Assessment of Circulating CCR6 Level in Acute Myocardial Infarction and its Association with Disease Severity.

Background: Acute myocardial infarction (AMI) pathophysiology is mediated by systemic, intraplaque myocardial inflammatory processes that occur mainly due to coronary artery thrombosis in an atherosclerotic plaque area. The G-protein-coupled chemokine receptor (Ccr6) is displayed on the surface of many types of leukocytes, that have been found in atherosclerotic plaques. It is a novel mediator of inflammation and immune response.

Association between Interleukin-17F 7488A/G and 7383A/G polymorphisms and susceptibility to juvenile idiopathic arthritis.

Background: Interleukin-17F (IL-17F), one of the cytokines, is crucial in the pathophysiology of juvenile idiopathic arthritis (JIA). Therefore, we aimed to determine the relation between IL17F 7488A/G and IL17F 7383A/G single-nucleotide polymorphisms and JIA susceptibility and to explain their impact on the disease activity.

Methods: Genomic DNA of 70 patients with JIA and 70 age and sex-matched controls were extracted and typed for IL17F 7488A/G and IL17F 7383A/G single-nucleotide polymorphisms, using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls.

DEFB1 gene polymorphisms modify vitiligo extent and response to NB-UVB phototherapy.

Human beta defensin-1(hBD-1); an antimicrobial peptide, has immune regulatory effects which may be involved in autoimmunity. The aims were to evaluate the association between defensin beta 1 (DEFB1) (-44 C/G) and (-20 G/A) gene polymorphisms with the risk of vitiligo development, the extent of the disease and the response to NB-UVB treatment in a sample of Egyptian population. 178 active nonsegmental vitiligo patients and 182 control subjects were included in this prospective case control study.

Serum TWEAK: A cutoff between segmental and nonsegmental vitiligo.

Background: TWEAK/Fn14 is expressed in many tissues including the skin, playing an important role in many inflammatory, autoimmune, and neoplastic cutaneous disorders.

Aims: To assess the serum levels of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in vitiligo patients.

Methods: This case-control study included 100 subjects (50 vitiligo patients and 50 control subjects) recruited from Dermatology Outpatient Clinic, Benha University.

Tumor Necrosis Factor-like Weak Inducer of Apoptosis: A Novel Serum Marker in Patients with Severe Alopecia.

Background: Alopecia areata (AA) is a common form of nonscarring hair loss of scalp and/or body. Genetic predisposition, autoimmunity, and environmental factors play a major role in the etiopathogenesis of AA. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a multifunctional cytokine expressed on various cell types and tissues and acts through binding to its sole receptor factor-inducible 14 (Fn14).

Serum TWEAK in acne vulgaris: An unknown soldier.

Background: TWEAK is an inflammatory cytokine which is involved in the development of many inflammatory disorders.

Aims: This study aimed to evaluate serum levels of TWEAK in patients with acne vulgaris.

Subjects And Methods: This case-controlled study included 100 acne vulgaris patients divided into two groups.

Assessment of IL-17F rs763780 gene polymorphism in immune thrombocytopenia.

Interleukin-17F rs763780 (7488A/G) gene polymorphism obviously affecting the expression and activity of IL17F and may affect primary immune thrombocytopenia (PIT) susceptibility and its clinical features in Egyptian children and adults. 105 ITP patients divided into (63 pediatric and 42 adult patient) and 112 age and sex matched healthy controls were enrolled in this case control study. All patients were subjected to history taking; clinical examination, CBC, bone marrow aspiration and genotyping of IL17F rs763780 polymorphism by (PCR-RFLP) technique.