PMID- 15271894
OWN - NLM
STAT- MEDLINE
DCOM- 20040820
LR  - 20181113
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 72
IP  - 8
DP  - 2004 Aug
TI  - Mycobacterium tuberculosis diverts alpha interferon-induced monocyte 
      differentiation from dendritic cells into immunoprivileged macrophage-like host 
      cells.
PG  - 4385-92
AB  - Dendritic cells (DCs) are critical for initiating a pathogen-specific T-cell 
      response. During chronic infections the pool of tissue DCs must be renewed by 
      recruitment of both circulating DC progenitors and in loco differentiating 
      monocytes. However, the interaction of monocytes with pathogens could affect 
      their differentiation. Mycobacterium tuberculosis has been shown to variably 
      interfere with the generation and function of antigen-presenting cells (APCs). In 
      this study we found that when alpha interferon (IFN-alpha) is used as an inductor 
      of monocyte differentiation, M. tuberculosis inhibits the generation of DCs, 
      forcing the generation of immunoprivileged macrophage-like cells instead. Cells 
      derived from M. tuberculosis-infected monocyte-derived macrophages (M. 
      tuberculosis-infected MoMphi) retained CD14 without acquiring CD1 molecules and 
      partially expressed B7.2 but did not up-regulate B7.1 and major 
      histocompatibility complex (MHC) class I and II molecules. They synthesized tumor 
      necrosis factor alpha and interleukin-10 (IL-10) but not IL-12. They also showed 
      a reduced ability to induce proliferation and functional polarization of 
      allogeneic T lymphocytes. Thus, in the presence of IFN-alpha, M. tuberculosis may 
      hamper the renewal of potent APCs, such as DCs, generating a safe habitat for 
      intracellular growth. M. tuberculosis-infected MoMphi, in fact, showed reduced 
      expression of both signal 1 (CD1, MHC classes I and II) and signal 2 (B7.1 and 
      B7.2), which are essential for mycobacterium-specific T-lymphocyte priming and/or 
      activation. These data further suggest that M. tuberculosis has the ability to 
      specifically interfere with monocyte differentiation. This ability may represent 
      an effective M. tuberculosis strategy for eluding immune surveillance and 
      persisting in the host.
FAU - Mariotti, Sabrina
AU  - Mariotti S
AD  - Dipartimento di Malattie Infettive, Parassitarie e Immunomediate, Istituto 
      Superiore di Sanita, Viale Regina Elena 299, 00161 Rome, Italy.
FAU - Teloni, Raffaela
AU  - Teloni R
FAU - Iona, Elisabetta
AU  - Iona E
FAU - Fattorini, Lanfranco
AU  - Fattorini L
FAU - Romagnoli, Giulia
AU  - Romagnoli G
FAU - Gagliardi, Maria Cristina
AU  - Gagliardi MC
FAU - Orefici, Graziella
AU  - Orefici G
FAU - Nisini, Roberto
AU  - Nisini R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Interferon-alpha)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Antigen Presentation
MH  - Cell Differentiation/*drug effects
MH  - Cells, Cultured
MH  - Coculture Techniques
MH  - Dendritic Cells/cytology/*immunology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor
MH  - Humans
MH  - Interferon-alpha/metabolism/*pharmacology
MH  - Lymphocyte Activation
MH  - Macrophages/*cytology/microbiology
MH  - Monocytes/*cytology
MH  - Mycobacterium tuberculosis/*pathogenicity
PMC - PMC470689
EDAT- 2004/07/24 05:00
MHDA- 2004/08/21 05:00
PMCR- 2004/08/01
CRDT- 2004/07/24 05:00
PHST- 2004/07/24 05:00 [pubmed]
PHST- 2004/08/21 05:00 [medline]
PHST- 2004/07/24 05:00 [entrez]
PHST- 2004/08/01 00:00 [pmc-release]
AID - 72/8/4385 [pii]
AID - 1661-03 [pii]
AID - 10.1128/IAI.72.8.4385-4392.2004 [doi]
PST - ppublish
SO  - Infect Immun. 2004 Aug;72(8):4385-92. doi: 10.1128/IAI.72.8.4385-4392.2004.