Abstract |
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 mice. 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) plague; the mutation, called CCR5Delta32, 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.
|
Authors | Stephen J Elvin, E Diane Williamson, Joanne C Scott, Jeremy N Smith, Guillermo Pérez De Lema, Silvia Chilla, Paul Clapham, Klaus Pfeffer, Detlef Schlöndorff, Bruno Luckow |
Journal | Nature
(Nature)
Vol. 430
Issue 6998
Pg. 417
(Jul 22 2004)
ISSN: 1476-4687 [Electronic] England |
PMID | 15272490
(Publication Type: Journal Article, Comment)
|
Chemical References |
|
Topics |
- Animals
- Evolution, Molecular
- Humans
- Macrophages
(cytology, immunology, metabolism, microbiology)
- Mice
- Mice, Inbred BALB C
- Mice, Inbred C57BL
- Models, Biological
- Phagocytosis
- Plague
(genetics, metabolism, microbiology)
- Receptors, CCR5
(deficiency, genetics, metabolism)
- Sequence Deletion
(genetics)
- Survival Rate
- Virulence
- White People
(genetics)
- Yersinia pestis
(pathogenicity, physiology)
|