Ambiguous role of CCR5 in Y. pestis infection
Stephen J. Elvin,
E. Diane Williamson (),
Joanne C. Scott,
Jeremy N. Smith,
Guillermo Pérez de Lema,
Silvia Chilla,
Paul Clapham,
Klaus Pfeffer,
Detlef Schlöndorff and
Bruno Luckow
Additional contact information
Stephen J. Elvin: Defence Science and Technology Laboratories, Porton Down
E. Diane Williamson: Defence Science and Technology Laboratories, Porton Down
Joanne C. Scott: Defence Science and Technology Laboratories, Porton Down
Jeremy N. Smith: Defence Science and Technology Laboratories, Porton Down
Guillermo Pérez de Lema: Klinikum der Universität München, Medizinische Poliklinik–Innenstadt
Silvia Chilla: Klinikum der Universität München, Medizinische Poliklinik–Innenstadt
Paul Clapham: University of Massachusetts
Klaus Pfeffer: Heinrich-Heine-Universität Düsseldorf
Detlef Schlöndorff: Klinikum der Universität München, Medizinische Poliklinik–Innenstadt
Bruno Luckow: Klinikum der Universität München, Medizinische Poliklinik–Innenstadt
Nature, 2004, vol. 430, issue 6998, 418-418
Abstract:
Abstract Arising from: J. Mecsas et al. Nature 427, 606 (2004) Mecsas and colleagues suggest that a deficiency in the chemokine receptor CCR5 in humans is unlikely to confer protection against plague, based on their study of Yersinia pestis infection in Ccr5-deficient mice1. They were testing the hypothesis that a mutation in the CCR5 gene, frequently found in Caucasians, may have been selected for in the past because it provided protection against (bubonic) plague2,3,4,5,6,7; the mutation, called CCR5Δ32, is characterized by a 32-base-pair deletion. We have also tested this hypothesis by using Y. pestis infection in mice and, in addition, we have done phagocytosis experiments with macrophages from wild-type and Ccr5-deficient mice. Although, like Mecsas et al., we did not see any difference in the survival of the two groups of mice, we did find that there was a significantly reduced uptake of Y. pestis by Ccr5-deficient macrophages in vitro. Our results indicate that the role of Ccr5 in Y. pestis infection may therefore be more complex than previously thought.
Date: 2004
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DOI: 10.1038/nature02822
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