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Exposure to anthrax toxin alters human leucocyte expression of anthrax toxin receptor 1
Author(s) -
Ingram R. J.,
Harris A.,
Ascough S.,
Metan G.,
Doganay M.,
Ballie L.,
Williamson E. D.,
Dyson H.,
Robinson J. H.,
Sriskandan S.,
Altmann D. M.
Publication year - 2013
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12090
Subject(s) - anthrax toxin , toxin , anthrax vaccines , microbiology and biotechnology , immunology , bacillus anthracis , biology , microbial toxins , virology , immune system , bacteria , immunization , recombinant dna , genetics , dna vaccination , gene , fusion protein
Summary Anthrax is a toxin‐mediated disease, the lethal effects of which are initiated by the binding of protective antigen ( PA ) with one of three reported cell surface toxin receptors ( ANTXR ). Receptor binding has been shown to influence host susceptibility to the toxins. Despite this crucial role for ANTXR in the outcome of disease, and the reported immunomodulatory consequence of the anthrax toxins during infection, little is known about ANTXR expression on human leucocytes. We characterized the expression levels of ANTXR 1 ( TEM 8) on human leucocytes using flow cytometry. In order to assess the effect of prior toxin exposure on ANTXR 1 expression levels, leucocytes from individuals with no known exposure, those exposed to toxin through vaccination and convalescent individuals were analysed. Donors could be defined as either ‘low’ or ‘high’ expressers based on the percentage of ANTXR 1‐positive monocytes detected. Previous exposure to toxins appears to modulate ANTXR 1 expression, exposure through active infection being associated with lower receptor expression. A significant correlation between low receptor expression and high anthrax toxin‐specific interferon ( IFN)‐ γ responses was observed in previously infected individuals. We propose that there is an attenuation of ANTXR 1 expression post‐infection which may be a protective mechanism that has evolved to prevent reinfection.

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