of severe disease. [source]

ORIGINAL ARTICLE: IL-6 as a Regulatory Factor of the Humoral Response During Pregnancy

AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 3 2008
Valeria Dubinsky
Problem, Regulatory factors seem to be essential to achieve transition from implantation window to placental vascularization. A novel function of interleukin (IL)-6 in the promotion of Th2 differentiation and inhibition of Th1 polarization has been demonstrated. Considering that Th2 response promotes antibody synthesis, we postulate that IL-6 could be modulating the quality of this response during pregnancy by increasing the proportion of blocking asymmetric antibodies. Method of study, We investigated expression of blocking-asymmetric-IgG during pregnancy of CBA/J × DBA/2 abortion model treated with IL-6, with regards to CBA/J × BALB/c. We also determined asymmetric-IgG production in IL-6-deficient pregnant mice. Results, We found that IL-6 treatment increased asymmetric-IgG in multiparous placentas from abortion combination whereas diminished abortion rate. Moreover, asymmetric-IgG proportion was diminished in sera from IL-6-deficient pregnant mice. Conclusion, Modulation of asymmetric antibody synthesis could be another mechanism implicated in the beneficial effect of IL-6 in prevention of murine recurrent abortion. [source]

Retinoid ameliorates experimental autoimmune myositis, with modulation of Th cell differentiation and antibody production in vivo

ARTHRITIS & RHEUMATISM, Issue 10 2009
Naho Ohyanagi
Objective Polymyositis and dermatomyositis are chronic inflammatory muscle diseases. Retinoids are compounds that bind to the retinoic acid binding site of retinoic acid receptors and have biologic activities similar to those of vitamin A. Recent studies indicate that retinoids promote Th2 differentiation and suppress Th1 and Th17 differentiation in vitro. The present study was undertaken to examine the effects of a synthetic retinoid, Am80, on experimental autoimmune myositis as well as on Th phenotype development and antibody production. Methods Experimental autoimmune myositis was induced in SJL/J mice by immunization with rabbit myosin. Am80 was administered orally once daily. Its effects were evaluated by measurement of the numbers of infiltrating inflammatory cells, production of inflammatory cytokines in muscle, production of Th-specific cytokines by myosin-stimulated splenic T cells, and production of antimyosin antibodies in serum. Results In mice with experimental autoimmune myositis, orally administered Am80 significantly reduced the number of infiltrating inflammatory cells and the expression of tumor necrosis factor , and interleukin-1, (IL-1,) in muscle. Moreover, Am80 increased production of interferon-,, IL-4, and IL-10, but not IL-17, by myosin-stimulated splenic T cells of mice with experimental autoimmune myositis, suggesting that it could enhance differentiation into Th1 and Th2, but not Th17, in vivo. Am80 also decreased serum levels of IgG2a and IgG2b antimyosin antibodies, but did not affect levels of IgG1 antimyosin antibodies. In addition, it suppressed chemokine expression and activator protein 1 activity in myoblasts in vitro. Conclusion The synthetic retinoid Am80 has an inhibitory effect on experimental autoimmune myositis. It might regulate the development of Th phenotype and antibody production in vivo, in addition to its effects on cytokine and chemokine production. [source]

The common G-allele of interleukin-18 single-nucleotide polymorphism is a genetic risk factor for atopic asthma.

CLINICAL & EXPERIMENTAL ALLERGY, Issue 2 2006
The SAPALDIA Cohort Study
Summary Background IL-18 is a pleiotrophic cytokine involved in both, T-helper type 1 (Th1) and Th2 differentiation. Recently genetic variants in the IL-18 gene have been associated with increased risk of atopy and asthma. Objective To examine the relationship of a genetic, haplotype-tagging promotor variant ,137G/C in the IL-18 gene with atopic asthma in a large, well-characterized and population-based study of adults. Methods Prospective cohort study design was used to collect interview and biological measurement data at two examination time-points 11 years apart. Multivariate logistic regression analysis was used to assess the association of genotype with asthma and atopy. Results The G-allele of the IL-18 promotor variant (,137G/C) was associated with a markedly increased risk for the prevalence of physician-diagnosed asthma with concomitant skin reactivity to common allergens. Stratification of the asthma cases by skin reactivity to common allergens revealed an exclusive association of IL-18 ,137 G-allele with an increased prevalence of atopic asthma (adjusted odds ratio (OR): 3.63; 95% confidence interval: (1.64,8.02) for GC or GG carriers vs. CC carriers), and no according association with asthma and concomitant negative skin reactivity (adjusted OR: 1.13; 0.66,1.94). The interaction between IL-18 ,137G/C genotype and positive skin prick test was statistically significant (P=0.029). None of 74 incident asthma cases with atopy at baseline exhibited the CC genotype. Conclusion Our results strongly suggest that this variant of the IL-18 gene is an important genetic determinant involved in the development of atopic asthma. [source]