We note that irradiation did alter the severity of infection, resulting in high parasite burdens in all groups, and a high number of infiltrating cells (Fig 5E–5G) Nonetheless, these experiments revealed that il1rl1-deficiency on radio-resistant cells, or in il1rl1-/- recipient, but not donor mice, recapitulated the phenotype of global knockouts, including reduced infiltrating myeloid and T cell numbers, and parasite burden, whereas il1rl1 expression on donor bone marrow, was dispensable (Fig 5E–5G). The gene discussed is IL1RL1; the disease is infection.