CD4(+) and CD8(+) T cells kill intracellular Mycobacterium tuberculosis by a perforin and Fas/Fas ligand-independent mechanism.
Identifieur interne : 000C63 ( Main/Corpus ); précédent : 000C62; suivant : 000C64CD4(+) and CD8(+) T cells kill intracellular Mycobacterium tuberculosis by a perforin and Fas/Fas ligand-independent mechanism.
Auteurs : D H Canaday ; R J Wilkinson ; Q. Li ; C V Harding ; R F Silver ; W H BoomSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2001.
English descriptors
- KwdEn :
- Antigens, Differentiation, T-Lymphocyte (genetics), Antigens, Differentiation, T-Lymphocyte (metabolism), Blood Bactericidal Activity (immunology), CD4-Positive T-Lymphocytes (immunology), CD4-Positive T-Lymphocytes (microbiology), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (microbiology), Cytotoxicity, Immunologic (MeSH), Fas Ligand Protein (MeSH), Granzymes (MeSH), Humans (MeSH), In Vitro Techniques (MeSH), Major Histocompatibility Complex (MeSH), Membrane Glycoproteins (genetics), Membrane Glycoproteins (immunology), Mycobacterium tuberculosis (growth & development), Mycobacterium tuberculosis (immunology), Perforin (MeSH), Pore Forming Cytotoxic Proteins (MeSH), RNA, Messenger (genetics), RNA, Messenger (metabolism), Serine Endopeptidases (genetics), Serine Endopeptidases (metabolism), Up-Regulation (MeSH), fas Receptor (genetics), fas Receptor (immunology).
- MESH :
- chemical , genetics : Antigens, Differentiation, T-Lymphocyte, Membrane Glycoproteins, RNA, Messenger, Serine Endopeptidases, fas Receptor.
- chemical , immunology : Membrane Glycoproteins, fas Receptor.
- chemical , metabolism : Antigens, Differentiation, T-Lymphocyte, RNA, Messenger, Serine Endopeptidases.
- growth & development : Mycobacterium tuberculosis.
- immunology : Blood Bactericidal Activity, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Mycobacterium tuberculosis.
- microbiology : CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes.
- Cytotoxicity, Immunologic, Fas Ligand Protein, Granzymes, Humans, In Vitro Techniques, Major Histocompatibility Complex, Perforin, Pore Forming Cytotoxic Proteins, Up-Regulation.
Abstract
Cytotoxic effector phenotype and function of MHC-restricted Mycobacterium tuberculosis (MTB)-reactive CD4(+) and CD8(+) T lymphocytes were analyzed from healthy tuberculin skin test-positive persons. After stimulation in vitro with MTB, both CD4(+) and CD8(+) T cells up-regulated mRNA expression for granzyme A and B, granulysin, perforin, and CD95L (Fas ligand). mRNA levels for these molecules were greater for resting CD8(+) than CD4(+) T cells. After MTB stimulation, mRNA levels were similar for both T cell subsets. Increased perforin and granulysin protein expression was confirmed in both in CD4(+) and CD8(+) T cells by flow cytometry. Both T cell subsets lysed MTB-infected monocytes. Biochemical inhibition of the granule exocytosis pathway in CD4(+) and CD8(+) T cells decreased cytolytic function by >90% in both T cell subsets. Ab blockade of the CD95-CD95L interaction decreased cytolytic function for both T cell populations by 25%. CD4(+) and CD8(+) T cells inhibited growth of intracellular MTB in autologous monocytes by 74% and 84%, respectively. However, inhibition of perforin activity, the CD95-CD95L interaction, or both CTL mechanisms did not affect CD4(+) and CD8(+) T cell mediated restriction of MTB growth. Thus, perforin and CD95-CD95L were not involved in CD4(+) and CD8(+) T cell mediated restriction of MTB growth.
