Alternative versus classical macrophage activation during experimental African trypanosomosis
The type I/type II cytokine balance may influence the development of different subsets of suppressive macrophages, i.e., classically activated macrophages (caMφ, type I) versus alternatively activated macrophages (aaMφ, type II). Recently, we showed that although mice infected with phospholipase C‐d...
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Veröffentlicht in: | Journal of leukocyte biology 2001-03, Vol.69 (3), p.387-396 |
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description | The type I/type II cytokine balance may influence the development of different subsets of suppressive macrophages, i.e., classically activated macrophages (caMφ, type I) versus alternatively activated macrophages (aaMφ, type II). Recently, we showed that although mice infected with phospholipase C‐deficient (PLC−/−) Trypanosoma brucei brucei exhibit a clear shift from type I to the type II cytokine production, wild type (WT)‐infected mice remain locked in a type I cytokine response. In the present study, phenotype and accessory cell function of macrophages elicited during WT and PLC−/− T. b. brucei infection were compared. Results indicate that caMφ develop in a type I cytokine environment in the early phase of WT and PLC−/− trypanosome infection, correlating with inhibition of T cell activation triggered by a mitogen, a superantigen, or an antigen. In the late stage of infection, only PLC−/−‐infected mice resisting the infection develop type II cytokine‐associated aaMφ correlating with impaired antigen‐ but not mitogen‐ or superantigen‐induced T cell activation. |
doi_str_mv | 10.1189/jlb.69.3.387 |
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Recently, we showed that although mice infected with phospholipase C‐deficient (PLC−/−) Trypanosoma brucei brucei exhibit a clear shift from type I to the type II cytokine production, wild type (WT)‐infected mice remain locked in a type I cytokine response. In the present study, phenotype and accessory cell function of macrophages elicited during WT and PLC−/− T. b. brucei infection were compared. Results indicate that caMφ develop in a type I cytokine environment in the early phase of WT and PLC−/− trypanosome infection, correlating with inhibition of T cell activation triggered by a mitogen, a superantigen, or an antigen. 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Recently, we showed that although mice infected with phospholipase C‐deficient (PLC−/−) Trypanosoma brucei brucei exhibit a clear shift from type I to the type II cytokine production, wild type (WT)‐infected mice remain locked in a type I cytokine response. In the present study, phenotype and accessory cell function of macrophages elicited during WT and PLC−/− T. b. brucei infection were compared. Results indicate that caMφ develop in a type I cytokine environment in the early phase of WT and PLC−/− trypanosome infection, correlating with inhibition of T cell activation triggered by a mitogen, a superantigen, or an antigen. In the late stage of infection, only PLC−/−‐infected mice resisting the infection develop type II cytokine‐associated aaMφ correlating with impaired antigen‐ but not mitogen‐ or superantigen‐induced T cell activation.</description><subject>Animals</subject><subject>antigen presentation</subject><subject>Antigen Presentation - immunology</subject><subject>Arginase - blood</subject><subject>Ascitic Fluid - metabolism</subject><subject>Ascitic Fluid - pathology</subject><subject>Concanavalin A - pharmacology</subject><subject>Enterotoxins - immunology</subject><subject>Enterotoxins - pharmacology</subject><subject>Epitopes, T-Lymphocyte - immunology</subject><subject>Female</subject><subject>immunosuppression</subject><subject>Interferon-gamma - biosynthesis</subject><subject>Interleukins - biosynthesis</subject><subject>Lymphocyte Activation - drug effects</subject><subject>Lymphocyte Activation - immunology</subject><subject>Macrophage Activation - drug effects</subject><subject>Macrophage Activation - immunology</subject><subject>Macrophages, Peritoneal - drug effects</subject><subject>Macrophages, Peritoneal - immunology</subject><subject>Macrophages, Peritoneal - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mitogens - pharmacology</subject><subject>Muramidase - immunology</subject><subject>Muramidase - pharmacology</subject><subject>Nitric Oxide - blood</subject><subject>Phenotype</subject><subject>phospholipase C</subject><subject>Superantigens - immunology</subject><subject>Superantigens - pharmacology</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - immunology</subject><subject>Trypanosoma brucei brucei</subject><subject>Trypanosoma brucei brucei - enzymology</subject><subject>Trypanosoma brucei brucei - genetics</subject><subject>trypanosome infection</subject><subject>Trypanosomiasis, African - blood</subject><subject>Trypanosomiasis, African - immunology</subject><subject>Type C Phospholipases - deficiency</subject><subject>Type C Phospholipases - genetics</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkD1v2zAQhokgRey42TIHWtIpUkhRpKTRDfoJA1mSsSBOImnToD5CSlb978NARrOl0y3Pve_dg9A1wQkhRXm_t1XCy4QmtMjP0JKUtIgpz-k5WuI8IzHLMF6gS-_3GGOacnyBFoSknOQFW6I_azso18JgDio6KOdHH9UWvDc12KiB2nX9DrYqgjogAevaSI7OtNtI_e2VM41qh0CutQsbbTS4Yw9t57um88Z_Rp80WK-uTnOFnr9_e3r4GW8ef_x6WG_iOmM8jzWknEnJAMKFiupKUsllVVAtGS4k4ExSVnCtMaE6gxRjKOsK0lQSnsk6pyv0Zc7tXfcyKj-IxvhaWQut6kYvcl4WZcrof8EgJaOcsQDezWAQ4L1TWvThV3BHQbB48y6Cd8FLQUXwHvCbU-5YNUq-wyfRASAzMBmrjh-Gid-br3gOvZ13dma7m4xTwjdgbahIxTRN_8pfAbKpnb0</recordid><startdate>200103</startdate><enddate>200103</enddate><creator>Namangala, Boniface</creator><creator>De