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Reply to “Streptococcus pyogenes and phagocytic killing”

Nature Medicine volume 8, pages 1045–1046 (2002)Cite this article

An Erratum to this article was published on 01 November 2002

Lei et al. reply

Although an extension concerning molecular mechanism responsible for the ability of Mac to inhibit phagocytosis and killing of group A Streptococcus (GAS) is potentially interesting, we have several concerns with the idea and data presented above. von Pawel-Rammingen et al. question the hypothesis that Mac/IdeS functions through molecular mimicry to block phagocytosis. We identified Mac protein by proteome analysis of supernatant proteins from GAS culture7 and subsequently showed that Mac is made during human infections, binds to human neutrophils (PMNs), diminishes IgG binding to CD16 and inhibits phagocytosis and killing of GAS. Based on the substantial homology of the central region of Mac with human CD11b, we proposed that molecular mimicry might form the basis for the inhibition of phagocytosis. The studies of von Pawel-Rammingen et al.3 confirmed our discovery of the biological function of Mac. Moreover, there is no significant difference between the idea they put forth here and the concept already published3.

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Figure 1: IdeSC94G binds to PMNs but does not protect against phagocytic killing.

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  1. Laboratory of Human Bacterial Pathogenesis Rocky Mountain Laboratories National Institute of Allergy and Infectious Diseases National Institutes of Health, Hamilton, Montana, USA

    Benfang Lei, Frank R. DeLeo & James M. Musser

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Lei, B., DeLeo, F. & Musser, J. Reply to “Streptococcus pyogenes and phagocytic killing”. Nat Med 8, 1045–1046 (2002). https://doi.org/10.1038/nm1002-1045

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