A method of reducing pathogenic T-helper cell activity in a human subject in need thereof is disclosed. The method comprises administering to the human subject, known to have a condition mediated by one or more differentiated T-helper cells responsive to Cd51, an effective amount of a nitroxide antioxidant, where the nitroxide antioxidant increases Cd51 expression, thereby reducing pathogenic T-helper cell activity. In some embodiments, the condition is an autoimmune disease.
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