THE MECHANISM OF ACTION OF ZADAXIN IS NOT COMPLETELY UNDERSTOOD BUT IS THOUGHT TO BE RELATED TO ITS IMMUNOMODULATING ACTIVITIES, CENTERED PRIMARILY AROUND AUGMENTATION OF T-CELL FUNCTION. IT HAS BEEN SHOWN TO PROMOTE T-CELL DIFFERENTIATION AND MATURATION; FOR EXAMPLE, CD4+, CD8+, AND CD3+ CELLS HAVE ALL BEEN SHOWN TO BE INCREASED. THYMOSIN ALPHA 1 HAS ALSO BEEN SHOWN TO INCREASE PRODUCTION OF IFN-G, IL-2, IL-3, AND EXPRESSION OF IL-2 RECEPTOR FOLLOWING ACTIVATION BY MITOGENS OR ANTIGENS, INCREASE NK CELL ACTIVITY, INCREASE PRODUCTION OF MIGRATORY INHIBITORY FACTOR (MIF), AND INCREASE ANTIBODY RESPONSE TO T-CELL DEPENDENT ANTIGENS. THYMOSIN ALPHA 1 HAS ALSO BEEN SHOWN TO ANTAGONIZE DEXAMETHASONE-INDUCED APOPTOSIS OF THYMOCYTES IN VITRO. IN VIVO ADMINISTRATION OF THYMOSIN ALPHA 1 TO ANIMALS IMMUNOSUPPRESSED BY CHEMOTHERAPY, TUMOR BURDEN, OR IRRADIATION SHOWED THAT THYMOSIN ALPHA 1 PROTECTS AGAINST CYTOTOXIC DAMAGE TO BONE MARROW, TUMOR PROGRESSION AND OPPORTUNISTIC INFECTIONS, THEREBY INCREASING SURVIVAL TIME AND NUMBER OF SURVIVORS. MANY OF THE IN VITRO AND IN VIVO EFFECTS OF THYMOSIN ALPHA 1 HAVE BEEN INTERPRETED AS INFLUENCES ON EITHER DIFFERENTIATION OF PLURIPOTENT STEM CELLS TO THYMOCYTES OR ACTIVATION OF THYMOCYTES INTO ACTIVATED T-CELLS.