Overall, Arg1 expression may compromise antimicrobial defenses in vivo during pathogen infection through three distinct mechanisms: 1) Arg1 depletes L-arginine from DCs, thereby preventing NOS2 from generating NO, which is effective in defending the organism against pathogen infections; 2) Arg1 from DCs competes for L-arginine required by T cells in the immune microenvironment; 3) Arg1-catalyzed generation of polyamines is essential for the growth of various parasites (27). Here, NOS2 is linked to infection.