Killing of Plasmodium falciparum by cytokine activated effector cells (neutrophils and macrophages)
Macrophages display natural antibody independent killing of asexual blood stages of Plasmodium falciparum in vitro. In contrast, the neutrophil killing of P. falciparum requires the presence of antibodies. Cytokines such as TNFα have very little effect on the macrophage-induced antiplasmodial activi...
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Veröffentlicht in: | Immunology letters 1990-08, Vol.25 (1), p.179-187 |
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creator | Ferrante, A. Kumaratilake, L. Rzepczyk, C.M. Dayer, J.-M. |
description | Macrophages display natural antibody independent killing of asexual blood stages of
Plasmodium falciparum in vitro. In contrast, the neutrophil killing of
P. falciparum requires the presence of antibodies. Cytokines such as TNFα have very little effect on the macrophage-induced antiplasmodial activity, but significantly increase the damage of parasites by neutrophils. Cytokines, TNFα, IFN-γ and TNFβ at very high concentrations were not toxic to
P. falciparum in culture. It is postulated that the basis for cytokine modulated antiplasmodial activity of leukocytes is increased expression of Fc and complement receptors, which leads to a more efficient interaction between the parasite and neutrophils. It is also postulated that the parasite evades natural macrophage killing mechanisms by inducing factors which supress this macrophage activity. Cytokine inhibitors may be induced during the course of a malarial infection. These could be involved in attempts to attain a balance between the host and the parasite, by protecting the parasite from the damaging effect of the immune system and protecting the host from the deleterious effects of cytokines. |
doi_str_mv | 10.1016/0165-2478(90)90112-4 |
format | Article |
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Plasmodium falciparum in vitro. In contrast, the neutrophil killing of
P. falciparum requires the presence of antibodies. Cytokines such as TNFα have very little effect on the macrophage-induced antiplasmodial activity, but significantly increase the damage of parasites by neutrophils. Cytokines, TNFα, IFN-γ and TNFβ at very high concentrations were not toxic to
P. falciparum in culture. It is postulated that the basis for cytokine modulated antiplasmodial activity of leukocytes is increased expression of Fc and complement receptors, which leads to a more efficient interaction between the parasite and neutrophils. It is also postulated that the parasite evades natural macrophage killing mechanisms by inducing factors which supress this macrophage activity. Cytokine inhibitors may be induced during the course of a malarial infection. These could be involved in attempts to attain a balance between the host and the parasite, by protecting the parasite from the damaging effect of the immune system and protecting the host from the deleterious effects of cytokines.</description><identifier>ISSN: 0165-2478</identifier><identifier>EISSN: 1879-0542</identifier><identifier>DOI: 10.1016/0165-2478(90)90112-4</identifier><identifier>PMID: 2126525</identifier><identifier>CODEN: IMLED6</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Antibodies, Protozoan - biosynthesis ; Biological and medical sciences ; Cytokine ; Cytokine inhibitor ; Cytokines - physiology ; Fundamental and applied biological sciences. Psychology ; Host-Parasite Interactions - immunology ; Humans ; Immunity, Cellular ; Interferon-gamma - physiology ; Invertebrates ; Life cycle. Host-agent relationship. Pathogenesis ; Lymphotoxin-alpha - physiology ; Macrophage ; Macrophages - immunology ; Malaria - blood ; Malaria - immunology ; Neutrophil ; Neutrophils - immunology ; Plasmodium falciparum ; Plasmodium falciparum - immunology ; Protozoa ; Tumor Necrosis Factor-alpha - physiology ; Tumour necrosis factor</subject><ispartof>Immunology letters, 1990-08, Vol.25 (1), p.179-187</ispartof><rights>1990</rights><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c484t-98730f4711ab1e8b8b3775fb66efcfd6893bba1e13d553c3a59328a771d52b8a3</citedby><cites>FETCH-LOGICAL-c484t-98730f4711ab1e8b8b3775fb66efcfd6893bba1e13d553c3a59328a771d52b8a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0165-2478(90)90112-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>309,310,314,778,782,787,788,3539,23913,23914,25123,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19296740$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2126525$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferrante, A.