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*Tuberculosis
The Journal of Immunology, 2005, 174: 4237-4243.
Copyright © 2005 by The American Association of Immunologists

Infection Biology of a Novel {alpha}-Crystallin of Mycobacterium tuberculosis: Acr21

Katalin A. Wilkinson2,*, Graham R. Stewart2,{dagger}, Sandra M. Newton*, H. Martin Vordermeier{ddagger}, John R. Wain{dagger}, Helen N. Murphy{dagger}, Katherine Horner{dagger}, Douglas B. Young{dagger} and Robert J. Wilkinson3,*,§

* Wellcome Trust Center for Research in Clinical Tropical Medicine and Department of Pediatric Infectious Diseases, Faculty of Medicine, Imperial College London, Wright Fleming Institute, London, {dagger} Center for Molecular Microbiology and Infection, Imperial College London, London, {ddagger} Department of Bacteriology, Veterinary Laboratories Agency, Weybridge, Surrey, and § Tuberculosis Service, Northwick Park Hospital, Harrow, United Kingdom

Heat shock proteins assist the survival of Mycobacterium tuberculosis (MTB) but also provide a signal to the immune response. The gene most strongly induced by heat shock in MTB is Rv0251c, which encodes Acr2, a novel member of the {alpha}-crystallin family of molecular chaperones. The expression of acr2 increased within 1 h after infection of monocytes or macrophages, reaching a peak of 18- to 55-fold by 24 h. Inhibition of superoxide action reduced the intracellular increase in acr2. Despite this contribution to the stress response of MTB, the gene for acr2 appears dispensable; a deletion mutant ({Delta}acr2) was unimpaired in log phase growth and persisted in IFN-{gamma}-activated human macrophages. Acr2 protein was strongly recognized by cattle with early primary Mycobacterium bovis infection and by healthy MTB-sensitized people. Within the latter group, those with recent exposure to infectious tuberculosis had, on average, 2.6 times the frequency of Acr2-specific IFN-{gamma}-secreting T cells than those with more remote exposure (p = 0.009). These data show that, by its up-regulation early after entry to cells, Acr2 gives away the presence of MTB to the immune response. The demonstration that there is infection stage-specific immunity to tuberculosis has implications for vaccine design.




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