أعضاء هيئة التدريس - جامعة بنها
Serum Levels of Tumor Necrosis Factor-Like Weak Inducer of Apoptosis (TWEAK) in Patients with Lichen Planus
• 2018
معلومات البحث
المؤلفون
Nehal Ahmed Abd El-Baky, Abd El-Aziz Ibrahim El-Taweel, Ahmed Mohamed Hamed , Amira Mohamed Noureldin Abdel Rahman
الكلمات المفتاحية
Not Available
المجلة العلمية
Not Available
الناشر
Not Available
المجلد
Not Available
العدد
Not Available
الصفحات
Not Available
publication.type
International
رابط البحث
Not Available
المواد المرفقة
Not Available
الملخص
Summary
Lichen planus is a chronic mucocutaneous autoimmune inflammatory disorder of the stratified squamous epithelium. Apoptosis of basal keratinocytes is a hall mark of LP. Lichen planus is a T-cell-mediated autoimmune disease. Inflammatory cells involved in this process consist of T helper and T cytotoxic lymphocytes, NK cells, and dendritic cells. T-cell activation is central to the pathogenesis of LP.
TNF-like weak inducer of apoptosis is a relatively new member of the TNF superfamily of ligands with proapoptotic effects. TWEAK/Fn14 signaling pathway participates in multiple biological activities, including the proliferation, differentiation, migration and death (apoptosis/necrosis) of cells, angiogenesis, and inflammatory responses.
The pathological functions of TWEAK are primarily attributed to its ability to induce the expression of several proinflammatory cytokines, chemokines, cell adhesion molecules, and matrix-degrading enzymes mainly through the activation of NF-κB.
The aim of the present study was to evaluate serum levels of TWEAK in patients with lichen planus in order to assess its role in the pathogenesis of lichen planus and also to assess the correlation between the serum levels of TWEAK and the different clinical parameters of the disease.
The current study included 50 patients with different clinical variants of LP. In addition to 50 apparently healthy individuals of matched age and sex as a control group.
The patients were subjected to full history taking, clinical examination and laboratory investigations including serum levels of TWEAK using ELISA technique.
The results of this study showed that
• Serum levels of TWEAK were significantly higher in patients with LP compared to healthy control subjects.
• There was a statistically positive correlation between serum levels of TWEAK and the disease activity.
• There was no statistically significant correlation between serum levels of TWEAK and patients' age, sex, BMI, smoking.
• Also, there was no correlation between serum levels of TWEAK and disease duration or affected area.
Conclusion
TWEAK is supposed to have a pivotal role in the pathogenesis of LP through several mechanisms and also in the disease activity and perpetuation. So, it can be used as marker for the disease activity.
Lichen planus is a chronic mucocutaneous autoimmune inflammatory disorder of the stratified squamous epithelium. Apoptosis of basal keratinocytes is a hall mark of LP. Lichen planus is a T-cell-mediated autoimmune disease. Inflammatory cells involved in this process consist of T helper and T cytotoxic lymphocytes, NK cells, and dendritic cells. T-cell activation is central to the pathogenesis of LP.
TNF-like weak inducer of apoptosis is a relatively new member of the TNF superfamily of ligands with proapoptotic effects. TWEAK/Fn14 signaling pathway participates in multiple biological activities, including the proliferation, differentiation, migration and death (apoptosis/necrosis) of cells, angiogenesis, and inflammatory responses.
The pathological functions of TWEAK are primarily attributed to its ability to induce the expression of several proinflammatory cytokines, chemokines, cell adhesion molecules, and matrix-degrading enzymes mainly through the activation of NF-κB.
The aim of the present study was to evaluate serum levels of TWEAK in patients with lichen planus in order to assess its role in the pathogenesis of lichen planus and also to assess the correlation between the serum levels of TWEAK and the different clinical parameters of the disease.
The current study included 50 patients with different clinical variants of LP. In addition to 50 apparently healthy individuals of matched age and sex as a control group.
The patients were subjected to full history taking, clinical examination and laboratory investigations including serum levels of TWEAK using ELISA technique.
The results of this study showed that
• Serum levels of TWEAK were significantly higher in patients with LP compared to healthy control subjects.
• There was a statistically positive correlation between serum levels of TWEAK and the disease activity.
• There was no statistically significant correlation between serum levels of TWEAK and patients' age, sex, BMI, smoking.
• Also, there was no correlation between serum levels of TWEAK and disease duration or affected area.
Conclusion
TWEAK is supposed to have a pivotal role in the pathogenesis of LP through several mechanisms and also in the disease activity and perpetuation. So, it can be used as marker for the disease activity.