DOI: 10.4049/jimmunol.167.5.2734
PubMed: 11509617
Links to Exploration step
pubmed:11509617Le document en format XML
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Li</name></author><author><name sortKey="Harding, C V" sort="Harding, C V" uniqKey="Harding C" first="C V" last="Harding">C V Harding</name></author><author><name sortKey="Silver, R F" sort="Silver, R F" uniqKey="Silver R" first="R F" last="Silver">R F Silver</name></author><author><name sortKey="Boom, W H" sort="Boom, W H" uniqKey="Boom W" first="W H" last="Boom">W H Boom</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2001">2001</date><idno type="RBID">pubmed:11509617</idno><idno type="pmid">11509617</idno><idno type="doi">10.4049/jimmunol.167.5.2734</idno><idno type="wicri:Area/Main/Corpus">000C63</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000C63</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">CD4(+) and CD8(+) T cells kill intracellular Mycobacterium tuberculosis by a perforin and Fas/Fas ligand-independent mechanism.</title><author><name sortKey="Canaday, D H" sort="Canaday, D H" uniqKey="Canaday D" first="D H" last="Canaday">D H Canaday</name><affiliation><nlm:affiliation>Division of Infectious Diseases, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, OH 44106, USA. dxc44@cwru.edu</nlm:affiliation></affiliation></author><author><name sortKey="Wilkinson, R J" sort="Wilkinson, R J" uniqKey="Wilkinson R" first="R J" last="Wilkinson">R J Wilkinson</name></author><author><name sortKey="Li, Q" sort="Li, Q" uniqKey="Li Q" first="Q" last="Li">Q. Li</name></author><author><name sortKey="Harding, C V" sort="Harding, C V" uniqKey="Harding C" first="C V" last="Harding">C V Harding</name></author><author><name sortKey="Silver, R F" sort="Silver, R F" uniqKey="Silver R" first="R F" last="Silver">R F Silver</name></author><author><name sortKey="Boom, W H" sort="Boom, W H" uniqKey="Boom W" first="W H" last="Boom">W H Boom</name></author></analytic><series><title level="j">Journal of immunology (Baltimore, Md. : 1950)</title><idno type="ISSN">0022-1767</idno><imprint><date when="2001" type="published">2001</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antigens, Differentiation, T-Lymphocyte (genetics)</term><term>Antigens, Differentiation, T-Lymphocyte (metabolism)</term><term>Blood Bactericidal Activity (immunology)</term><term>CD4-Positive T-Lymphocytes (immunology)</term><term>CD4-Positive T-Lymphocytes (microbiology)</term><term>CD8-Positive T-Lymphocytes (immunology)</term><term>CD8-Positive T-Lymphocytes (microbiology)</term><term>Cytotoxicity, Immunologic (MeSH)</term><term>Fas Ligand Protein (MeSH)</term><term>Granzymes (MeSH)</term><term>Humans (MeSH)</term><term>In Vitro Techniques (MeSH)</term><term>Major Histocompatibility Complex (MeSH)</term><term>Membrane Glycoproteins (genetics)</term><term>Membrane Glycoproteins (immunology)</term><term>Mycobacterium tuberculosis (growth & development)</term><term>Mycobacterium tuberculosis (immunology)</term><term>Perforin (MeSH)</term><term>Pore Forming Cytotoxic Proteins (MeSH)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Serine Endopeptidases (genetics)</term><term>Serine Endopeptidases (metabolism)</term><term>Up-Regulation (MeSH)</term><term>fas Receptor (genetics)</term><term>fas Receptor (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Antigens, Differentiation, T-Lymphocyte</term><term>Membrane Glycoproteins</term><term>RNA, Messenger</term><term>Serine Endopeptidases</term><term>fas Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Membrane Glycoproteins</term><term>fas Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, Differentiation, T-Lymphocyte</term><term>RNA, Messenger</term><term>Serine Endopeptidases</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Blood Bactericidal Activity</term><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term><term>Mycobacterium tuberculosis</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>CD4-Positive T-Lymphocytes</term><term>CD8-Positive T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cytotoxicity, Immunologic</term><term>Fas Ligand Protein</term><term>Granzymes</term><term>Humans</term><term>In Vitro Techniques</term><term>Major Histocompatibility Complex</term><term>Perforin</term><term>Pore Forming Cytotoxic Proteins</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Cytotoxic effector phenotype and function of MHC-restricted Mycobacterium tuberculosis (MTB)-reactive CD4(+) and CD8(+) T lymphocytes were analyzed from healthy tuberculin skin test-positive persons. After stimulation in vitro with MTB, both CD4(+) and CD8(+) T cells up-regulated mRNA expression for granzyme A and B, granulysin, perforin, and CD95L (Fas ligand). mRNA levels for these molecules were greater for resting CD8(+) than CD4(+) T cells. After MTB stimulation, mRNA levels were similar for both T cell subsets. Increased perforin and granulysin protein expression was confirmed in both in CD4(+) and CD8(+) T cells by flow cytometry. Both T cell subsets lysed MTB-infected monocytes. Biochemical inhibition of the granule exocytosis pathway in CD4(+) and CD8(+) T cells decreased cytolytic function by >90% in both T cell subsets. Ab blockade of the CD95-CD95L interaction decreased cytolytic function for both T cell populations by 25%. CD4(+) and CD8(+) T cells inhibited growth of intracellular MTB in autologous monocytes by 74% and 84%, respectively. However, inhibition of perforin activity, the CD95-CD95L interaction, or both CTL mechanisms did not affect CD4(+) and CD8(+) T cell mediated restriction of MTB growth. Thus, perforin and CD95-CD95L were not involved in CD4(+) and CD8(+) T cell mediated restriction of MTB growth.