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Differential migration of human monocyte-derived dendritic cells after infection with prevalent clinical strains of Mycobacterium tuberculosis
Abstract Dendritic cells (DCs) play a key role in the host immune response to infections. Mycobacterium tuberculosis (MTB) can inhibit the maturation of DCs and impair their ability to stimulate T cell proliferation. Here, we assessed in vitro migratory behavior of human monocyte-derived DCs (MoDC)...
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Published in: | Immunobiology (1979) 2008-01, Vol.213 (7), p.567-575 |
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container_title | Immunobiology (1979) |
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creator | Rajashree, P Supriya, P Das, Sulochana D |
description | Abstract Dendritic cells (DCs) play a key role in the host immune response to infections. Mycobacterium tuberculosis (MTB) can inhibit the maturation of DCs and impair their ability to stimulate T cell proliferation. Here, we assessed in vitro migratory behavior of human monocyte-derived DCs (MoDC) when infected with various MTB strains (H37Rv and prevalent clinical strains S7 and S10 from South India). The migration of Rv and S7 infected MoDC towards secondary lymphoid chemokine (CCL21) was 50% lower after 1 day of infection compared to LPS stimulation. This reduced cell migration may be due to a block in the chemokine receptor switch from CCR5 to CCR7 expression on MoDC. Only clinical strain S10 infected MoDC showed an up-regulation of CCR7 and down-regulation of CCR5 expression, similar to LPS stimulated MoDC. While Rv and S7 infected MoDC did not display any alteration in expression of these receptors. Similarly, Rv and S7 infected MoDC did not induce IL-8, IP-10 and MCP-1 chemokine production. This reduction in chemokine levels was reflected in the reduced chemoattraction of CD4+ T cells also. These findings suggest that there is variation in the stimulation of MoDC with different clinical strains of MTB and this variation may be dependent upon the virulence of the strain. |
doi_str_mv | 10.1016/j.imbio.2008.01.007 |
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Mycobacterium tuberculosis (MTB) can inhibit the maturation of DCs and impair their ability to stimulate T cell proliferation. Here, we assessed in vitro migratory behavior of human monocyte-derived DCs (MoDC) when infected with various MTB strains (H37Rv and prevalent clinical strains S7 and S10 from South India). The migration of Rv and S7 infected MoDC towards secondary lymphoid chemokine (CCL21) was 50% lower after 1 day of infection compared to LPS stimulation. This reduced cell migration may be due to a block in the chemokine receptor switch from CCR5 to CCR7 expression on MoDC. Only clinical strain S10 infected MoDC showed an up-regulation of CCR7 and down-regulation of CCR5 expression, similar to LPS stimulated MoDC. While Rv and S7 infected MoDC did not display any alteration in expression of these receptors. Similarly, Rv and S7 infected MoDC did not induce IL-8, IP-10 and MCP-1 chemokine production. This reduction in chemokine levels was reflected in the reduced chemoattraction of CD4+ T cells also. These findings suggest that there is variation in the stimulation of MoDC with different clinical strains of MTB and this variation may be dependent upon the virulence of the strain.</description><identifier>ISSN: 0171-2985</identifier><identifier>EISSN: 1878-3279</identifier><identifier>DOI: 10.1016/j.imbio.2008.01.007</identifier><identifier>PMID: 18656704</identifier><language>eng</language><publisher>Netherlands: Elsevier GmbH</publisher><subject>Adolescent ; Adult ; Advanced Basic Science ; Allergy and Immunology ; Cell Movement - physiology ; Cells, Cultured ; Chemokine CCL2 - biosynthesis ; Chemokine CXCL10 - biosynthesis ; Chemokines ; Chemotaxis ; Clinical isolates ; Dendritic cells ; Dendritic Cells - microbiology ; Dendritic Cells - physiology ; Down-Regulation ; Humans ; Interleukin-8 - biosynthesis ; Middle Aged ; Migration ; Monocytes ; Mycobacterium