Elution profile of IgG on a Protein A agarose affinity column. Open in a separate window Fig. patients with the patchy, persistent type of alopecia. Furthermore, sera from AA patients had lower levels of SOD activity as compared to control sera. Conclusion This is the first report showing an association between OH-modified SOD and AA. These novel results demonstrate that OH radical-mediated changes in SOD present unique neo-epitopes that might contribute to antigen-driven antibody induction in AA. strong class=”kwd-title” Keywords: Alopecia areata, Autoimmunity, OH-SOD, Reactive oxygen varieties, Superoxide dismutase Intro Alopecia areata (AA) is definitely a non-scarring, autoimmune, inflammatory condition resulting in hair loss. It is relatively common, with an incidence of 0.15% worldwide1. Although the exact pathogenesis is unfamiliar, autoimmune reactions have been implicated in AA2. Due to an aberrant T cells response observed against numerous self antigens, AA is now considered to be an autoimmune disease3. This etiology has been proposed on the basis of evidence such as its association with numerous SIBA autoimmune diseases4 and the presence of autoantibodies and various underlying immunologic abnormalities in the affected sites5. However, the precise mechanism of autoantibody generation in AA remains unclear5,6. It is well recorded that oxidative stress plays a vital part in AA as SIBA well as other pores and skin disorders7,8,9,10,11,12. Numerous studies have shown that AA is definitely associated with improved formation of free radicals and a decrease in antioxidant potential7,8,9,10,13,14,15. This may result in oxidative damage to cell parts, including proteins and nucleic acids, as seen in several other autoimmune diseases16,17,18. Superoxide dismutase (SOD) is definitely a perfect antioxidant enzyme that eliminates the effects of superoxide, therefore limiting the toxicity from reactive oxygen species (ROS)19. Hence, SOD is considered an important regulator of oxidative stress. SOD dysfunction has been reported in individuals with AA7,8,9,15, while SOD antigenicity has been observed in numerous chronic conditions20. It is assumed that since SOD may be constantly exposed to oxidative stress, alterations SIBA may occur in the enzyme’s conformation and function, resulting in changes of its biological properties. Consequently, this study was designed to test the hypothesis that oxidative by-products such as hydroxyl radicaldamaged SOD help to initiate autoimmunity in AA. To test this hypothesis, the presence of circulating autoantibodies in AA individuals directed against ROS-modified SOD (ROS-SOD) was investigated. This novel study helps the association between ROS-SOD and AA pathogenesis and provides evidence that ROS-damaged SOD could be an important biomarker for the evaluation of oxidative stress in AA individuals. MATERIALS AND METHODS Patient recruitment The study was carried out in accordance with the Code of Ethics for Study Involving Humans from the World Medical Association (Declaration of Helsinki, as revised in Tokyo 2004). The study was authorized by the local ethics committee of the College of Medicine, Qassim University or college, Kingdom of Saudi Arabia. Study subjects were recruited through the NR4A2 dermatology outpatient medical center of Qassim University or college, Buraidah, Kingdom of Saudi Arabia, and educated consent was from each subject. The study group included 26 AA subjects (5 females and 21 males) and their age range was 19~45 years (meanstandard deviation [SD], 31.47.32 years). The duration of the disease ranged from one month to 18 years. Subjects were classified relating to Alopecia Areata Basis Clinical Assessment Recommendations21, where subjects with less than 100% scalp hair loss for 1 year were classified as AA patchy prolonged (AAP; n=21), while those with 100% scalp and body hair loss were classified as alopecia universalis (AU; n=5). Except for one subject who was treated with systemic corticosteroids and 10 subjects who have been.