Trehalose 6,6′-dimycolate – A coat to regulate tuberculosis immunopathogenesis
Abstract Tuberculosis (TB) remains a significant public health burden worldwide. Treatment of this disease requires a minimum of six months and there is no vaccine available for the most common form of the disease. Increasing evidence suggests that the mycobacterial glycolipid trehalose 6,6′ dimycol...
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| Veröffentlicht in: | Tuberculosis (Edinburgh, Scotland) Scotland), 2013-12, Vol.93, p.S3-S9 |
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| container_title | Tuberculosis (Edinburgh, Scotland) |
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| creator | Welsh, Kerry J Hunter, Robert L Actor, Jeffrey K |
| description | Abstract Tuberculosis (TB) remains a significant public health burden worldwide. Treatment of this disease requires a minimum of six months and there is no vaccine available for the most common form of the disease. Increasing evidence suggests that the mycobacterial glycolipid trehalose 6,6′ dimycolate (TDM; cord factor) plays a key role in the pathogenesis of TB disease. TDM protects the TB bacilli from macrophage-mediated killing, inhibits effective antigen presentation, and reduces the formation of protective T-cell responses. TDM promotes initiation of granuloma formation and likely plays a role in caseation. Furthermore, TDM may contribute to the development of post primary disease. Receptors for TDM were recently described and are expected to contribute to our knowledge of the molecular pathogenesis of TB disease. In this manner, understanding TDM may prove promising towards development of targeted TB therapeutics to limit clinical pathologies. |
| doi_str_mv | 10.1016/S1472-9792(13)70003-9 |
| format | Article |
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Treatment of this disease requires a minimum of six months and there is no vaccine available for the most common form of the disease. Increasing evidence suggests that the mycobacterial glycolipid trehalose 6,6′ dimycolate (TDM; cord factor) plays a key role in the pathogenesis of TB disease. TDM protects the TB bacilli from macrophage-mediated killing, inhibits effective antigen presentation, and reduces the formation of protective T-cell responses. TDM promotes initiation of granuloma formation and likely plays a role in caseation. Furthermore, TDM may contribute to the development of post primary disease. Receptors for TDM were recently described and are expected to contribute to our knowledge of the molecular pathogenesis of TB disease. 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Treatment of this disease requires a minimum of six months and there is no vaccine available for the most common form of the disease. Increasing evidence suggests that the mycobacterial glycolipid trehalose 6,6′ dimycolate (TDM; cord factor) plays a key role in the pathogenesis of TB disease. TDM protects the TB bacilli from macrophage-mediated killing, inhibits effective antigen presentation, and reduces the formation of protective T-cell responses. TDM promotes initiation of granuloma formation and likely plays a role in caseation. Furthermore, TDM may contribute to the development of post primary disease. Receptors for TDM were recently described and are expected to contribute to our knowledge of the molecular pathogenesis of TB disease. In this manner, understanding TDM may prove promising towards development of targeted TB therapeutics to limit clinical pathologies.</description><subject>Adjuvants, Immunologic - pharmacology</subject><subject>Cord Factor</subject><subject>Cord Factors - pharmacology</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Granuloma, Respiratory Tract - drug therapy</subject><subject>Granuloma, Respiratory Tract - immunology</subject><subject>Granuloma, Respiratory Tract - pathology</subject><subject>Humans</subject><subject>Infectious Disease</subject><subject>Male</subject><subject>Mycobacterium tuberculosis - drug effects</subject><subject>Mycobacterium tuberculosis - immunology</subject><subject>Pulmonary/Respiratory</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - pathology</subject><subject>Trehalose 6,6′-dimycolate</subject><subject>Tuberculosis - immunology</subject><subject>Tuberculosis - pathology</subject><subject>Tuberculosis - prevention & control</subject><subject>Tuberculosis