2012
DOI: 10.1177/0192623311430694
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Cytokine Pathways in Allergic Disease

Abstract: Cytokines are critical in allergic intercellular communication networks, and they contribute to disease pathology through the recruitment and activation of pro-inflammatory leukocytes and in chronic disease to pro-fibrotic/remodeling events. Th2 cytokines predominate primarily in mild to moderate allergic asthma, although clinical trials with inhibitors of IL-4 and IL-5 have not provided the robust efficacy observed in animal models of allergy. These results not only highlight the complexity of allergic diseas… Show more

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Cited by 54 publications
(40 citation statements)
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References 137 publications
(186 reference statements)
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“…15) Since IL-10 level is strongly correlated to IgE titer, 28) and AD is often involved in the infiltration IgE, the significant reduction of the IL-10 level could lead to inhibition of IgE. 29,30) Interestingly, our result revealed a consistent decrement pattern of IL-10 and IgE level in HW group as compared to PW group. Viewed together, HW might affect the immune balance through the suppression of TARC, inflammatory cytokines, and IgE levels in DNCB-induced AD mice.…”
Section: )supporting
confidence: 52%
“…15) Since IL-10 level is strongly correlated to IgE titer, 28) and AD is often involved in the infiltration IgE, the significant reduction of the IL-10 level could lead to inhibition of IgE. 29,30) Interestingly, our result revealed a consistent decrement pattern of IL-10 and IgE level in HW group as compared to PW group. Viewed together, HW might affect the immune balance through the suppression of TARC, inflammatory cytokines, and IgE levels in DNCB-induced AD mice.…”
Section: )supporting
confidence: 52%
“…Th2 cells are suspected as the key culprit in the pathophysiology of atopic disorders [1]. Interleukin 17A (IL-17A), commonly known as IL-17, is produced by T helper 17 (Th17) subset of CD4 + T cells.…”
Section: Introductionmentioning
confidence: 99%
“…IL-33 may be released by damaged cells during infection or trauma—suggesting it functions as an alarmin (Moussion et al 2008). Pathogens, allergens, and other environmental agents may also trigger tissue damage that results in IL-33 secretion (Wang et al 2011; Yamaguchi et al 2012; Bartemes et al 2012; Williams et al 2012; Barlow et al 2012). Moreover, IL-33 expression in bronchial asthma correlates with disease severity (Prefontaine et al 2010).…”
Section: Introductionmentioning
confidence: 99%