PittsburghV1, Main, Exploration, bibRecord, 003967

Chemokines in tuberculosis: The good, the bad and the ugly

Identifieur interne : 003967 ( Main/Exploration ); précédent : 003966; suivant : 003968

Chemokines in tuberculosis: The good, the bad and the ugly

Auteurs : Leticia Monin [États-Unis] ; Shabaana A. Khader [États-Unis]

Source :

Seminars in immunology [ 1044-5323 ] ; 2014.

RBID : PMC:4314384

Descripteurs français

KwdFr :
- Cellules myéloïdes (anatomopathologie), Cellules myéloïdes (immunologie), Cellules myéloïdes (microbiologie), Chimiokines (génétique), Chimiokines (immunologie), Humains, Immunité innée, Interactions hôte-pathogène (immunologie), Lymphocytes (anatomopathologie), Lymphocytes (immunologie), Lymphocytes (microbiologie), Mycobacterium tuberculosis (immunologie), Poumon (anatomopathologie), Poumon (immunologie), Poumon (microbiologie), Régulation de l'expression des gènes, Transduction du signal, Tuberculose latente (anatomopathologie), Tuberculose latente (immunologie), Tuberculose latente (microbiologie), Tuberculose pulmonaire (anatomopathologie), Tuberculose pulmonaire (immunologie), Tuberculose pulmonaire (microbiologie), Équilibre Th1-Th2.
MESH :
- anatomopathologie : Cellules myéloïdes, Lymphocytes, Poumon, Tuberculose latente, Tuberculose pulmonaire.
- génétique : Chimiokines.
- immunologie : Cellules myéloïdes, Chimiokines, Interactions hôte-pathogène, Lymphocytes, Mycobacterium tuberculosis, Poumon, Tuberculose latente, Tuberculose pulmonaire.
- microbiologie : Cellules myéloïdes, Lymphocytes, Poumon, Tuberculose latente, Tuberculose pulmonaire.
- Humains, Immunité innée, Régulation de l'expression des gènes, Transduction du signal, Équilibre Th1-Th2.

English descriptors

KwdEn :
- Chemokines (genetics), Chemokines (immunology), Gene Expression Regulation, Host-Pathogen Interactions (immunology), Humans, Immunity, Innate, Latent Tuberculosis (immunology), Latent Tuberculosis (microbiology), Latent Tuberculosis (pathology), Lung (immunology), Lung (microbiology), Lung (pathology), Lymphocytes (immunology), Lymphocytes (microbiology), Lymphocytes (pathology), Mycobacterium tuberculosis (immunology), Myeloid Cells (immunology), Myeloid Cells (microbiology), Myeloid Cells (pathology), Signal Transduction, Th1-Th2 Balance, Tuberculosis, Pulmonary (immunology), Tuberculosis, Pulmonary (microbiology), Tuberculosis, Pulmonary (pathology).
MESH :
- chemical , genetics : Chemokines.
- chemical , immunology : Chemokines.
- immunology : Host-Pathogen Interactions, Latent Tuberculosis, Lung, Lymphocytes, Mycobacterium tuberculosis, Myeloid Cells, Tuberculosis, Pulmonary.
- microbiology : Latent Tuberculosis, Lung, Lymphocytes, Myeloid Cells, Tuberculosis, Pulmonary.
- pathology : Latent Tuberculosis, Lung, Lymphocytes, Myeloid Cells, Tuberculosis, Pulmonary.
- Gene Expression Regulation, Humans, Immunity, Innate, Signal Transduction, Th1-Th2 Balance.

Abstract

Mycobacterium tuberculosis (Mtb) infects about one third of the world’s population, with a majority of infected individuals exhibiting latent asymptomatic infection, while 5–10% of infected individuals progress to active pulmonary disease. Research in the past two decades has elucidated critical host immune mechanisms that mediate Mtb control. Among these, chemokines have been associated with numerous key processes that lead to Mtb containment, from recruitment of myeloid cells into the lung to activation of adaptive immunity, formation of protective granulomas and vaccine recall responses. However, imbalances in several key chemokine mediators can alter the delicate balance of cytokines and cellular responses that promote mycobacterial containment, instead precipitating terminal tissue destruction and spread of Mtb infection. In this review, we will describe recent insights in the involvement of chemokines in host responses to Mtb infection and Mtb containment (the good), chemokines contributing to inflammation during TB (the bad), and the role of chemokines in driving cavitation and lung pathology (the ugly).

