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Article: Impaired accumulation and function of memory CD4 T cells in human IL-12 receptor β1 deficiency

TitleImpaired accumulation and function of memory CD4 T cells in human IL-12 receptor β1 deficiency
Authors
Issue Date2003
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal Of Immunology, 2003, v. 170 n. 1, p. 597-603 How to Cite?
AbstractDefects in IL-12 production or IL-12 responsiveness result in a vulnerability to infection with non-viral intracellular organisms, but the immunological mechanisms responsible for this susceptibility remain poorly understood. We present an immunological analysis of a patient with disseminated Salmonella enteritidis and a homozygous splice acceptor mutation in the IL-12Rβ1-chain gene. This mutation resulted in the absence of IL-12Rβ1 protein on PBMC and an inability of T cells to specifically bind IL-12 or produce IFN-γ in response to either IL-12 or IL-23. The accumulation of memory (CD45R0high) CD4 T cells that were CCR7high (putative central memory cells) was normal or increased for age. Central memory CD4 T cells of the patient and age-matched controls were similar in having a low to undetectable capacity to produce IFN-γ after polyclonal stimulation. In contrast, the patient had a substantial decrease in the number of CCR7neg/dull CD45R0high memory CD4 T cells (putative effector memory cells), and these differed from control cells in having a minimal ability to produce IFN-γ after polyclonal stimulation. Importantly, tetanus toxoid-specific IFN-γ production by PBMC from the patient was also significantly reduced compared with that in age-matched controls, indicating that signaling via the IL-12Rβ1-chain is generally necessary for the in vivo accumulation of human memory CD4 T cells with Th1 function. These results are also consistent with a model in which the IL-12Rβ1 subunit is necessary for the conversion of central memory CD4 T cells into effector memory cells.
Persistent Identifierhttp://hdl.handle.net/10722/170324
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCleary, AMen_US
dc.contributor.authorTu, Wen_US
dc.contributor.authorEnright, Aen_US
dc.contributor.authorGiffon, Ten_US
dc.contributor.authorDewaalMalefyt, Ren_US
dc.contributor.authorGutierrez, Ken_US
dc.contributor.authorLewis, DBen_US
dc.date.accessioned2012-10-30T06:07:30Z-
dc.date.available2012-10-30T06:07:30Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Immunology, 2003, v. 170 n. 1, p. 597-603en_US
dc.identifier.issn0022-1767en_US
dc.identifier.urihttp://hdl.handle.net/10722/170324-
dc.description.abstractDefects in IL-12 production or IL-12 responsiveness result in a vulnerability to infection with non-viral intracellular organisms, but the immunological mechanisms responsible for this susceptibility remain poorly understood. We present an immunological analysis of a patient with disseminated Salmonella enteritidis and a homozygous splice acceptor mutation in the IL-12Rβ1-chain gene. This mutation resulted in the absence of IL-12Rβ1 protein on PBMC and an inability of T cells to specifically bind IL-12 or produce IFN-γ in response to either IL-12 or IL-23. The accumulation of memory (CD45R0high) CD4 T cells that were CCR7high (putative central memory cells) was normal or increased for age. Central memory CD4 T cells of the patient and age-matched controls were similar in having a low to undetectable capacity to produce IFN-γ after polyclonal stimulation. In contrast, the patient had a substantial decrease in the number of CCR7neg/dull CD45R0high memory CD4 T cells (putative effector memory cells), and these differed from control cells in having a minimal ability to produce IFN-γ after polyclonal stimulation. Importantly, tetanus toxoid-specific IFN-γ production by PBMC from the patient was also significantly reduced compared with that in age-matched controls, indicating that signaling via the IL-12Rβ1-chain is generally necessary for the in vivo accumulation of human memory CD4 T cells with Th1 function. These results are also consistent with a model in which the IL-12Rβ1 subunit is necessary for the conversion of central memory CD4 T cells into effector memory cells.en_US
dc.languageengen_US
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_US
dc.relation.ispartofJournal of Immunologyen_US
dc.subject.meshAdolescenten_US
dc.subject.meshCd4-Positive T-Lymphocytes - Immunology - Metabolismen_US
dc.subject.meshCell Membrane - Genetics - Immunologyen_US
dc.subject.meshCell Movement - Genetics - Immunologyen_US
dc.subject.meshChilden_US
dc.subject.meshChild, Preschoolen_US
dc.subject.meshExons - Geneticsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunologic Deficiency Syndromes - Genetics - Immunologyen_US
dc.subject.meshImmunologic Memory - Geneticsen_US
dc.subject.meshInterferon-Gamma - Biosynthesisen_US
dc.subject.meshInterleukin-12 - Deficiency - Genetics - Metabolism - Physiologyen_US
dc.subject.meshInterleukin-12 Subunit P40en_US
dc.subject.meshInterleukin-23en_US
dc.subject.meshInterleukin-23 Subunit P19en_US
dc.subject.meshInterleukins - Deficiency - Geneticsen_US
dc.subject.meshLeukocytes, Mononuclear - Immunology - Metabolismen_US
dc.subject.meshLymphocyte Activation - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshPoint Mutationen_US
dc.subject.meshProtein Subunits - Deficiency - Genetics - Physiologyen_US
dc.subject.meshRna Splicing - Geneticsen_US
dc.subject.meshRna, Messenger - Biosynthesis - Blooden_US
dc.subject.meshReceptors, Interleukin - Biosynthesis - Deficiency - Genetics - Physiologyen_US
dc.subject.meshReceptors, Interleukin-12en_US
dc.subject.meshSalmonella Infections - Genetics - Immunologyen_US
dc.subject.meshT-Lymphocyte Subsets - Immunology - Metabolismen_US
dc.subject.meshTh1 Cells - Immunology - Metabolismen_US
dc.titleImpaired accumulation and function of memory CD4 T cells in human IL-12 receptor β1 deficiencyen_US
dc.typeArticleen_US
dc.identifier.emailTu, W:wwtu@hkucc.hku.hken_US
dc.identifier.authorityTu, W=rp00416en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.4049/jimmunol.170.1.597-
dc.identifier.pmid12496448-
dc.identifier.scopuseid_2-s2.0-0037218610en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037218610&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume170en_US
dc.identifier.issue1en_US
dc.identifier.spage597en_US
dc.identifier.epage603en_US
dc.identifier.isiWOS:000180106600075-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCleary, AM=7006746184en_US
dc.identifier.scopusauthoridTu, W=7006479236en_US
dc.identifier.scopusauthoridEnright, A=7004081418en_US
dc.identifier.scopusauthoridGiffon, T=6507596983en_US
dc.identifier.scopusauthoridDewaalMalefyt, R=6504211676en_US
dc.identifier.scopusauthoridGutierrez, K=7004343486en_US
dc.identifier.scopusauthoridLewis, DB=7404750928en_US

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