</creatorcontrib><creatorcontrib>Kumaratilake, L.</creatorcontrib><creatorcontrib>Rzepczyk, C.M.</creatorcontrib><creatorcontrib>Dayer, J.-M.</creatorcontrib><title>Killing of Plasmodium falciparum by cytokine activated effector cells (neutrophils and macrophages)</title><title>Immunology letters</title><addtitle>Immunol Lett</addtitle><description>Macrophages display natural antibody independent killing of asexual blood stages of
Plasmodium falciparum in vitro. In contrast, the neutrophil killing of
P. falciparum requires the presence of antibodies. Cytokines such as TNFα have very little effect on the macrophage-induced antiplasmodial activity, but significantly increase the damage of parasites by neutrophils. Cytokines, TNFα, IFN-γ and TNFβ at very high concentrations were not toxic to
P. falciparum in culture. It is postulated that the basis for cytokine modulated antiplasmodial activity of leukocytes is increased expression of Fc and complement receptors, which leads to a more efficient interaction between the parasite and neutrophils. It is also postulated that the parasite evades natural macrophage killing mechanisms by inducing factors which supress this macrophage activity. Cytokine inhibitors may be induced during the course of a malarial infection. These could be involved in attempts to attain a balance between the host and the parasite, by protecting the parasite from the damaging effect of the immune system and protecting the host from the deleterious effects of cytokines.</description><subject>Animals</subject><subject>Antibodies, Protozoan - biosynthesis</subject><subject>Biological and medical sciences</subject><subject>Cytokine</subject><subject>Cytokine inhibitor</subject><subject>Cytokines - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Host-Parasite Interactions - immunology</subject><subject>Humans</subject><subject>Immunity, Cellular</subject><subject>Interferon-gamma - physiology</subject><subject>Invertebrates</subject><subject>Life cycle. Host-agent relationship. Pathogenesis</subject><subject>Lymphotoxin-alpha - physiology</subject><subject>Macrophage</subject><subject>Macrophages - immunology</subject><subject>Malaria - blood</subject><subject>Malaria - immunology</subject><subject>Neutrophil</subject><subject>Neutrophils - immunology</subject><subject>Plasmodium falciparum</subject><subject>Plasmodium falciparum - immunology</subject><subject>Protozoa</subject><subject>Tumor Necrosis Factor-alpha - physiology</subject><subject>Tumour necrosis factor</subject><issn>0165-2478</issn><issn>1879-0542</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEuLFTEQhYMo43X0Hyhko8wsWvPsJJsBGXzhgC50HfKojNF-XJPugfvvTXsv485FUVXUqcPhQ-g5Ja8pof2bVrJjQukLQy4NoZR14gHaUa1MR6RgD9HuXvIYPan1JyFUcsHP0BmjrJdM7lD4nIchT7d4Tvjr4Oo4x7yOOLkh5L0rbfQHHA7L_CtPgF1Y8p1bIGJICcIyFxxgGCq-mGBdyrz_kdvipohHF7bV3UK9fIoeNb8Kz079HH1__-7b9cfu5suHT9dvb7ogtFg6oxUnSShKnaegvfZcKZl830MKKfbacO8dBcqjlDxwJw1n2ilFo2ReO36OXh1992X-vUJd7Jjrls9NMK_V0p4IprRoQnEUtoy1Fkh2X_LoysFSYje2dgNnN3DWEPuXrd3eXpz8Vz9CvH86wWz3l6e7q8ENqbgp5PrP2zDTK0Ga7uqogwbjLkOxNWSYAsRcGlQb5_z_IH8ABu-WMw</recordid><startdate>19900801</startdate><enddate>19900801</enddate><creator>Ferrante, A.</creator><creator>Kumaratilake, L.</creator><creator>Rzepczyk, C.M.</creator><creator>Dayer, J.-M.</creator><general>Elsevier B.V</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></search><sort><creationdate>19900801</creationdate><title>Killing of Plasmodium falciparum by cytokine activated effector cells (neutrophils and macrophages)</title><author>Ferrante, A. ; Kumaratilake, L. ; Rzepczyk, C.M. ; Dayer, J.