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[PMID]:28129122
[Au] Autor:Locke FL; Neelapu SS; Bartlett NL; Siddiqi T; Chavez JC; Hosing CM; Ghobadi A; Budde LE; Bot A; Rossi JM; Jiang Y; Xue AX; Elias M; Aycock J; Wiezorek J; Go WY
[Ad] Endereço:Department of Blood and Marrow Transplantation, Moffitt Cancer Center, Tampa, FL 33612, USA. Electronic address: frederick.locke@moffitt.org.
[Ti] Título:Phase 1 Results of ZUMA-1: A Multicenter Study of KTE-C19 Anti-CD19 CAR T Cell Therapy in Refractory Aggressive Lymphoma.
[So] Source:Mol Ther;25(1):285-295, 2017 Jan 04.
[Is] ISSN:1525-0024
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Outcomes for patients with refractory diffuse large B cell lymphoma (DLBCL) are poor. In the multicenter ZUMA-1 phase 1 study, we evaluated KTE-C19, an autologous CD3ζ/CD28-based chimeric antigen receptor (CAR) T cell therapy, in patients with refractory DLBCL. Patients received low-dose conditioning chemotherapy with concurrent cyclophosphamide (500 mg/m ) and fludarabine (30 mg/m ) for 3 days followed by KTE-C19 at a target dose of 2 × 10 CAR T cells/kg. The incidence of dose-limiting toxicity (DLT) was the primary endpoint. Seven patients were treated with KTE-C19 and one patient experienced a DLT of grade 4 cytokine release syndrome (CRS) and neurotoxicity. Grade ≥3 CRS and neurotoxicity were observed in 14% (n = 1/7) and 57% (n = 4/7) of patients, respectively. All other KTE-C19-related grade ≥3 events resolved within 1 month. The overall response rate was 71% (n = 5/7) and complete response (CR) rate was 57% (n = 4/7). Three patients have ongoing CR (all at 12+ months). CAR T cells demonstrated peak expansion within 2 weeks and continued to be detectable at 12+ months in patients with ongoing CR. This regimen of KTE-C19 was safe for further study in phase 2 and induced durable remissions in patients with refractory DLBCL.
[Mh] Termos MeSH primário: Antígenos CD19/imunologia
Antígenos CD28/metabolismo
Linfoma não Hodgkin/imunologia
Linfoma não Hodgkin/terapia
Complexo Receptor-CD3 de Antígeno de Linfócitos T/metabolismo
Proteínas Recombinantes de Fusão
Linfócitos T/imunologia
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores
Antígenos CD28/genética
Terapia Combinada
Progressão da Doença
Resistência a Medicamentos Antineoplásicos
Feminino
Seguimentos
Seres Humanos
Imunofenotipagem
Imunoterapia Adotiva/efeitos adversos
Imunoterapia Adotiva/métodos
Linfoma Difuso de Grandes Células B/diagnóstico
Linfoma Difuso de Grandes Células B/imunologia
Linfoma Difuso de Grandes Células B/terapia
Linfoma não Hodgkin/diagnóstico
Masculino
Meia-Idade
Estadiamento de Neoplasias
Complexo Receptor-CD3 de Antígeno de Linfócitos T/genética
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Antigens, CD19); 0 (Biomarkers); 0 (CD28 Antigens); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Recombinant Fusion Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170128
[St] Status:MEDLINE