TDM</subject><issn>1472-9792</issn><issn>1873-281X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtuFDEQhi0EIiFwBFAvg0RD-dF-bEBRxEuKhARBYme57ZrEobs92N1Is8sduAlHyknwzCQs2LCyVfr-v1QfIU8pvKRA5asvVCjWGmXYMeXPFQDw1twjh1Qr3jJNv92v_zvkgDwq5QpqDjQ8JAdMcK2lkIfk83nGSzekgo18IW-uf7chjhufBjdjc3P9qzlpfHJzM6cm48WyG89Lj9kvNRRLE8dxmdLazZfpAieso8fkwcoNBZ_cvkfk67u356cf2rNP7z-enpy1XjCY2w5lp1cIiDJIQXvphWe984EZQLNyrOOeBsW56oUWTHWoA5NaUKM8hdDzI3K8713n9GPBMtsxFo_D4CZMS7FUGFAdcAMV7faoz6mUjCu7znF0eWMp2K1Ou9Npt64s5Xan05qae3a7YulHDH9Td_4q8GYPYD30Z8Rsi484eQwxo59tSPG_K17_0-CHOEXvhu-4wXKVljxVi5bawizsS7YdlO8aDP8Dkc-bVQ</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Welsh, Kerry J</creator><creator>Hunter, Robert L</creator><creator>Actor, Jeffrey K</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20131201</creationdate><title>Trehalose 6,6′-dimycolate – A coat to regulate tuberculosis immunopathogenesis</title><author>Welsh, Kerry J ; Hunter, Robert L ; Actor, Jeffrey K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-5e658fe0ee6d641b6c4c2bacd290e9fa253c1d7337b484275e8d2684197c10db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adjuvants, Immunologic - pharmacology</topic><topic>Cord Factor</topic><topic>Cord Factors - pharmacology</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Granuloma, Respiratory Tract - drug therapy</topic><topic>Granuloma, Respiratory Tract - immunology</topic><topic>Granuloma, Respiratory Tract - pathology</topic><topic>Humans</topic><topic>Infectious Disease</topic><topic>Male</topic><topic>Mycobacterium tuberculosis - drug effects</topic><topic>Mycobacterium tuberculosis - immunology</topic><topic>Pulmonary/Respiratory</topic><topic>T-Lymphocytes - drug effects</topic><topic>T-Lymphocytes - pathology</topic><topic>Trehalose 6,6′-dimycolate</topic><topic>Tuberculosis - immunology</topic><topic>Tuberculosis - pathology</topic><topic>Tuberculosis - prevention & control</topic><topic>Tuberculosis TDM</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Welsh, Kerry J</creatorcontrib><creatorcontrib>Hunter, Robert L</creatorcontrib><creatorcontrib>Actor, Jeffrey K</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Tuberculosis (Edinburgh, Scotland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Welsh, Kerry J</au><au>Hunter, Robert L</au><au>Actor, Jeffrey K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Trehalose 6,6′-dimycolate – A coat to regulate tuberculosis immunopathogenesis</atitle><jtitle>Tuberculosis (Edinburgh, Scotland)</jtitle><addtitle>Tuberculosis (Edinb)</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>93</volume><spage>S3</spage><epage>S9</epage><pages>S3-S9</pages><issn>1472-9792</issn><eissn>1873-281X</eissn><abstract>Abstract Tuberculosis (TB) remains a significant public health burden worldwide. Treatment of this disease requires a minimum of six months and there is no vaccine available for the most common form of the disease. Increasing evidence suggests that the mycobacterial glycolipid trehalose 6,6′ dimycolate (TDM; cord factor) plays a key role in the pathogenesis of TB disease. TDM protects the TB bacilli from macrophage-mediated killing, inhibits effective antigen presentation, and reduces the formation of protective T-cell responses. TDM promotes initiation of granuloma formation and likely plays a role in caseation. Furthermore, TDM may contribute to the development of post primary disease. Receptors for TDM were recently described and are expected to contribute to our knowledge of the molecular pathogenesis of TB disease. In this manner, understanding TDM may prove promising towards development of targeted TB therapeutics to limit clinical pathologies.</abstract><cop>Scotland</cop><pub>Elsevier Ltd</pub><pmid>24388646</pmid><doi>10.1016/S1472-9792(13)70003-9</doi></addata></record> |
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| ispartof | Tuberculosis (Edinburgh, Scotland), 2013-12, Vol.93, p.S3-S9 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Adjuvants, Immunologic - pharmacology Cord Factor Cord Factors - pharmacology Disease Progression Female Granuloma, Respiratory Tract - drug therapy Granuloma, Respiratory Tract - immunology Granuloma, Respiratory Tract - pathology Humans Infectious Disease Male Mycobacterium tuberculosis - drug effects Mycobacterium tuberculosis - immunology Pulmonary/Respiratory T-Lymphocytes - drug effects T-Lymphocytes - pathology Trehalose 6,6′-dimycolate Tuberculosis - immunology Tuberculosis - pathology Tuberculosis - prevention & control Tuberculosis TDM |
| title | Trehalose 6,6′-dimycolate – A coat to regulate tuberculosis immunopathogenesis |
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