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4314384

DOI: 10.1016/j.smim.2014.09.004
PubMed: 25444549
PubMed Central: 4314384

Affiliations:

Le document en format XML

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<term>Chemokines (immunology)</term>
<term>Gene Expression Regulation</term>
<term>Host-Pathogen Interactions (immunology)</term>
<term>Humans</term>
<term>Immunity, Innate</term>
<term>Latent Tuberculosis (immunology)</term>
<term>Latent Tuberculosis (microbiology)</term>
<term>Latent Tuberculosis (pathology)</term>
<term>Lung (immunology)</term>
<term>Lung (microbiology)</term>
<term>Lung (pathology)</term>
<term>Lymphocytes (immunology)</term>
<term>Lymphocytes (microbiology)</term>
<term>Lymphocytes (pathology)</term>
<term>Mycobacterium tuberculosis (immunology)</term>
<term>Myeloid Cells (immunology)</term>
<term>Myeloid Cells (microbiology)</term>
<term>Myeloid Cells (pathology)</term>
<term>Signal Transduction</term>
<term>Th1-Th2 Balance</term>
<term>Tuberculosis, Pulmonary (immunology)</term>
<term>Tuberculosis, Pulmonary (microbiology)</term>
<term>Tuberculosis, Pulmonary (pathology)</term>
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<term>Cellules myéloïdes (immunologie)</term>
<term>Cellules myéloïdes (microbiologie)</term>
<term>Chimiokines (génétique)</term>
<term>Chimiokines (immunologie)</term>
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<term>Immunité innée</term>
<term>Interactions hôte-pathogène (immunologie)</term>
<term>Lymphocytes (anatomopathologie)</term>
<term>Lymphocytes (immunologie)</term>
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<term>Poumon (immunologie)</term>
<term>Poumon (microbiologie)</term>
<term>Régulation de l'expression des gènes</term>
<term>Transduction du signal</term>
<term>Tuberculose latente (anatomopathologie)</term>
<term>Tuberculose latente (immunologie)</term>
<term>Tuberculose latente (microbiologie)</term>
<term>Tuberculose pulmonaire (anatomopathologie)</term>
<term>Tuberculose pulmonaire (immunologie)</term>
<term>Tuberculose pulmonaire (microbiologie)</term>
<term>Équilibre Th1-Th2</term>
</keywords>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Chemokines</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules myéloïdes</term>
<term>Lymphocytes</term>
<term>Poumon</term>
<term>Tuberculose latente</term>
<term>Tuberculose pulmonaire</term>
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<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules myéloïdes</term>
<term>Chimiokines</term>
<term>Interactions hôte-pathogène</term>
<term>Lymphocytes</term>
<term>Mycobacterium tuberculosis</term>
<term>Poumon</term>
<term>Tuberculose latente</term>
<term>Tuberculose pulmonaire</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Host-Pathogen Interactions</term>
<term>Latent Tuberculosis</term>
<term>Lung</term>
<term>Lymphocytes</term>
<term>Mycobacterium tuberculosis</term>
<term>Myeloid Cells</term>
<term>Tuberculosis, Pulmonary</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Cellules myéloïdes</term>
<term>Lymphocytes</term>
<term>Poumon</term>
<term>Tuberculose latente</term>
<term>Tuberculose pulmonaire</term>
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<term>Lymphocytes</term>
<term>Myeloid Cells</term>
<term>Tuberculosis, Pulmonary</term>
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<term>Lymphocytes</term>
<term>Myeloid Cells</term>
<term>Tuberculosis, Pulmonary</term>
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<term>Humans</term>
<term>Immunity, Innate</term>
<term>Signal Transduction</term>
<term>Th1-Th2 Balance</term>
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<front><div type="abstract" xml:lang="en"><p id="P1"><italic>Mycobacterium tuberculosis</italic>
 (<italic>Mtb</italic>
) infects about one third of the world’s population, with a majority of infected individuals exhibiting latent asymptomatic infection, while 5–10% of infected individuals progress to active pulmonary disease. Research in the past two decades has elucidated critical host immune mechanisms that mediate <italic>Mtb</italic>
 control. Among these, chemokines have been associated with numerous key processes that lead to <italic>Mtb</italic>
 containment, from recruitment of myeloid cells into the lung to activation of adaptive immunity, formation of protective granulomas and vaccine recall responses. However, imbalances in several key chemokine mediators can alter the delicate balance of cytokines and cellular responses that promote mycobacterial containment, instead precipitating terminal tissue destruction and spread of <italic>Mtb</italic>
 infection. In this review, we will describe recent insights in the involvement of chemokines in host responses to <italic>Mtb</italic>
 infection and <italic>Mtb</italic>
 containment (the good), chemokines contributing to inflammation during TB (the bad), and the role of chemokines in driving cavitation and lung pathology (the ugly).</p>
</div>
</front>
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Chemokines in tuberculosis: The good, the bad and the ugly

Chemokines in tuberculosis: The good, the bad and the ugly

Source :

Descripteurs français

English descriptors

Abstract

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