Leishmania donovani: Evolution and Architecture of the Splenic Cellular Immune Response Related to Control of Infection
Melby, P. C., Tabares, A., Restrepo, B. I., Cardona, A. E., McGuff, H. S., and Teale, J. M. 2001. Leishmania donovani: Evolution and architecture of the splenic cellular immune response related to control of infection. Experimental Parasitology99, 17–25. Infection with the protozoan Leishmania donov...
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description | Melby, P. C., Tabares, A., Restrepo, B. I., Cardona, A. E., McGuff, H. S., and Teale, J. M. 2001. Leishmania donovani: Evolution and architecture of the splenic cellular immune response related to control of infection. Experimental Parasitology99, 17–25. Infection with the protozoan Leishmania donovani in humans is usually subclinical. Parasites probably persist for the life of the host and the low-level infection is controlled by the cellular immune response. To better understand the mechanisms related to the control of infection, we studied the evolution and architecture of the splenic cellular immune response in a murine model that is most representative of human subclinical infection. Following systemic inoculation with L. donovani, the parasites were primarily localized to the macrophage-rich splenic red pulp. There was an initial increase in the numbers of T cells and dendritic cells in the periarteriolar lymphoid sheath and marginal zone, but the red pulp (where parasitized macrophages were prominent) remained free of these cells until later in the course of infection. Thus, T cells did not colocalize with parasitized red pulp macrophages until later in the course of infection. Early in the course of infection, IL-10 production within the marginal zone and TGF-β production by cells in the red pulp were prominent. These macrophage-inhibitory cytokines may contribute to the establishment of the infection and early parasite replication. By day 28 of infection, when the visceral parasite burden began to decline, the number of IL-10-producing spleen cells was back to the baseline level, but IFN-γ production was higher and the number of IL-12-producing cells was increased dramatically. At this time T cells and dendritic cells had moved out of the lymphoid follicle and marginal zone into the red pulp where the parasites were located. These findings therefore suggest that control of infection is associated with IFN-γ and IL-12 production and migration of T cells and dendritic cells to the site of chronic parasitism. |
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C., Tabares, A., Restrepo, B. I., Cardona, A. E., McGuff, H. S., and Teale, J. M. 2001. Leishmania donovani: Evolution and architecture of the splenic cellular immune response related to control of infection. Experimental Parasitology99, 17–25. Infection with the protozoan Leishmania donovani in humans is usually subclinical. Parasites probably persist for the life of the host and the low-level infection is controlled by the cellular immune response. To better understand the mechanisms related to the control of infection, we studied the evolution and architecture of the splenic cellular immune response in a murine model that is most representative of human subclinical infection. Following systemic inoculation with L. donovani, the parasites were primarily localized to the macrophage-rich splenic red pulp. There was an initial increase in the numbers of T cells and dendritic cells in the periarteriolar lymphoid sheath and marginal zone, but the red pulp (where parasitized macrophages were prominent) remained free of these cells until later in the course of infection. Thus, T cells did not colocalize with parasitized red pulp macrophages until later in the course of infection. Early in the course of infection, IL-10 production within the marginal zone and TGF-β production by cells in the red pulp were prominent. These macrophage-inhibitory cytokines may contribute to the establishment of the infection and early parasite replication. By day 28 of infection, when the visceral parasite burden began to decline, the number of IL-10-producing spleen cells was back to the baseline level, but IFN-γ production was higher and the number of IL-12-producing cells was increased dramatically. At this time T cells and dendritic cells had moved out of the lymphoid follicle and marginal zone into the red pulp where the parasites were located. These findings therefore suggest that control of infection is associated with IFN-γ and IL-12 production and migration of T cells and dendritic cells to the site of chronic parasitism.