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The interferon-γ (IFNγ)–inducible IRG proteins are a distinctive cytoplasmic GTPase family encoded by about 20 genes in the C57BL/6 mouse [1]. All four IRG genes that have been knocked out (Irgm1, Irgm3, Irgd, Irga6) have caused more or less striking susceptibility phenotypes to Toxoplasma gondii ([2], [3] and O. Liesenfeld, I. Parvanova, J. Zerrahn, S-J. Han, F. Heinrich, et al., unpublished data). However, one single member of the IRG family, Irgm1 (formerly called LRG-47), stands out because it has additionally been implicated in a remarkable range of resistances in the mouse: resistance to Trypanosoma cruzi [4], Leishmania major [5], Listeria monocytogenes [2], Mycobacterium tuberculosis [6], Mycobacterium avium [7], Chlamydia trachomatis [8], and Salmonella typhimurium [9]. These are all intracellular but otherwise very different organisms—some are protozoa, some Gram-negative bacteria, some Gram-positive, some living inside a vacuole or phagosome, and some free in the cytosol. Thus, Irgm1 appears to have exceptional properties of disease resistance not shared by other members of the IRG family.

The Mouse Resistance Protein Irgm1 (LRG-47): A Regulator or an Effector of Pathogen Defense?