Background: Alopecia areata is an autoimmune condition that shows no symptoms of inflammation on the surface of the skin. The cause of hair loss in AA patients is still a mystery, however T cells and proinflammatory cytokines are thought to play a role. Many variables, including genetic predisposition, play a role in the development of an overactive immune response. Desmosomes, the cell adhesion junctions created by epithelial cells, are the source of our serum marker, type-1 transmembrane glycoproteins. Cell and tissue-specific expression patterns for the three Dsc genes expressed in mammals are evident. At Benha University Hospital's dermatology outpatient clinic, 60 individuals with AA were included in the research. In addition, a control group of 30 healthy adults of the same age and sex was used. All patients (100 percent) in this research had a quick onset of symptoms. Only 6.3 percent and 3.3 percent of the patients, respectively, had an intermitted or regressive course of action. The median length was three months, although it varied from two days to eleven years. Fewer than a quarter of the participants in our research (20 percent) had a history of the disease running in their families. Our findings indicated that 50% of patients had atopy and pitting of the nails (51.7 percent ). AD was found in more than a third of the patients (38.3 percent ). The median number of patches seen in this study was 1.5, with a range of one to nine. More than three-quarters of the patients were afflicted with occipital encephalitis, followed by parietal encephalitis, totalis encephalitis, vertex encephalitis, frontal encephalitis, ophiasis, and beard encephalitis (1.7 percent ). According to our findings, 68.3% of the patients had undergone prior therapy, and more than a third (41.6%) had a positive response.