Moreover, the previous studies suggested that silencing or deletion of SOCS3 in the animal model leads to the aggravation of airway hyper-responsiveness and other inflammatory conditions. The increased expression of SOCS3 has been observed in the patients with allergic conditions. SOCS3 controls the IL-6 mediated signaling cascade through the negative feedback mechanism. IL-6 initiates JAK-STAT signaling cascade and the expression of Suppressor of Cytokine Signaling 3 (SOCS3), a signaling molecule which regulates the immune responses to inflammation and infection. IL-6 is a potent inducer of Janus Kinase-Signal Transducers and Activators of Transcription (JAK-STAT) signaling cascade. IL-6 is a crucial immune system regulator that is involved in the survival and maturation of mast cells thereby it is associated with the prognosis of allergy. This vast spectrum of pro-inflammatory cytokines implies that it is a Th2 cell mediated response that leads to late phase allergic response. Cross-talk through the activity of pro-inflammatory cytokines such as interferon γ (IFN- γ), interleukin-6 (IL-6), IL-13, IL-5, IL-4, granulocyte macrophage colony stimulating factor (GM-CSF) and other chemokines is essential to regulate allergic responses. IgE-mediated inflammation, triggered by IgE-specific antigen, is regulated by the cascade of defense signaling involving FcεR (high affinity receptor of IgE) on the surface of mast cells. According to American Academy of Allergy, Asthma, and Immunology, 10–40% of the world population has been reported with allergen sensitization to foreign antigens. The incidence of allergy is increasing day by day in the various regions of the world. Hypersensitivity of the immune system, due to elevated level of immunoglobulin E (IgE), instigates the allergic inflammation that leads to atopic conditions, including rhinitis, conjunctivitis, asthma, food allergy and anaphylaxis, after the exposure to a specific associated allergen. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper.įunding: The study was supported by National University of Sciences and Technology (NUST) as a part of student research fund. Received: JanuAccepted: JPublished: June 28, 2019Ĭopyright: © 2019 Jannat et al. PLoS ONE 14(6):Įditor: Lucienne Chatenoud, Université Paris Descartes, FRANCE Notably, the study established SOCS3 and IL-6 as potential targets for the diagnosis/prognosis of allergy and for the development of reliable therapeutic strategies to control atopic conditions in the near future.Ĭitation: Jannat A, Khan M, Shabbir M, Badshah Y (2019) Expression of suppressor of cytokine signaling 3 (SOCS3) and interleukin-6 (-174-G/C) polymorphism in atopic conditions. Therefore establishing the role of IL-6 (-174-G/C) polymorphism on the expression of SOCS3 and IL-6 in atopic cases.
Expression of SOCS3 and IL-6 serum levels were found to be highly correlated. Furthermore, the polymorphic study of IL-6 promoter region (IL-6 174-G/C) in atopic population has reasserted the importance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. Female population was found to be at a higher risk to develop atopic condition than male population as females exhibited higher expression of both SOCS3 and IL-6 than males. Moreover, IL-6 has, also, been found significantly enhanced in the serum level of atopic cases (26.4 pg/ml) as compared to control cases (3.686 pg/ml). The expression study of SOCS3 through real-time PCR analysis revealed, a 5.9 mean fold increase in SOCS3 expression in atopic cases in comparison to control cases. The given study focuses on the assessment of crosstalk between SOCS3 and IL-6 to unravel the molecular significance of SOCS3 and IL-6 in the diagnosis and prognosis of allergy. IL-6 mediated defense responses are tightly regulated by Suppressor of Cytokine Signaling 3 (SOCS3), an inhibitory molecules of Janus Kinase-Signal Transducers and Activators of Transcription (JAK-STAT) signaling, in a negative feedback mechanism. IgE-mediated inflammation is regulated by the cascade of defense related signaling molecules including interleukin-6 (IL-6) that plays pivotal role in the survival and maturation of mast cells during an allergic reaction. Hypersensitivity of the immune system is caused by elevated immunoglobulin E (IgE) levels in the serum, in response to a discrete allergen leading to allergic reactions.
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