This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Dugué, C.
Right arrow Articles by Renaudineau, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dugué, C.
Right arrow Articles by Renaudineau, Y.

 Previous Article  |  Next Article 

Infection and Immunity, January 2004, p. 301-309, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.301-309.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Effects of Anti-Endothelial Cell Antibodies in Leprosy and Malaria

Christophe Dugué,1 Ronald Perraut,2 Pierre Youinou,1* and Yves Renaudineau1

Laboratory of Immunology, Brest University Medical School Hospital, Brest, France,1 Pasteur Institute, Dakar, Senegal2

Received 27 August 2003/ Returned for modification 8 October 2003/ Accepted 20 October 2003

As a result of damaging endothelial cells (ECs), Mycobacterium leprae triggers the production of antibodies (Abs). These anti-EC Abs (AECAs) can be divided into two types. The first type nonspecifically reacts with components of the cytosol (CY) and can be detected by enzyme-linked immunosorbent assay (ELISA). The second specifically reacts with the EC membrane (MB) and requires fluorescence-activated cell sorter (FACS) analysis to be detected. The presence of both types of AECAs was determined in 68 leprosy patients. The ELISA was positive for 35 of them but also for 30 of 34 malaria patients and 17 of 50 healthy African controls. However, whereas FACS analysis showed MB reactivity in only three malaria patients and four controls, this reactivity was found in 27 leprosy patients, more of those having the lepromatous than the tuberculoid form. Specificity for MB, which we failed to absorb by incubation with CY lysates, predominated over that for CY in leprosy, unlike malaria, where the EC reactivity was restricted to the CY. Western blot analysis and two-dimensional electrophoresis revealed that calreticulin, vimentin, tubulin, and heat shock protein 70 were targeted by AECAs from leprosy patients, but other proteins remained unidentified. These auto-Abs, but not those from malaria patients, did activate ECs, as indicated by the E-selectin and intercellular adhesion molecule 1 upregulation, and/or induced them into apoptosis, as documented by four different methods. Our findings suggest that, in some but not all leprosy patients, AECAs may play a role in pathogenesis.

* Corresponding author. Mailing address: Laboratory of Immunology, Brest University Medical School Hospital, BP 824, F29609 Brest Cedex, France. Phone: 33-298-22-33-84. Fax: 33-298-22-38-47. E-mail: youinou{at}univ-brest.fr.

Editor: W. A. Petri, Jr.

Infection and Immunity, January 2004, p. 301-309, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.301-309.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Alard, J.-E., Dueymes, M., Mageed, R. A., Saraux, A., Youinou, P., Jamin, C. (2009). Mitochondrial heat shock protein (HSP) 70 synergizes with HSP60 in transducing endothelial cell apoptosis induced by anti-HSP60 autoantibody. FASEB J. 23: 2772-2779 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»