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IFN-- and TNF-independent vitamin D-inducible human suppression of mycobacteria: the role of cathelicidin LL-37

Martineau, A. R., K. A. Wilkinson, S. M. Newton, R. A. Floto, A. W. Norman, K. Skolimowska, R. N. Davidson, O. E. Sørensen, B. Kampmann, C. J. Griffiths, and R. J. Wilkinson. 2007. IFN-- and TNF-independent vitamin D-inducible human suppression of mycobacteria: the role of cathelicidin LL-37. J. Immunol. 178: 7190–7198 .

In the Introduction, Materials and Methods, Discussion, Fig. 4D, and the Fig. 4 legend, all but one reference made to IRGC should be to IRGM. The sentence on page 7191, repeated on page 7194, "There has been no investigation of the human homolog of LRG-47 (IRGC) in humans" is incorrect. There are two human homologs; the one under investigation in our publication was in fact IRGM. Materials and Methods correctly describe primers to detect the transcript of IRGM, not IRGC. Furthermore, although the statement on page 7197 "Humans have only one intact p47 GTPase (IRGC) whose expression has been reported from testis but not THP-1 cells" is correct, it has little relevance to our work because we only measured the transcript of IRGM.

The authors wish to clarify that the sole IRG-family (p47) GTPase transcript measured in this work was the product of IRGM. The human IRGM gene product is a 181-aa fragment expressed constitutively in many cell types under the probable control of the long terminal repeat of an endogenous retrovirus (Bekpen, C., J. P. Hunn, C. Rohde, I. Parvanova, L. Guethlein, D. M. Dunn, E. Glowalla, M. Leptin, and J. C. Howard. 2005. The interferon-inducible p47 (IRG) GTPases in vertebrates: loss of the cell autonomous resistance mechanism in the human lineage. Genome Biol. 6: 492). It has been implicated in autophagy and intrinsic resistance to mycobacterial infection in human macrophages (Singh, S. B., A. S. Davis, G. A. Taylor, and V. Deretic. 2006. Human IRGM induces autophagy to eliminate intracellular mycobacteria. Science 313: 1438–1441) and has recently been implicated in a genetic screen as a major susceptibility factor in Crohn’s Disease (Parkes, M., J. C. Barrett, N. J. Prescott, M. Tremelling, C. A. Anderson, S. A. Fisher, R. G. Roberts, E. R. Nimmo, F. R. Cummings, D. Soars et al. 2007. Nat. Genet. 39: 830–832).

The authors apologize for any confusion caused and are grateful to colleagues in the field for bringing the errors to their attention. In particular, the authors wish to acknowledge Dr. Jonathan Howard of the University of Cologne Institute for Genetics (Cologne, Germany) for pointing out these errors and for helpful discussion and advice on preparing the erratum. Overall, the findings with IRGM were modest and do not form a major part of the conclusions, particularly those concerning Cathelicidin LL-37 and its role in resistance to tuberculosis.

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