tuberculosis ; Mycobacterium tuberculosis - immunology ; Mycobacterium tuberculosis - pathogenicity ; Receptors, CCR5 - metabolism ; Receptors, CCR7 - metabolism ; Receptors, Chemokine - metabolism ; Up-Regulation ; Virulence</subject><ispartof>Immunobiology (1979), 2008-01, Vol.213 (7), p.567-575</ispartof><rights>Elsevier GmbH</rights><rights>2008 Elsevier GmbH</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-4179f50f88a00159a0a91d44de07b09db5e7bee446a1eb57e88515be232034ca3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0171298508000259$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3549,27924,27925,45780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18656704$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rajashree, P</creatorcontrib><creatorcontrib>Supriya, P</creatorcontrib><creatorcontrib>Das, Sulochana D</creatorcontrib><title>Differential migration of human monocyte-derived dendritic cells after infection with prevalent clinical strains of Mycobacterium tuberculosis</title><title>Immunobiology (1979)</title><addtitle>Immunobiology</addtitle><description>Abstract Dendritic cells (DCs) play a key role in the host immune response to infections. Mycobacterium tuberculosis (MTB) can inhibit the maturation of DCs and impair their ability to stimulate T cell proliferation. Here, we assessed in vitro migratory behavior of human monocyte-derived DCs (MoDC) when infected with various MTB strains (H37Rv and prevalent clinical strains S7 and S10 from South India). The migration of Rv and S7 infected MoDC towards secondary lymphoid chemokine (CCL21) was 50% lower after 1 day of infection compared to LPS stimulation. This reduced cell migration may be due to a block in the chemokine receptor switch from CCR5 to CCR7 expression on MoDC. Only clinical strain S10 infected MoDC showed an up-regulation of CCR7 and down-regulation of CCR5 expression, similar to LPS stimulated MoDC. While Rv and S7 infected MoDC did not display any alteration in expression of these receptors. Similarly, Rv and S7 infected MoDC did not induce IL-8, IP-10 and MCP-1 chemokine production. This reduction in chemokine levels was reflected in the reduced chemoattraction of CD4+ T cells also. These findings suggest that there is variation in the stimulation of MoDC with different clinical strains of MTB and this variation may be dependent upon the virulence of the strain.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Advanced Basic Science</subject><subject>Allergy and Immunology</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Chemokine CXCL10 - biosynthesis</subject><subject>Chemokines</subject><subject>Chemotaxis</subject><subject>Clinical isolates</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - microbiology</subject><subject>Dendritic Cells - physiology</subject><subject>Down-Regulation</subject><subject>Humans</subject><subject>Interleukin-8 - biosynthesis</subject><subject>Middle Aged</subject><subject>Migration</subject><subject>Monocytes</subject><subject>Mycobacterium tuberculosis</subject><subject>Mycobacterium tuberculosis - immunology</subject><subject>Mycobacterium tuberculosis - pathogenicity</subject><subject>Receptors, CCR5 - metabolism</subject><subject>Receptors, CCR7 - metabolism</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Up-Regulation</subject><subject>Virulence</subject><issn>0171-2985</issn><issn>1878-3279</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqFksFu1DAQhiMEotvCEyAhn-CUME7i2DmAVBUKSEUcgLPlOBM6S2IvdrJoX4JnxukuQuIAJ1--_7dmvsmyJxwKDrx5sS1o6sgXJYAqgBcA8l624UqqvCplez_bAJc8L1slzrLzGLcAvC2lepidcdWIRkK9yX6-pmHAgG4mM7KJvgYzk3fMD-x2mYxjk3feHmbMewy0x5716PpAM1lmcRwjM8OMgZEb0N4lf9B8y3YB92ZMrcyO5Mim7jgHQy6uzR8O1nfGphwtE5uXDoNdRh8pPsoeDGaM-Pj0XmRfrt98vnqX33x8-_7q8ia3dV3Pec1lOwgYlDJpKNEaMC3v67pHkB20fSdQdoh13RiOnZColOCiw7IqoaqtqS6y58feXfDfF4yzniiu8xiHfolaqQoqEBIS-eyfZNNWompVk8DqCNrgYww46F2gyYSD5qBXYXqr74TpVZgGrpOwlHp6ql-6Cfs_mZOhBLw8ApjWsScMOlpCZ7GnkDaue0__-eDVX_nfRr7hAePWL8GlTWuuY6lBf1pvZj0ZUABQirb6BRB7wHE</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Rajashree, P</creator><creator>Supriya, P</creator><creator>Das, Sulochana