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11509617</PMID><DateCompleted><Year>2001</Year><Month>12</Month><Day>05</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1767</ISSN><JournalIssue CitedMedium="Print"><Volume>167</Volume><Issue>5</Issue><PubDate><Year>2001</Year><Month>Sep</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J Immunol</ISOAbbreviation></Journal><ArticleTitle>CD4(+) and CD8(+) T cells kill intracellular Mycobacterium tuberculosis by a perforin and Fas/Fas ligand-independent mechanism.</ArticleTitle><Pagination><MedlinePgn>2734-42</MedlinePgn></Pagination><Abstract><AbstractText>Cytotoxic effector phenotype and function of MHC-restricted Mycobacterium tuberculosis (MTB)-reactive CD4(+) and CD8(+) T lymphocytes were analyzed from healthy tuberculin skin test-positive persons. After stimulation in vitro with MTB, both CD4(+) and CD8(+) T cells up-regulated mRNA expression for granzyme A and B, granulysin, perforin, and CD95L (Fas ligand). mRNA levels for these molecules were greater for resting CD8(+) than CD4(+) T cells. After MTB stimulation, mRNA levels were similar for both T cell subsets. Increased perforin and granulysin protein expression was confirmed in both in CD4(+) and CD8(+) T cells by flow cytometry. Both T cell subsets lysed MTB-infected monocytes. Biochemical inhibition of the granule exocytosis pathway in CD4(+) and CD8(+) T cells decreased cytolytic function by >90% in both T cell subsets. Ab blockade of the CD95-CD95L interaction decreased cytolytic function for both T cell populations by 25%. CD4(+) and CD8(+) T cells inhibited growth of intracellular MTB in autologous monocytes by 74% and 84%, respectively. However, inhibition of perforin activity, the CD95-CD95L interaction, or both CTL mechanisms did not affect CD4(+) and CD8(+) T cell mediated restriction of MTB growth. Thus, perforin and CD95-CD95L were not involved in CD4(+) and CD8(+) T cell mediated restriction of MTB growth.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Canaday</LastName><ForeName>D H</ForeName><Initials>DH</Initials><AffiliationInfo><Affiliation>Division of Infectious Diseases, Case Western Reserve University School of Medicine and University Hospitals of Cleveland, Cleveland, OH 44106, USA. dxc44@cwru.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wilkinson</LastName><ForeName>R J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Q</ForeName><Initials>Q</Initials></Author><Author ValidYN="Y"><LastName>Harding</LastName><ForeName>C V</ForeName><Initials>CV</Initials></Author><Author ValidYN="Y"><LastName>Silver</LastName><ForeName>R F</ForeName><Initials>RF</Initials></Author><Author ValidYN="Y"><LastName>Boom</LastName><ForeName>W H</ForeName><Initials>WH</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI 27243</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI 95383</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL 59858</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>K08 AI 01581</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Immunol</MedlineTA><NlmUniqueID>2985117R</NlmUniqueID><ISSNLinking>0022-1767</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000945">Antigens, Differentiation, T-Lymphocyte</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C505661">FASLG protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053222">Fas Ligand Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C075005">GNLY protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052899">Pore Forming Cytotoxic Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019014">fas Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>126465-35-8</RegistryNumber><NameOfSubstance UI="D054353">Perforin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber><NameOfSubstance UI="C509213">GZMB protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber><NameOfSubstance UI="D053804">Granzymes</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.-</RegistryNumber><NameOfSubstance UI="D012697">Serine Endopeptidases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.21.78</RegistryNumber><NameOfSubstance UI="C509212">GZMA protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000945" MajorTopicYN="N">Antigens, Differentiation, T-Lymphocyte</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001770" MajorTopicYN="N">Blood Bactericidal Activity</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015496" MajorTopicYN="N">CD4-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="Y">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003602" MajorTopicYN="N">Cytotoxicity, Immunologic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053222" MajorTopicYN="N">Fas Ligand Protein</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053804" MajorTopicYN="N">Granzymes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D066298" MajorTopicYN="N">In Vitro Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008285" MajorTopicYN="N">Major Histocompatibility Complex</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008562" MajorTopicYN="N">Membrane Glycoproteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009169" MajorTopicYN="N">Mycobacterium tuberculosis</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054353" MajorTopicYN="N">Perforin</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052899" MajorTopicYN="N">Pore Forming Cytotoxic Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012697" MajorTopicYN="N">Serine Endopeptidases</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019014" MajorTopicYN="N">fas Receptor</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2001</Year><Month>8</Month><Day>18</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>1</Month><Day>5</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2001</Year><Month>8</Month><Day>18</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11509617</ArticleId><ArticleId IdType="doi">10.4049/jimmunol.167.5.2734</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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