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Gene expression studies in murine asthma models demonstrated thymulins ability to shift immune balance away from Th2 dominance: [3] Increased IFN- expression, stimulating Th1 cells Reduced IL-13 secretion (Th2-associated mediator) Decreased eotaxin (eosinophil chemotactic factor) Lower eosinophil, neutrophil, and mononuclear cell infiltration in bronchoalveolar lavage fluid Zinc deficiency investigations show that reduced thymulin activity impairs Th1 cell proliferation while leaving Th2 function intact, resulting in measurable Th1/Th2 imbalance