D</creator><general>Elsevier GmbH</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><scope>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>20080101</creationdate><title>Differential migration of human monocyte-derived dendritic cells after infection with prevalent clinical strains of Mycobacterium tuberculosis</title><author>Rajashree, P ; Supriya, P ; Das, Sulochana D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-4179f50f88a00159a0a91d44de07b09db5e7bee446a1eb57e88515be232034ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Advanced Basic Science</topic><topic>Allergy and Immunology</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Chemokine CXCL10 - biosynthesis</topic><topic>Chemokines</topic><topic>Chemotaxis</topic><topic>Clinical isolates</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - microbiology</topic><topic>Dendritic Cells - physiology</topic><topic>Down-Regulation</topic><topic>Humans</topic><topic>Interleukin-8 - biosynthesis</topic><topic>Middle Aged</topic><topic>Migration</topic><topic>Monocytes</topic><topic>Mycobacterium tuberculosis</topic><topic>Mycobacterium tuberculosis - immunology</topic><topic>Mycobacterium tuberculosis - pathogenicity</topic><topic>Receptors, CCR5 - metabolism</topic><topic>Receptors, CCR7 - metabolism</topic><topic>Receptors, Chemokine - metabolism</topic><topic>Up-Regulation</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rajashree, P</creatorcontrib><creatorcontrib>Supriya, P</creatorcontrib><creatorcontrib>Das, Sulochana D</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><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Immunobiology (1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rajashree, P</au><au>Supriya, P</au><au>Das, Sulochana D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential migration of human monocyte-derived dendritic cells after infection with prevalent clinical strains of Mycobacterium tuberculosis</atitle><jtitle>Immunobiology (1979)</jtitle><addtitle>Immunobiology</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>213</volume><issue>7</issue><spage>567</spage><epage>575</epage><pages>567-575</pages><issn>0171-2985</issn><eissn>1878-3279</eissn><abstract>Abstract Dendritic cells (DCs) play a key role in the host immune response to infections. Mycobacterium tuberculosis (MTB) can inhibit the maturation of DCs and impair their ability to stimulate T cell proliferation. Here, we assessed in vitro migratory behavior of human monocyte-derived DCs (MoDC) when infected with various MTB strains (H37Rv and prevalent clinical strains S7 and S10 from South India). The migration of Rv and S7 infected MoDC towards secondary lymphoid chemokine (CCL21) was 50% lower after 1 day of infection compared to LPS stimulation. This reduced cell migration may be due to a block in the chemokine receptor switch from CCR5 to CCR7 expression on MoDC. Only clinical strain S10 infected MoDC showed an up-regulation of CCR7 and down-regulation of CCR5 expression, similar to LPS stimulated MoDC. While Rv and S7 infected MoDC did not display any alteration in expression of these receptors. Similarly, Rv and S7 infected MoDC did not induce IL-8, IP-10 and MCP-1 chemokine production. 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subjects | Adolescent Adult Advanced Basic Science Allergy and Immunology Cell Movement - physiology Cells, Cultured Chemokine CCL2 - biosynthesis Chemokine CXCL10 - biosynthesis Chemokines Chemotaxis Clinical isolates Dendritic cells Dendritic Cells - microbiology Dendritic Cells - physiology Down-Regulation Humans Interleukin-8 - biosynthesis Middle Aged Migration Monocytes Mycobacterium tuberculosis Mycobacterium tuberculosis - immunology Mycobacterium tuberculosis - pathogenicity Receptors, CCR5 - metabolism Receptors, CCR7 - metabolism Receptors, Chemokine - metabolism Up-Regulation Virulence |
title | Differential migration of human monocyte-derived dendritic cells after infection with prevalent clinical strains of Mycobacterium tuberculosis |
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