Treatment with anti-L3T4 (CD4) monoclonal antibody reduces the inflammatory response in toxoplasmic encephalitis
Toxoplasma gondii is an important cause of disease of the central nervous system in patients with AIDS. Among the variety of immunologic disorders encountered by AIDS patients is a depletion of CD4+ subpopulation of lymphocytes. In order to determine the role of this population of T lymphocytes in t...
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Veröffentlicht in: | The Journal of immunology (1950) 1989-02, Vol.142 (3), p.954-958 |
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creator | Israelski, DM Araujo, FG Conley, FK Suzuki, Y Sharma, S Remington, JS |
description | Toxoplasma gondii is an important cause of disease of the central nervous system in patients with AIDS. Among the variety of immunologic disorders encountered by AIDS patients is a depletion of CD4+ subpopulation of lymphocytes. In order to determine the role of this population of T lymphocytes in the generation of toxoplasmic encephalitis, mice chronically infected with T. gondii were treated with mAb GK1.5 directed against the cell surface glycoprotein L3T4 (CD4) of T lymphocytes. Histopathologic sections of brains of control and treated animals were examined at regular intervals during and after completion of treatment. The results demonstrated significantly less inflammation in brains of mice during treatment with GK1.5 mAb. In addition, recrudescence of the inflammatory process occurred after discontinuation of treatment. Similar results were observed in experiments in which different strains of mice and T. gondii were used. |
doi_str_mv | 10.4049/jimmunol.142.3.954 |
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Among the variety of immunologic disorders encountered by AIDS patients is a depletion of CD4+ subpopulation of lymphocytes. In order to determine the role of this population of T lymphocytes in the generation of toxoplasmic encephalitis, mice chronically infected with T. gondii were treated with mAb GK1.5 directed against the cell surface glycoprotein L3T4 (CD4) of T lymphocytes. Histopathologic sections of brains of control and treated animals were examined at regular intervals during and after completion of treatment. The results demonstrated significantly less inflammation in brains of mice during treatment with GK1.5 mAb. In addition, recrudescence of the inflammatory process occurred after discontinuation of treatment. Similar results were observed in experiments in which different strains of mice and T. gondii were used.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.142.3.954</identifier><identifier>PMID: 2783605</identifier><identifier>CODEN: JOIMA3</identifier><language>eng</language><publisher>Bethesda, MD: Am Assoc Immnol</publisher><subject>Animals ; Antibodies, Monoclonal - therapeutic use ; Antigens, Differentiation, T-Lymphocyte - immunology ; Biological and medical sciences ; Brain - pathology ; Encephalitis - immunology ; Encephalitis - pathology ; Encephalitis - therapy ; Female ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Hypersensitivity, Delayed - pathology ; Immunobiology ; Lymphoid cells: ontogeny, maturation, markers, receptors, circulation and recirculation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Rats ; Toxoplasma gondii ; Toxoplasmosis, Animal - immunology ; Toxoplasmosis, Animal - pathology ; Toxoplasmosis, Animal - therapy</subject><ispartof>The Journal of immunology (1950), 1989-02, Vol.142 (3), p.954-958</ispartof><rights>1990 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-45a2f0626b38e8c2a0f5fe5ad564d7a9c9cc274e3bf21b78e3f219d8a26c0c0a3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=6686113$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2783605$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Israelski, DM</creatorcontrib><creatorcontrib>Araujo, FG</creatorcontrib><creatorcontrib>Conley, FK</creatorcontrib><creatorcontrib>Suzuki, Y</creatorcontrib><creatorcontrib>Sharma, S</creatorcontrib><creatorcontrib>Remington, JS</creatorcontrib><title>Treatment with anti-L3T4 (CD4) monoclonal antibody reduces the inflammatory response in toxoplasmic encephalitis</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Toxoplasma gondii is an important cause of disease of the central nervous system in patients with AIDS. Among the variety of immunologic disorders encountered by AIDS patients is a depletion of CD4+ subpopulation of lymphocytes. In order to determine the role of this population of T lymphocytes in the generation of toxoplasmic encephalitis, mice chronically infected with T. gondii were treated with mAb GK1.5 directed against the cell surface glycoprotein L3T4 (CD4) of T lymphocytes. Histopathologic sections of brains of control and treated animals were examined at regular intervals during and after completion of treatment. The results demonstrated significantly less inflammation in brains of mice during treatment with GK1.5 mAb. In addition, recrudescence of the inflammatory process occurred after discontinuation of treatment. Similar results were observed in experiments in which different strains of mice and T. gondii were used.