In the present study, we follow in detail the evolution of both Th2 and Treg parameters over the course of infection, with particular focus on CTLA-4 (CD152), glucocorticoid-induced tolerance-associated receptor (GITR), CD103, TGF-β and Foxp3 within both CD4+CD25+ and CD4+CD25– subsets, as well as the functional characteristics of Treg populations. The gene discussed is ITGAE; the disease is infection.