Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis
The world’s most successful intracellular bacterial pathogen, Mycobacterium tuberculosis (MTB), survives inside macrophages by blocking phagosome maturation and establishes chronic infection characterized by the formation of granulomas. Trehalose-6,6-dimycolate (TDM), the mycobacterial cord factor,...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2013-01-01
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| Series: | Frontiers in Immunology |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fimmu.2013.00005/full |
| _version_ | 1818151907246473216 |
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| author | Roland eLang |
| author_facet | Roland eLang |
| author_sort | Roland eLang |
| collection | DOAJ |
| description | The world’s most successful intracellular bacterial pathogen, Mycobacterium tuberculosis (MTB), survives inside macrophages by blocking phagosome maturation and establishes chronic infection characterized by the formation of granulomas. Trehalose-6,6-dimycolate (TDM), the mycobacterial cord factor, is the most abundant cell wall lipid of virulent mycobacteria, is sufficient to cause granuloma formation, and has long been known to be a major virulence factor of MTB. Recently, TDM has been shown to activate the Syk-Card9 signaling pathway in macrophages through binding to the C-type lectin receptor Mincle. The Mincle-Card9 pathway is required for activation of macrophages by TDM in vitro and for granuloma formation in vivo following injection of TDM. Whether this pathway is also exploited by MTB to reprogram the macrophage into a comfortable niche has not been explored yet. Several recent studies have investigated the phenotype of Mincle-deficient mice in mycobacterial infection, yielding divergent results in terms of a role for Mincle in host resistance. Here, we review these studies, discuss possible reasons for discrepant results and highlight open questions in the role of Mincle and other C-type lectin receptors in the infection biology of MTB. |
| first_indexed | 2024-12-11T13:46:17Z |
| format | Article |
| id | doaj.art-db3ac424e39047bebfade5bc2334162a |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-12-11T13:46:17Z |
| publishDate | 2013-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-db3ac424e39047bebfade5bc2334162a2022-12-22T01:04:30ZengFrontiers Media S.A.Frontiers in Immunology1664-32242013-01-01410.3389/fimmu.2013.0000539929Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosisRoland eLang0University Hospital ErlangenThe world’s most successful intracellular bacterial pathogen, Mycobacterium tuberculosis (MTB), survives inside macrophages by blocking phagosome maturation and establishes chronic infection characterized by the formation of granulomas. Trehalose-6,6-dimycolate (TDM), the mycobacterial cord factor, is the most abundant cell wall lipid of virulent mycobacteria, is sufficient to cause granuloma formation, and has long been known to be a major virulence factor of MTB. Recently, TDM has been shown to activate the Syk-Card9 signaling pathway in macrophages through binding to the C-type lectin receptor Mincle. The Mincle-Card9 pathway is required for activation of macrophages by TDM in vitro and for granuloma formation in vivo following injection of TDM. Whether this pathway is also exploited by MTB to reprogram the macrophage into a comfortable niche has not been explored yet. Several recent studies have investigated the phenotype of Mincle-deficient mice in mycobacterial infection, yielding divergent results in terms of a role for Mincle in host resistance. Here, we review these studies, discuss possible reasons for discrepant results and highlight open questions in the role of Mincle and other C-type lectin receptors in the infection biology of MTB.http://journal.frontiersin.org/Journal/10.3389/fimmu.2013.00005/fullTuberculosismycobacteriacord factorTDMMincleC-type lectin receptor |
| spellingShingle | Roland eLang Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis Frontiers in Immunology Tuberculosis mycobacteria cord factor TDM Mincle C-type lectin receptor |
| title | Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis |
| title_full | Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis |
| title_fullStr | Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis |
| title_full_unstemmed | Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis |
| title_short | Recognition of the mycobacterial cord factor by Mincle: relevance for granuloma formation and resistance to tuberculosis |
| title_sort | recognition of the mycobacterial cord factor by mincle relevance for granuloma formation and resistance to tuberculosis |
| topic | Tuberculosis mycobacteria cord factor TDM Mincle C-type lectin receptor |
| url | http://journal.frontiersin.org/Journal/10.3389/fimmu.2013.00005/full |
| work_keys_str_mv | AT rolandelang recognitionofthemycobacterialcordfactorbyminclerelevanceforgranulomaformationandresistancetotuberculosis |