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Infection and Immunity, December 2001, p. 7461-7470, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7461-7470.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Influence of Mycobacterium bovis Bacillus Calmette Guérin on In Vitro Induction of CD1 Molecules in Human Adherent Mononuclear Cells

Anna Giuliani,1,2 Salvatore P. Prete,1 Grazia Graziani,1 Angelo Aquino,1 Alessandra Balduzzi,1 Masahiko Sugita,3 Michael B. Brenner,3 Elena Iona,4 Lanfranco Fattorini,4 Graziella Orefici,4 Steven A. Porcelli,5,* and Enzo Bonmassar6

Department of Neuroscience, University of Rome "Tor Vergata,"1 Institute of Neurobiology and Molecular Medicine, National Council of Research (CNR),2 Laboratory of Bacteriology and Medical Mycology, "Istituto Superiore di Sanità,"4 and "Istituto Dermopatico dell'Immacolata" (IDI-IRCCS),6 Rome, Italy; Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 021153; and Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 104615

Received 30 May 2001/Returned for modification 13 July 2001/Accepted 11 September 2001

Nonpeptide antigens (including glycolipids of microbial origin) can be presented to T cells by CD1 molecules expressed on monocyte-derived dendritic cells. These HLA unrestricted responses appear to play a role in host immunity against Mycobacterium tuberculosis and other pathogenic bacteria. It is known that vaccination with Mycobacterium bovis bacillus Calmette-Guérin (BCG) has limited efficacy in many clinical settings, although the reasons for its inadequacy remain unclear. Here we have investigated the influence of BCG on the induction of CD1b on human monocytes by granulocyte-macrophage colony-stimulating factor (GM-CSF), which is believed to be the principal inducer of this antigen-presenting molecule. Although BCG alone led to a slight induction of CD1b expression, this agent reduced markedly the ability of GM-CSF to induce high levels of CD1b that were typically observed in uninfected cells. Inhibition of CD1b expression in BCG-infected monocytes was apparent at both the mRNA transcript and CD1b protein levels. Down-regulation of CD1b expression by BCG was mediated, at least in part, by one or more soluble factors and could not be reversed with high concentrations of GM-CSF or a variety of other cytokines. The present results suggest that BCG could diminish the efficiency of CD1-restricted T-cell responses against nonpeptide mycobacterial antigens by reducing CD1 expression on antigen-presenting cells. These findings have potential implications for understanding the nature of the immune response elicited by BCG in humans and suggest potential strategies that could be important for the development of better vaccines for the prevention of tuberculosis.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461. Phone: (718) 430-3228, -3227, or -3226. Fax: (718) 430-8711. E-mail: porcelli{at}aecom.yu.edu.

Infection and Immunity, December 2001, p. 7461-7470, Vol. 69, No. 12
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.12.7461-7470.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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