-M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c484t-98730f4711ab1e8b8b3775fb66efcfd6893bba1e13d553c3a59328a771d52b8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Animals</topic><topic>Antibodies, Protozoan - biosynthesis</topic><topic>Biological and medical sciences</topic><topic>Cytokine</topic><topic>Cytokine inhibitor</topic><topic>Cytokines - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Host-Parasite Interactions - immunology</topic><topic>Humans</topic><topic>Immunity, Cellular</topic><topic>Interferon-gamma - physiology</topic><topic>Invertebrates</topic><topic>Life cycle. Host-agent relationship. Pathogenesis</topic><topic>Lymphotoxin-alpha - physiology</topic><topic>Macrophage</topic><topic>Macrophages - immunology</topic><topic>Malaria - blood</topic><topic>Malaria - immunology</topic><topic>Neutrophil</topic><topic>Neutrophils - immunology</topic><topic>Plasmodium falciparum</topic><topic>Plasmodium falciparum - immunology</topic><topic>Protozoa</topic><topic>Tumor Necrosis Factor-alpha - physiology</topic><topic>Tumour necrosis factor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ferrante, A.</creatorcontrib><creatorcontrib>Kumaratilake, L.</creatorcontrib><creatorcontrib>Rzepczyk, C.M.</creatorcontrib><creatorcontrib>Dayer, J.-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><jtitle>Immunology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ferrante, A.</au><au>Kumaratilake, L.</au><au>Rzepczyk, C.M.</au><au>Dayer, J.-M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Killing of Plasmodium falciparum by cytokine activated effector cells (neutrophils and macrophages)</atitle><jtitle>Immunology letters</jtitle><addtitle>Immunol Lett</addtitle><date>1990-08-01</date><risdate>1990</risdate><volume>25</volume><issue>1</issue><spage>179</spage><epage>187</epage><pages>179-187</pages><issn>0165-2478</issn><eissn>1879-0542</eissn><coden>IMLED6</coden><abstract>Macrophages display natural antibody independent killing of asexual blood stages of
Plasmodium falciparum in vitro. In contrast, the neutrophil killing of
P. falciparum requires the presence of antibodies. Cytokines such as TNFα have very little effect on the macrophage-induced antiplasmodial activity, but significantly increase the damage of parasites by neutrophils. Cytokines, TNFα, IFN-γ and TNFβ at very high concentrations were not toxic to
P. falciparum in culture. It is postulated that the basis for cytokine modulated antiplasmodial activity of leukocytes is increased expression of Fc and complement receptors, which leads to a more efficient interaction between the parasite and neutrophils. It is also postulated that the parasite evades natural macrophage killing mechanisms by inducing factors which supress this macrophage activity. Cytokine inhibitors may be induced during the course of a malarial infection. These could be involved in attempts to attain a balance between the host and the parasite, by protecting the parasite from the damaging effect of the immune system and protecting the host from the deleterious effects of cytokines.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>2126525</pmid><doi>10.1016/0165-2478(90)90112-4</doi><tpages>9</tpages></addata></record> |
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subjects | Animals Antibodies, Protozoan - biosynthesis Biological and medical sciences Cytokine Cytokine inhibitor Cytokines - physiology Fundamental and applied biological sciences. Psychology Host-Parasite Interactions - immunology Humans Immunity, Cellular Interferon-gamma - physiology Invertebrates Life cycle. Host-agent relationship. Pathogenesis Lymphotoxin-alpha - physiology Macrophage Macrophages - immunology Malaria - blood Malaria - immunology Neutrophil Neutrophils - immunology Plasmodium falciparum Plasmodium falciparum - immunology Protozoa Tumor Necrosis Factor-alpha - physiology Tumour necrosis factor |
title | Killing of Plasmodium falciparum by cytokine activated effector cells (neutrophils and macrophages) |
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