原创力文档cytotoxic activity of dendritic cells as a possible mechanism of negative regulation of t lymphocytes in pulmonary tuberculosis细胞毒性的树突细胞的可能机制- t淋巴细胞在肺结核的监管.pdfVIP
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cytotoxic activity of dendritic cells as a possible mechanism of negative regulation of t lymphocytes in pulmonary tuberculosis细胞毒性的树突细胞的可能机制- t淋巴细胞在肺结核的监管
Hindawi Publishing Corporation
Clinical and Developmental Immunology
Volume 2012, Article ID 628635, 9 pages
doi:10.1155/2012/628635
Research Article
Cytotoxic Activity of Dendritic Cells as a Possible Mechanism of
Negative Regulation of T Lymphocytes in Pulmonary Tuberculosis
Ludmila V. Sakhno,1 Marina A. Tikhonova,1 Tamara V. Tyrinova,1 Olga Yu. Leplina,1
Ekaterina Ya. Shevela,1 Sergey D. Nikonov,2 Oleg A. Zhdanov,2 Alexander A. Ostanin,1
and Elena R. Chernykh1
1 Research Institute of Clinical Immunology, Russian Academy of Medical Sciences (RAMS), Siberian Branch (SB),
Novosibirsk 630099, Russia
2 Novosibirsk Tuberculosis Clinical Hospital No. 1, Novosibirsk 630099, Russia
Correspondence should be addressed to Ludmila V. Sakhno, lsahno53@mail.ru
Received 3 July 2012; Revised 23 August 2012; Accepted 31 August 2012
Academic Editor: Mario Clerici
Copyright © 2012 Ludmila V. Sakhno et al. This is an open access article distributed under the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly
cited.
The PD-1/B7-H1-mediated induction of T cell apoptosis/anergy as a possible mechanism of immune response failure was studied
in 76 patients with pulmonary tuberculosis (TB) with normal and low-proliferative response to antigens of M. tuberculosis (purified
protein derivative (PPD)). It was revealed that dendritic cells (DCs), generated in vitro from patient blood monocytes with GM-
CSF + IFN-α, were characterized by increased B7-H1 expression, upproduction of IL-10, and reducing of allostimulatory activity
in mixed lymphocyte culture (MLC). Moreover, DCs of patients with TB were able to enhance T cell apoptosis and to block T-cell
division in MLC. It w
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