TNF-alpha single nucleotide polymorphisms in atopic dermatitis

Behniafard, Nasrin; Gharagozlou, Mohammad; Farhadi, Elham; Khaledi, Mojdeh; Sotoudeh, Soheila; Darabi, Behzad; Fathi, Seyed Mohammad; Moghaddam, Zahra Gholizadeh; Mahmoudi, Mahdi; Aghamohammadi, Asghar; Amirzargar, Ali Akbar; Rezaei, Nima

doi:10.1684/ecn.2012.0323

Cited by 28 publications

(24 citation statements)

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“…16 TNF-a, as a proinflammatory cytokine, plays a key role in the inflammation of AD. 17 In this study, we showed for the first time in the literature that tacrolimus can affect the function of monocytes by suppressing the expression of cytokines and chemokines. These findings suggest that in addition to inhibiting the activation of T cells, tacrolimus may exert therapeutic effects on AD by modulating the expression of AD-related cytokines and chemokines in monocytes.…”

Section: Discussionmentioning

confidence: 70%

“…16 TNF-a is a proinflammatory cytokine and is considered a potential biomarker of AD. 17 TNF-a levels rapidly increase after mechanical trauma and skin barrier disruption, inducing the production of chemoattractants and adhesion molecules, and subsequently facilitating the recruitment and proliferation of leukocytes in the skin. 4 Calcineurin inhibitors (CNIs), such as tacrolimus, are widely used as topical agents to treat AD by modulating Tcell activity.…”

Section: Introductionmentioning

confidence: 99%

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Tacrolimus suppresses atopic dermatitis-associated cytokines and chemokines in monocytes

Chang

Lin

Kuo

et al. 2016

Journal of Microbiology, Immunology and Infection

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Section: Discussionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Tacrolimus suppresses atopic dermatitis-associated cytokines and chemokines in monocytes

Chang

Lin

Kuo

et al. 2016

Journal of Microbiology, Immunology and Infection

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“…A previous study on QP with methods of ELISA by Yuan-Yuan and Lin-Feng [27] had demonstrated that 100% QP and 75% QP significantly decrease the levels of IL-5 after 2-weeks treatment in DNFB-induced AD-like lesions. In addition, the 100% QP elevated the levels of TNF- α in skin ( P < 0.05), which had an unclear relation with mechanism of AD [28, 29]. Resulted from that study, QP showed no effect on IL-1 β (produced mainly by macrophagocyte) and IL-2 expression in skin (Table 5).…”

Section: Discussionmentioning

confidence: 97%

Anti-Inflammatory Effect of Qingpeng Ointment in Atopic Dermatitis-Like Murine Model

Jiang

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Qingpeng ointment (QP) is a Chinese medicine which has been used in treatment of atopic dermatitis (AD) in China. AD-like lesions were induced in BALB/c mice by repeated application of 2,4-dinitrofluorobenzene (DNFB) on shaved backs. The mice were then treated for 2 weeks with QP of different concentrations and Mometasone Furoate cream (MF), respectively. Macroscopic and microscopic changes of the skin lesions were observed after the treatment. The levels of serum immunoglobulin (Ig) E, tissue interferon (IFN)-γ, and interleukin (IL)-4 and IL-17A and the levels of involucrin, filaggrin, and kallikrein7 in epidermis were measured. The results show severe dermatitis with immune profiles similar to human acute AD. A significant infiltration of CD4+ T and mast cells was observed in dermis of lesion but inhibited by QP after a 2-week treatment with it. The production of IgE, IL-4 and the mRNA expression of IL-17A were also suppressed, but the level of IFN-γ was increased. MF suppressed all production of these cytokines and IgE. Accordingly, the mechanism of QP on AD might correlate with its ability of modulating the immune dysfunctions rather than suppressing them. It had no effect on expressions of involucrin and filaggrin, except that its vehicle decreased the level of kallikrein7.

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“…Some studies showed that 308G/A polymorphism of TNF-α gene is related to higher susceptibility for atopic dermatitis, asthma, ankylosis spondylitis and increase mortality in meningococcal infection [34][35][36][37]. Lahat et al suggested that altered TNF-α levels play a role in the pathogenesis of FS [38].…”

Section: Discussionmentioning

confidence: 99%