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...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of immunology (1950) 1989-02, Vol.142 (3), p.954-958
Hauptverfasser: Israelski, DM, Araujo, FG, Conley, FK, Suzuki, Y, Sharma, S, Remington, JS
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 958
container_issue 3
container_start_page 954
container_title The Journal of immunology (1950)
container_volume 142
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
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_78847646</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>15114327</sourcerecordid><originalsourceid>FETCH-LOGICAL-c433t-45a2f0626b38e8c2a0f5fe5ad564d7a9c9cc274e3bf21b78e3f219d8a26c0c0a3</originalsourceid><addsrcrecordid>eNqFkUuL1EAQxxtR1nH1CwhCDiJ6yNjvJEcZnzDgZTw3lU7H9NKP2N0h7rc34467R08F9X9UwQ-hlwTvOebd-xvr_RKi2xNO92zfCf4I7YgQuJYSy8dohzGlNWlk8xQ9y_kGYywx5VfoijYtk1js0HxKBoo3oVSrLVMFodj6yE68env4yN9VPoaoXQzg_kp9HG6rZIZFm1yVyVQ2jA68hxLTWchzDPm8rUr8HWcH2VtdmaDNPIGzxebn6MkILpsXl3mNfnz-dDp8rY_fv3w7fDjWmjNWai6AjlhS2bPWtJoCHsVoBAxC8qGBTnda04Yb1o-U9E1r2Da7oQUqNdYY2DV6c9c7p_hrMbkob7M2zkEwccmqaVveSC7_aySCEM5osxnpnVGnmHMyo5qT9ZBuFcHqzEP946E2HoqpjccWenVpX3pvhvvIBcCmv77okDW4MUHQNt_bpGwlIezhycn-nFabjMoenNtKiVrX9eHeH5z2pEg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>15114327</pqid></control><display><type>article</type><title>Treatment with anti-L3T4 (CD4) monoclonal antibody reduces the inflammatory response in toxoplasmic encephalitis</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Israelski, DM ; Araujo, FG ; Conley, FK ; Suzuki, Y ; Sharma, S ; Remington, JS</creator><creatorcontrib>Israelski, DM ; Araujo, FG ; Conley, FK ; Suzuki, Y ; Sharma, S ; Remington, JS</creatorcontrib><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><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&amp;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. Psychology</topic><topic>Fundamental immunology</topic><topic>Hypersensitivity, Delayed - pathology</topic><topic>Immunobiology</topic><topic>Lymphoid cells: ontogeny, maturation, markers, receptors, circulation and recirculation</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C3H</topic><topic>Rats</topic><topic>Toxoplasma gondii</topic><topic>Toxoplasmosis, Animal - immunology</topic><topic>Toxoplasmosis, Animal - pathology</topic><topic>Toxoplasmosis, Animal - therapy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Israelski, DM</creatorcontrib><creatorcontrib>Araujo, FG</creatorcontrib><creatorcontrib>Conley, FK</creatorcontrib><creatorcontrib>Suzuki, Y</creatorcontrib><creatorcontrib>Sharma, S</creatorcontrib><creatorcontrib>Remington, JS</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>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Israelski, DM</au><au>Araujo, FG</au><au>Conley, FK</au><au>Suzuki, Y</au><au>Sharma, S</au><au>Remington, JS</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Treatment with anti-L3T4 (CD4) monoclonal antibody reduces the inflammatory response in toxoplasmic encephalitis</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>1989-02-01</date><risdate>1989</risdate><volume>142</volume><issue>3</issue><spage>954</spage><epage>958</epage><pages>954-958</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><coden>JOIMA3</coden><abstract>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.</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>
fulltext fulltext
identifier ISSN: 0022-1767
ispartof The Journal of immunology (1950), 1989-02, Vol.142 (3), p.954-958
issn 0022-1767
1550-6606
language eng
recordid cdi_proquest_miscellaneous_78847646
source MEDLINE; Alma/SFX Local Collection
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
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T05%3A18%3A53IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Treatment%20with%20anti-L3T4%20(CD4)%20monoclonal%20antibody%20reduces%20the%20inflammatory%20response%20in%20toxoplasmic%20encephalitis&rft.jtitle=The%20Journal%20of%20immunology%20(1950)&rft.au=Israelski,%20DM&rft.date=1989-02-01&rft.volume=142&rft.issue=3&rft.spage=954&rft.epage=958&rft.pages=954-958&rft.issn=0022-1767&rft.eissn=1550-6606&rft.coden=JOIMA3&rft_id=info:doi/10.4049/jimmunol.142.3.954&rft_dat=%3Cproquest_cross%3E15114327%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=15114327&rft_id=info:pmid/2783605&rfr_iscdi=true