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Scientific Overview Research Interest Summary Principal Investigators    Yuri Bushkin, Ph.D.
   Loren Day, Ph.D.
   Karl Drlica, Ph.D.
   David Dubnau, Ph.D.
   Marila Gennaro, M.D.
   Gilla Kaplan, Ph.D.
   Fred Kramer, Ph.D.
   Barry Kreiswirth, Ph.D.
   Leonard Mindich, Ph.D.
   Harvey Penefsky, Ph.D.
   David Perlin, Ph.D.
   Richard Pine, Ph.D.
   Abraham Pinter, Ph.D.
   Issar Smith, Ph.D.
   Patricia Soteropoulos, Ph.D.
   Sanjay Tyagi, Ph.D.
   David Wah, Ph.D.
   Shuishu Wang, Ph.D.

   Research Faculty
   Xilin Zhao, Ph.D.

Junior Faculty Members Research Grants
 
Gilla Kaplan, Ph.D.
 



Recent Articles

Hanekom WA, Mendillo M, Manca C, Haslett PA, Siddiqui MR, Barry C 3rd, Kaplan G. (2003).
Mycobacterium tuberculosis inhibits maturation of human monocyte-derived dendritic cells in vitro.
J Infect Dis. 2003 Jul 15;188(2):257-66. Epub 2003 Jul 09
PMID: 12854081

To induce effector immunity, dendritic cells (DCs) must differentiate into fully mature cells. We show that, after human monocyte-derived DCs were infected with virulent Mycobacterium tuberculosis, up-regulation of cellular-surface maturation markers was minimal and reversible. In the presence of a potent stimulus for maturation (tumor necrosis factor [TNF]-alpha, interleukin [IL]-1beta, and prostaglandin E2 [PGE2]), M. tuberculosis inhibited phenotypic DC maturation. M. tuberculosis-infected DCs had an impaired ability to induce allogeneic lymphoproliferation and activated autologous memory CD4+ and CD8+ T cells optimally only in the presence of TNF-alpha, IL-1beta, and PGE2. Thus, virulent M. tuberculosis inhibits phenotypic and functional maturation of human monocyte-derived DCs. This mechanism, which has been described elsewhere for various viruses and for the virulent mycobacterium M. leprae, may be a novel mechanism that this pathogen uses to evade the host's immune response.


 
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