Depleting CD4+ T helper cells by anti-CD4 treatment completely abrogated the protective effects of PGRN on CDI-associated mortality and morbidity (Figure 6a, b) and also increased the mortality and morbidity of untreated mice after CDI, demonstrating that CD4+ T helper cells were an essential downstream effector cell in PGRN-mediated protection. The gene discussed is CD4; the disease is clostridium difficile infection.