Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo.

Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Research Abstract Details 

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Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Abstract Text:

Eleanor Z Kincaid,Andrea J Wolf,Ludovic Desvignes,Sebabrata Mahapatra,Dean C Crick,Patrick J Brennan,Martin S Pavelka,Joel D Ernst,

Mycobacterium tuberculosis is an exceptionally successful human pathogen. A major component of this success is the ability of the bacteria to infect immunocompetent individuals and to evade eradication by an adaptive immune response that includes production of the macrophage-activating cytokine, IFN-gamma. Although IFN-gamma is essential for arrest of progressive tuberculosis, it is insufficient for efficacious macrophage killing of the bacteria, which may be due to the ability of M. tuberculosis to inhibit selected macrophage responses to IFN-gamma. In vitro studies have determined that mycobacterial lipoproteins and other components of the M. tuberculosis cell envelope, acting as agonists for TLR2, inhibit IFN-gamma induction of MHC class II. In addition, M. tuberculosis peptidoglycan and IL-6 secreted by infected macrophages inhibit IFN-gamma induction of MHC class II in a TLR2-independent manner. To determine whether TLR2-dependent inhibition of macrophage responses to IFN-gamma is quantitatively dominant over the TLR2-independent mechanisms in vivo, we prepared mixed bone marrow chimeric mice in which the hemopoietic compartment was reconstituted with a mixture of TLR(+/+) and TLR2(-/-) cells. When the chimeric mice were infected with M. tuberculosis, the expression of MHC class II on TLR2(+/+) and TLR2(-/-) macrophages from the lungs of individual infected chimeric mice was indistinguishable. These results indicate that TLR2-dependent and -independent mechanisms of inhibition of responses to IFN-gamma are equivalent in vivo, and that M. tuberculosis uses multiple pathways to abrogate the action of an important effector of adaptive immunity. This work was supported by National Institutes of Health Grants AI 065357-AI 020010.

Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Publishing Authors By Initials

EZ Kincaid,AJ Wolf,L Desvignes,S Mahapatra,DC Crick,PJ Brennan,MS Pavelka,JD Ernst,

For similar bacterial infections and mycoses: bacterial infections: gram-positive bacterial infections: actinomycetales infections: mycobacterium infections: tuberculosis: tuberculosis, pulmonary research abstracts see: bacterial infections and mycoses: bacterial infections: gram-positive bacterial infections: actinomycetales infections: mycobacterium infections: tuberculosis: tuberculosis, pulmonary research

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Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 179

Page Numbers: 3187-95

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Sep

YEAR: 2007

Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Keywords Mesh Terms:

KEYWORDS: Tuberculosis, Pulmonary

MESH TERMS: immunology

Chemical & Substance for Abstract: Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo. Information

Substance Name: Interferon Type II

Registry Number: 82115-62-6

Grant and Affiliation Information for Codominance of TLR2-dependent and TLR2-independent modulation of MHC class II in Mycobacterium tuberculosis infection in vivo.

AFFILIATION: Division of Infectious Diseases, Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.

Country: United States

AGENCY: United States NIAID

GRANT: AI 47311

ACRONYM: AI

MEDLINETA: J Immunol

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