Baetselier, Patrick</creator><creator>Noël, Wim</creator><creator>Brys, Lea</creator><creator>Beschin, Alain</creator><general>Society for Leukocyte Biology</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>7T5</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope></search><sort><creationdate>200103</creationdate><title>Alternative versus classical macrophage activation during experimental African trypanosomosis</title><author>Namangala, Boniface ; De Baetselier, Patrick ; Noël, Wim ; Brys, Lea ; Beschin, Alain</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4567-fa265dd5aa003e3fbd3d6db83fd508da04d3586ff013f4a200a9cba22d164dc73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>antigen presentation</topic><topic>Antigen Presentation - immunology</topic><topic>Arginase - blood</topic><topic>Ascitic Fluid - metabolism</topic><topic>Ascitic Fluid - pathology</topic><topic>Concanavalin A - pharmacology</topic><topic>Enterotoxins - immunology</topic><topic>Enterotoxins - pharmacology</topic><topic>Epitopes, T-Lymphocyte - immunology</topic><topic>Female</topic><topic>immunosuppression</topic><topic>Interferon-gamma - biosynthesis</topic><topic>Interleukins - biosynthesis</topic><topic>Lymphocyte Activation - drug effects</topic><topic>Lymphocyte Activation - immunology</topic><topic>Macrophage Activation - drug effects</topic><topic>Macrophage Activation - immunology</topic><topic>Macrophages, Peritoneal - drug effects</topic><topic>Macrophages, Peritoneal - immunology</topic><topic>Macrophages, Peritoneal - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mitogens - pharmacology</topic><topic>Muramidase - immunology</topic><topic>Muramidase - pharmacology</topic><topic>Nitric Oxide - blood</topic><topic>Phenotype</topic><topic>phospholipase C</topic><topic>Superantigens - immunology</topic><topic>Superantigens - pharmacology</topic><topic>T-Lymphocytes - drug effects</topic><topic>T-Lymphocytes - immunology</topic><topic>Trypanosoma brucei brucei</topic><topic>Trypanosoma brucei brucei - enzymology</topic><topic>Trypanosoma brucei brucei - genetics</topic><topic>trypanosome infection</topic><topic>Trypanosomiasis, African - blood</topic><topic>Trypanosomiasis, African - immunology</topic><topic>Type C Phospholipases - deficiency</topic><topic>Type C Phospholipases - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Namangala, Boniface</creatorcontrib><creatorcontrib>De Baetselier, Patrick</creatorcontrib><creatorcontrib>Noël, Wim</creatorcontrib><creatorcontrib>Brys, Lea</creatorcontrib><creatorcontrib>Beschin, Alain</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Namangala, Boniface</au><au>De Baetselier, Patrick</au><au>Noël, Wim</au><au>Brys, Lea</au><au>Beschin, Alain</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alternative versus classical macrophage activation during experimental African trypanosomosis</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2001-03</date><risdate>2001</risdate><volume>69</volume><issue>3</issue><spage>387</spage><epage>396</epage><pages>387-396</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>The type I/type II cytokine balance may influence the development of different subsets of suppressive macrophages, i.e., classically activated macrophages (caMφ, type I) versus alternatively activated macrophages (aaMφ, type II). Recently, we showed that although mice infected with phospholipase C‐deficient (PLC−/−) Trypanosoma brucei brucei exhibit a clear shift from type I to the type II cytokine production, wild type (WT)‐infected mice remain locked in a type I cytokine response. In the present study, phenotype and accessory cell function of macrophages elicited during WT and PLC−/− T. b. brucei infection were compared. Results indicate that caMφ develop in a type I cytokine environment in the early phase of WT and PLC−/− trypanosome infection, correlating with inhibition of T cell activation triggered by a mitogen, a superantigen, or an antigen. In the late stage of infection, only PLC−/−‐infected mice resisting the infection develop type II cytokine‐associated aaMφ correlating with impaired antigen‐ but not mitogen‐ or superantigen‐induced T cell activation.</abstract><cop>United States</cop><pub>Society for Leukocyte Biology</pub><pmid>11261785</pmid><doi>10.1189/jlb.69.3.387</doi><tpages>10</tpages></addata></record> |
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source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals |
subjects | Animals antigen presentation Antigen Presentation - immunology Arginase - blood Ascitic Fluid - metabolism Ascitic Fluid - pathology Concanavalin A - pharmacology Enterotoxins - immunology Enterotoxins - pharmacology Epitopes, T-Lymphocyte - immunology Female immunosuppression Interferon-gamma - biosynthesis Interleukins - biosynthesis Lymphocyte Activation - drug effects Lymphocyte Activation - immunology Macrophage Activation - drug effects Macrophage Activation - immunology Macrophages, Peritoneal - drug effects Macrophages, Peritoneal - immunology Macrophages, Peritoneal - metabolism Mice Mice, Inbred BALB C Mitogens - pharmacology Muramidase - immunology Muramidase - pharmacology Nitric Oxide - blood Phenotype phospholipase C Superantigens - immunology Superantigens - pharmacology T-Lymphocytes - drug effects T-Lymphocytes - immunology Trypanosoma brucei brucei Trypanosoma brucei brucei - enzymology Trypanosoma brucei brucei - genetics trypanosome infection Trypanosomiasis, African - blood Trypanosomiasis, African - immunology Type C Phospholipases - deficiency Type C Phospholipases - genetics |
title | Alternative versus classical macrophage activation during experimental African trypanosomosis |
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