</description><identifier>ISSN: 0014-4894</identifier><identifier>EISSN: 1090-2449</identifier><identifier>DOI: 10.1006/expr.2001.4640</identifier><identifier>PMID: 11708830</identifier><identifier>CODEN: EXPAAA</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Cricetinae ; Cytokines - biosynthesis ; Dendritic Cells - immunology ; Disease Models, Animal ; Experimental protozoal diseases and models ; g-Interferon ; Immunity, Cellular ; Immunohistochemistry ; Infectious diseases ; Leishmania donovani ; Leishmania donovani - immunology ; Leishmaniasis, Visceral - immunology ; Macrophages - parasitology ; Male ; Medical sciences ; Mesocricetus ; Mice ; Mice, Inbred BALB C ; Parasitic diseases ; protozoa ; Protozoal diseases ; Spleen - immunology ; Spleen - pathology ; T-Lymphocytes - immunology</subject><ispartof>Experimental parasitology, 2001-09, Vol.99 (1), p.17-25</ispartof><rights>2001 Academic Press</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-12e75db0f5de11ad00729ff7fd19bd1950d91088263e550f13addbb6a66bb5233</citedby><cites>FETCH-LOGICAL-c401t-12e75db0f5de11ad00729ff7fd19bd1950d91088263e550f13addbb6a66bb5233</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/expr.2001.4640$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14145908$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11708830$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Melby, Peter C.</creatorcontrib><creatorcontrib>Tabares, Adriana</creatorcontrib><creatorcontrib>Restrepo, Blanca I.</creatorcontrib><creatorcontrib>Cardona, Astrid E.</creatorcontrib><creatorcontrib>McGuff, H.Stan</creatorcontrib><creatorcontrib>Teale, Judy M.</creatorcontrib><title>Leishmania donovani: Evolution and Architecture of the Splenic Cellular Immune Response Related to Control of Infection</title><title>Experimental parasitology</title><addtitle>Exp Parasitol</addtitle><description>Melby, P. C., Tabares, A., Restrepo, B. I., Cardona, A. E., McGuff, H. S., and Teale, J. M. 2001. Leishmania donovani: Evolution and architecture of the splenic cellular immune response related to control of infection. Experimental Parasitology99, 17–25. Infection with the protozoan Leishmania donovani in humans is usually subclinical. Parasites probably persist for the life of the host and the low-level infection is controlled by the cellular immune response. To better understand the mechanisms related to the control of infection, we studied the evolution and architecture of the splenic cellular immune response in a murine model that is most representative of human subclinical infection. Following systemic inoculation with L. donovani, the parasites were primarily localized to the macrophage-rich splenic red pulp. There was an initial increase in the numbers of T cells and dendritic cells in the periarteriolar lymphoid sheath and marginal zone, but the red pulp (where parasitized macrophages were prominent) remained free of these cells until later in the course of infection. Thus, T cells did not colocalize with parasitized red pulp macrophages until later in the course of infection. Early in the course of infection, IL-10 production within the marginal zone and TGF-β production by cells in the red pulp were prominent. These macrophage-inhibitory cytokines may contribute to the establishment of the infection and early parasite replication. By day 28 of infection, when the visceral parasite burden began to decline, the number of IL-10-producing spleen cells was back to the baseline level, but IFN-γ production was higher and the number of IL-12-producing cells was increased dramatically. At this time T cells and dendritic cells had moved out of the lymphoid follicle and marginal zone into the red pulp where the parasites were located. These findings therefore suggest that control of infection is associated with IFN-γ and IL-12 production and migration of T cells and dendritic cells to the site of chronic parasitism.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cricetinae</subject><subject>Cytokines - biosynthesis</subject><subject>Dendritic Cells - immunology</subject><subject>Disease Models, Animal</subject><subject>Experimental protozoal diseases and models</subject><subject>g-Interferon</subject><subject>Immunity, Cellular</subject><subject>Immunohistochemistry</subject><subject>Infectious diseases</subject><subject>Leishmania donovani</subject><subject>Leishmania donovani - immunology</subject><subject>Leishmaniasis, Visceral - immunology</subject><subject>Macrophages - parasitology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesocricetus</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Parasitic diseases</subject><subject>protozoa</subject><subject>Protozoal diseases</subject><subject>Spleen - immunology</subject><subject>Spleen - pathology</subject><subject>T-Lymphocytes - immunology</subject><issn>0014-4894</issn><issn>1090-2449</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU2LFDEQhoMo7rh69Si56K3HSjrpD2_LsOrAgODHOaSTChPpTsake1b_vWlmYE_iIaQIT71U6iHkNYMtA2je4-9T2nIAthWNgCdkw6CHigvRPyWb8iwq0fXihrzI-ScAdIyL5-SGsRa6roYNeTigz8dJB6-pjSGeS_WB3p_juMw-BqqDpXfJHP2MZl4S0ujofET67TRi8IbucByXUSe6n6YlIP2K-RRDXotRz2jpHOkuhjnFcW3dB1dySvBL8szpMeOr631Lfny8_777XB2-fNrv7g6VEcDminFspR3ASYuMaQvQ8t651lnWD-VIsD0rX-FNjVKCY7W2dhga3TTDIHld35J3l9xTir8WzLOafDZlaB0wLlm1nHes5uy_IOs4l1Ku4PYCmhRzTujUKflJpz-KgVqdqNWJWp2o1UlpeHNNXoYJ7SN-lVCAt1dAZ6NHl3QwPj9yggnZQ1e47sJhWdjZY1LZeAwGrU9lq8pG_68Z_gJKpakK</recordid><startdate>20010901</startdate><enddate>20010901</enddate><creator>Melby, Peter C.</creator><creator>Tabares, Adriana</creator><creator>Restrepo, Blanca I.</creator><creator>Cardona, Astrid E.</creator><creator>McGuff, H.Stan</creator><creator>Teale, Judy M.