کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3385386 | 1220591 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Perfil de citosinas relacionadas con linfocitos Th17: rol fisiopatológico y potencial uso como biomarcadores de actividad del lupus eritematoso sistémico
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
ایمونولوژی، آلرژی و روماتولوژی
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چکیده انگلیسی
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease expressed in genetically predisposed individuals. The interaction of a trigger factor together with the failure of the mechanisms for handling potential reactive autoantigens leads to the development of immune complex responsible for the damage of the target organs. Elements of both innate and adaptive immunity have been implicated in the pathophysiology of the disease, but given the heterogeneity of the SLE, we still do not have a biological marker of activity of the disease with high sensitivity, specificity and predictive value. Recently, a cell population was described as lymphocytes T helper 17 (Th17), so called because of their production of Interleukin 17 (IL-17), cytokine that mediates physiological and pathophysiological processes implicated in the development of inflammatory conditions such as SLE. It has been postulated that serum IL-17 may be a biomarker that meets these parameters; however, data on this topic is still incomplete. We present a review of the ontogenetic mechanisms of Th17 lymphocytes, an explanation of its pathophysiological role in SLE and clinical studies that support and discuss the role of Th17 lymphocytes related cytokines as biomarkers of disease activity in SLE.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Revista Colombiana de ReumatologÃa - Volume 22, Issue 4, December 2015, Pages 217-224
Journal: Revista Colombiana de ReumatologÃa - Volume 22, Issue 4, December 2015, Pages 217-224
نویسندگان
Héctor Hernán Cubides, Claudia Marcela Mora K., Leydi Viviana Parra I., John Londono P.,