</description><subject>Animals</subject><subject>Antibodies, Monoclonal - therapeutic use</subject><subject>Antigens, Differentiation, T-Lymphocyte - immunology</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Encephalitis - immunology</subject><subject>Encephalitis - pathology</subject><subject>Encephalitis - therapy</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Fundamental immunology</subject><subject>Hypersensitivity, Delayed - pathology</subject><subject>Immunobiology</subject><subject>Lymphoid cells: ontogeny, maturation, markers, receptors, circulation and recirculation</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Rats</subject><subject>Toxoplasma gondii</subject><subject>Toxoplasmosis, Animal - immunology</subject><subject>Toxoplasmosis, Animal - pathology</subject><subject>Toxoplasmosis, Animal - therapy</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1989</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUuL1EAQxxtR1nH1CwhCDiJ6yNjvJEcZnzDgZTw3lU7H9NKP2N0h7rc34467R08F9X9UwQ-hlwTvOebd-xvr_RKi2xNO92zfCf4I7YgQuJYSy8dohzGlNWlk8xQ9y_kGYywx5VfoijYtk1js0HxKBoo3oVSrLVMFodj6yE68env4yN9VPoaoXQzg_kp9HG6rZIZFm1yVyVQ2jA68hxLTWchzDPm8rUr8HWcH2VtdmaDNPIGzxebn6MkILpsXl3mNfnz-dDp8rY_fv3w7fDjWmjNWai6AjlhS2bPWtJoCHsVoBAxC8qGBTnda04Yb1o-U9E1r2Da7oQUqNdYY2DV6c9c7p_hrMbkob7M2zkEwccmqaVveSC7_aySCEM5osxnpnVGnmHMyo5qT9ZBuFcHqzEP946E2HoqpjccWenVpX3pvhvvIBcCmv77okDW4MUHQNt_bpGwlIezhycn-nFabjMoenNtKiVrX9eHeH5z2pEg</recordid><startdate>19890201</startdate><enddate>19890201</enddate><creator>Israelski, DM</creator><creator>Araujo, FG</creator><creator>Conley, FK</creator><creator>Suzuki, Y</creator><creator>Sharma, S</creator><creator>Remington, JS</creator><general>Am Assoc Immnol</general><general>American Association of Immunologists</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>19890201</creationdate><title>Treatment with anti-L3T4 (CD4) monoclonal antibody reduces the inflammatory response in toxoplasmic encephalitis</title><author>Israelski, DM ; Araujo, FG ; Conley, FK ; Suzuki, Y ; Sharma, S ; Remington, JS</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-45a2f0626b38e8c2a0f5fe5ad564d7a9c9cc274e3bf21b78e3f219d8a26c0c0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1989</creationdate><topic>Animals</topic><topic>Antibodies, Monoclonal - therapeutic use</topic><topic>Antigens, Differentiation, T-Lymphocyte - immunology</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Encephalitis - immunology</topic><topic>Encephalitis - pathology</topic><topic>Encephalitis - therapy</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. 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Among the variety of immunologic disorders encountered by AIDS patients is a depletion of CD4+ subpopulation of lymphocytes. In order to determine the role of this population of T lymphocytes in the generation of toxoplasmic encephalitis, mice chronically infected with T. gondii were treated with mAb GK1.5 directed against the cell surface glycoprotein L3T4 (CD4) of T lymphocytes. Histopathologic sections of brains of control and treated animals were examined at regular intervals during and after completion of treatment. The results demonstrated significantly less inflammation in brains of mice during treatment with GK1.5 mAb. In addition, recrudescence of the inflammatory process occurred after discontinuation of treatment. Similar results were observed in experiments in which different strains of mice and T. gondii were used.</abstract><cop>Bethesda, MD</cop><pub>Am Assoc Immnol</pub><pmid>2783605</pmid><doi>10.4049/jimmunol.142.3.954</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antibodies, Monoclonal - therapeutic use Antigens, Differentiation, T-Lymphocyte - immunology Biological and medical sciences Brain - pathology Encephalitis - immunology Encephalitis - pathology Encephalitis - therapy Female Fundamental and applied biological sciences. Psychology Fundamental immunology Hypersensitivity, Delayed - pathology Immunobiology Lymphoid cells: ontogeny, maturation, markers, receptors, circulation and recirculation Mice Mice, Inbred BALB C Mice, Inbred C3H Rats Toxoplasma gondii Toxoplasmosis, Animal - immunology Toxoplasmosis, Animal - pathology Toxoplasmosis, Animal - therapy |
title | Treatment with anti-L3T4 (CD4) monoclonal antibody reduces the inflammatory response in toxoplasmic encephalitis |
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