الفهرس 
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Abstract
Alopecia areata is a dermatological disease characterized by non-scarring hair loss of the scalp and/or body, with an unpredictable and variable evolution in the patients.
Diverse studies have established that AA affects 1-2% of the general population with an estimated life time risk of 1.7%.
However, prevalence can vary between 0.1 and 6.9% depending on the population studied. Many studies have described an association with various types of thyroid disease, including simple goiter, myxoedema, Grave‟s disease and Hashimoto‟s thyroiditis. One large American study reported a rate of 8% compared with a rate of 2% in the general population. Most but not all studies have confirmed this association.
The course of AA in both children and adults is unpredictable. However, it has been established that a poor prognosis could be due to the early age of onset, the extent of hair loss, nail abnormalities, a positive family history for AA and comorbidity with autoimmune diseases. Severe cases occur more frequently before puberty and have less than a 10% chance of regaining hair despite treatments.
UL16 binding protein-3 (ULBP3) belongs to a class of proteins known as natural killer (NK) cell ligands, which serve to attract immune cells marked by a natural killer cell receptor known as NKG2D. Which are then poised to injure the hair follicle. Interestingly, NK ligands are also expressed in the affected organs of humans and animal models of the other three diseases: the joint lining in rheumatoid arthritis, the islet cells of the pancreas in type 1 diabetes and the gut in celiac disease.
In humans, NKG2D is expressed on natural killer (NK) cells cluster differentiation 8+ (CD8+) αβ T cells, γδ T cells, some NK-T cells, and a rare population of CD4+/CD28– T cells. NKG2D can deliver an activation signal to NK cells and, under some conditions, can act as a costimulatory receptor for TCR-mediated activation of T cells, in a similar manner as CD28. Under normal circumstances in the adult, NKG2D ligand expression is generally low or absent, but is induced under conditions of transformation. In the normal hair follicle, ULBP3 is turned off, because usually the hair follicle is invisible to the immune system. In active lesions from alopecia areata patients, however, the gene was activated in the outermost layer of the hair follicle, called the dermal sheath.
The perturbations in the hair follicle microenvironment contribute to the initiation of AA. ULBP3 has been postulated that NKG2D ligands, if over expressed in genetically susceptible individuals, can trigger an autoimmune response against the tissue expressing the ligand. To probe this hypothesis in the setting of AA, there is marked upregulation of ULBP3 expression in the dermal sheath as well as the dermal papilla, but not in control individuals or those with other inflammatory scalp disorders. It has also been found in hair follicles in scalp biopsy specimens from patients with active disease. It is now postulated that the characteristic T cell “swarm of bees” infiltrate seen in alopecia areata is the result of T cells being attracted to the hair follicle by NKG2D-activating ligands. Many drugs currently being used or being evaluated for other autoimmune diseases that
Summary
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work through these mechanisms might prove to be very effective in alopecia areata.
The aim of this study is to detect UL16 binding protein 3 (ULBP3) expression in AA patients and to correlate its expression with the available clinical data. The study recruited 85 subjects, 55 AA patients and 30 controls. All patients were subjected to detailed history taking and examination. 4mm scalp punch biopsies were taken form sites where the disease was active. Scalp biopsy specimens form healthy volunteers were included as controls. Samples were washed with saline and then homogenized in RLT lyses buffer (Qiagen RN ease mini kit. Helden. Germany) and stored at -80о until analyzed for doing real-time polymerase chain reaction (PCR) for estimation of ULBP3.
The results revealed higher level of ULBP3 gene in cases was statistically significant compared with controls (P = 0.001) statistically non-significant relationship between ULBP3 gene expression and clinical data of the studied cases.
Statistically significant positive correlations between ULBP3 gene expression and age of patients in years (P=0.038) and disease duration in years (P=0.005)
Statistically significant negative correlations between Kavak‟s classification and age of patients in years , statistically non-significant correlations between Kavak‟s classification and disease duration in years, SALT score and ULBP3 gene expression among studied cases.