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>20010901</creationdate><title>Leishmania donovani: Evolution and Architecture of the Splenic Cellular Immune Response Related to Control of Infection</title><author>Melby, Peter C. ; Tabares, Adriana ; Restrepo, Blanca I. ; Cardona, Astrid E. ; McGuff, H.Stan ; Teale, Judy M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-12e75db0f5de11ad00729ff7fd19bd1950d91088263e550f13addbb6a66bb5233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cricetinae</topic><topic>Cytokines - biosynthesis</topic><topic>Dendritic Cells - immunology</topic><topic>Disease Models, Animal</topic><topic>Experimental protozoal diseases and models</topic><topic>g-Interferon</topic><topic>Immunity, Cellular</topic><topic>Immunohistochemistry</topic><topic>Infectious diseases</topic><topic>Leishmania donovani</topic><topic>Leishmania donovani - immunology</topic><topic>Leishmaniasis, Visceral - immunology</topic><topic>Macrophages - parasitology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesocricetus</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Parasitic diseases</topic><topic>protozoa</topic><topic>Protozoal diseases</topic><topic>Spleen - immunology</topic><topic>Spleen - pathology</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Melby, Peter C.</creatorcontrib><creatorcontrib>Tabares, Adriana</creatorcontrib><creatorcontrib>Restrepo, Blanca I.</creatorcontrib><creatorcontrib>Cardona, Astrid E.</creatorcontrib><creatorcontrib>McGuff, H.Stan</creatorcontrib><creatorcontrib>Teale, Judy M.</creatorcontrib><collection>Pascal-Francis</collection><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>Experimental parasitology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Melby, Peter C.</au><au>Tabares, Adriana</au><au>Restrepo, Blanca I.</au><au>Cardona, Astrid E.</au><au>McGuff, H.Stan</au><au>Teale, Judy M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leishmania donovani: Evolution and Architecture of the Splenic Cellular Immune Response Related to Control of Infection</atitle><jtitle>Experimental parasitology</jtitle><addtitle>Exp Parasitol</addtitle><date>2001-09-01</date><risdate>2001</risdate><volume>99</volume><issue>1</issue><spage>17</spage><epage>25</epage><pages>17-25</pages><issn>0014-4894</issn><eissn>1090-2449</eissn><coden>EXPAAA</coden><abstract>Melby, P. C., Tabares, A., Restrepo, B. I., Cardona, A. E., McGuff, H. S., and Teale, J. M. 2001. Leishmania donovani: Evolution and architecture of the splenic cellular immune response related to control of infection. Experimental Parasitology99, 17–25. Infection with the protozoan Leishmania donovani in humans is usually subclinical. Parasites probably persist for the life of the host and the low-level infection is controlled by the cellular immune response. To better understand the mechanisms related to the control of infection, we studied the evolution and architecture of the splenic cellular immune response in a murine model that is most representative of human subclinical infection. Following systemic inoculation with L. donovani, the parasites were primarily localized to the macrophage-rich splenic red pulp. There was an initial increase in the numbers of T cells and dendritic cells in the periarteriolar lymphoid sheath and marginal zone, but the red pulp (where parasitized macrophages were prominent) remained free of these cells until later in the course of infection. Thus, T cells did not colocalize with parasitized red pulp macrophages until later in the course of infection. Early in the course of infection, IL-10 production within the marginal zone and TGF-β production by cells in the red pulp were prominent. These macrophage-inhibitory cytokines may contribute to the establishment of the infection and early parasite replication. By day 28 of infection, when the visceral parasite burden began to decline, the number of IL-10-producing spleen cells was back to the baseline level, but IFN-γ production was higher and the number of IL-12-producing cells was increased dramatically. At this time T cells and dendritic cells had moved out of the lymphoid follicle and marginal zone into the red pulp where the parasites were located. These findings therefore suggest that control of infection is associated with IFN-γ and IL-12 production and migration of T cells and dendritic cells to the site of chronic parasitism.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>11708830</pmid><doi>10.1006/expr.2001.4640</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Biological and medical sciences Cricetinae Cytokines - biosynthesis Dendritic Cells - immunology Disease Models, Animal Experimental protozoal diseases and models g-Interferon Immunity, Cellular Immunohistochemistry Infectious diseases Leishmania donovani Leishmania donovani - immunology Leishmaniasis, Visceral - immunology Macrophages - parasitology Male Medical sciences Mesocricetus Mice Mice, Inbred BALB C Parasitic diseases protozoa Protozoal diseases Spleen - immunology Spleen - pathology T-Lymphocytes - immunology |
title | Leishmania donovani: Evolution and Architecture of the Splenic Cellular Immune Response Related to Control of Infection |
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