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[PMID]:28109957
[Au] Autor:Fishman S; Lewis MD; Siew LK; De Leenheer E; Kakabadse D; Davies J; Ziv D; Margalit A; Karin N; Gross G; Wong FS
[Ad] Endereço:Laboratory of Immunology, MIGAL - Galilee Research Institute, Kiryat Shmona 11016, Israel; Department of Immunology, Rappaport Family Institute for Research in the Medical Sciences, Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3525433, Israel.
[Ti] Título:Adoptive Transfer of mRNA-Transfected T Cells Redirected against Diabetogenic CD8 T Cells Can Prevent Diabetes.
[So] Source:Mol Ther;25(2):456-464, 2017 Feb 01.
[Is] ISSN:1525-0024
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chimeric major histocompatibility complex (MHC) molecules supplemented with T cell receptor (TCR) signaling motifs function as activation receptors and can redirect gene-modified T cells against pathogenic CD8 T cells. We have shown that ß microglobulin (ß m) operates as a universal signaling component of MHC-I molecules when fused with the CD3-ζ chain. Linking the H-2K -binding insulin B chain peptide insulin B chain, amino acids 15-23 (InsB ) to the N terminus of ß m/CD3-ζ, redirected polyclonal CD8 T cells against pathogenic CD8 T cells in a peptide-specific manner in the non-obese diabetic (NOD) mouse. Here, we describe mRNA electroporation for delivering peptide/ß m/CD3-ζ genes to a reporter T cell line and purified primary mouse CD8 T cells. The peptide/ß m/CD3-ζ products paired with endogenous MHC-I chains and transmitted strong activation signals upon MHC-I cross-linking. The reporter T cell line transfected with InsB /ß m/CD3-ζ mRNA was activated by an InsB -H-2K -specific CD8 T cell hybrid only when the transfected T cells expressed H-2K . Primary NOD CD8 T cells expressing either InsB /ß m/CD3-ζ or islet-specific glucose-6-phosphatase catalytic subunit-related protein, amino acids 206-214 (IGRP )/ß m/CD3-ζ killed their respective autoreactive CD8 T cell targets in vitro. Furthermore, transfer of primary CD8 T cells transfected with InsB /ß m/CD3-ζ mRNA significantly reduced insulitis and protected NOD mice from diabetes. Our results demonstrate that mRNA encoding chimeric MHC-I receptors can redirect effector CD8 against diabetogenic CD8 T cells, offering a new approach for the treatment of type 1 diabetes.
[Mh] Termos MeSH primário: Transferência Adotiva
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/metabolismo
Diabetes Mellitus Tipo 1/genética
Diabetes Mellitus Tipo 1/imunologia
Imunomodulação
RNA Mensageiro/genética
Linfócitos T/imunologia
Linfócitos T/metabolismo
[Mh] Termos MeSH secundário: Animais
Citotoxicidade Imunológica
Diabetes Mellitus Tipo 1/prevenção & controle
Diabetes Mellitus Tipo 1/terapia
Modelos Animais de Doenças
Feminino
Expressão Gênica
Ordem dos Genes
Vetores Genéticos/genética
Insulina/imunologia
Camundongos
Camundongos Endogâmicos NOD
Complexo Receptor-CD3 de Antígeno de Linfócitos T/genética
Proteínas Recombinantes de Fusão/genética
Transfecção
Microglobulina-2 beta/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); 0 (RNA, Messenger); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Recombinant Fusion Proteins); 0 (beta 2-Microglobulin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170123
[St] Status:MEDLINE


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[PMID]:27183595
[Au] Autor:Glassman CR; Parrish HL; Deshpande NR; Kuhns MS
[Ad] Endereço:Department of Immunobiology, The University of Arizona College of Medicine, Tucson, AZ 85724;
[Ti] Título:The CD4 and CD3δε Cytosolic Juxtamembrane Regions Are Proximal within a Compact TCR-CD3-pMHC-CD4 Macrocomplex.
[So] Source:J Immunol;196(11):4713-22, 2016 Jun 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TCRs relay information about peptides embedded within MHC molecules (pMHC) to the ITAMs of the associated CD3γε, CD3δε, and CD3ζζ signaling modules. CD4 then recruits the Src kinase p56(Lck) (Lck) to the TCR-CD3 complex to phosphorylate the ITAMs, initiate intracellular signaling, and drive CD4(+) T cell fate decisions. Whereas the six ITAMs of CD3ζζ are key determinants of T cell development, activation, and the execution of effector functions, multiple models predict that CD4 recruits Lck proximal to the four ITAMs of the CD3 heterodimers. We tested these models by placing FRET probes at the cytosolic juxtamembrane regions of CD4 and the CD3 subunits to evaluate their relationship upon pMHC engagement in mouse cell lines. The data are consistent with a compact assembly in which CD4 is proximal to CD3δε, CD3ζζ resides behind the TCR, and CD3γε is offset from CD3δε. These results advance our understanding of the architecture of the TCR-CD3-pMHC-CD4 macrocomplex and point to regions of high CD4-Lck + ITAM concentrations therein. The findings thus have implications for TCR signaling, as phosphorylation of the CD3 ITAMs by CD4-associated Lck is important for CD4(+) T cell fate decisions.
[Mh] Termos MeSH primário: Antígenos CD4/imunologia
Membrana Celular/imunologia
Citosol/imunologia
Complexo Principal de Histocompatibilidade/imunologia
Complexo Receptor-CD3 de Antígeno de Linfócitos T/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Transferência Ressonante de Energia de Fluorescência
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD4 Antigens); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160517
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1502110


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[PMID]:27154354
[Au] Autor:Bishop GA
[Ad] Endereço:Department of Microbiology, The University of Iowa, Iowa City, Iowa, USA; gail-bishop@uiowa.edu.
[Ti] Título:TRAF3 as a powerful and multitalented regulator of lymphocyte functions.
[So] Source:J Leukoc Biol;100(5):919-926, 2016 Nov.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This review summarizes the current state of knowledge regarding the roles of the signaling adapter protein tumor necrosis factor receptor (TNFR)-associated factor 3 in regulating the functions of B and T lymphocytes. In B lymphocytes, TNFR-associated factor 3 inhibits signaling by TNFR superfamily receptors, Toll-like receptors, and interleukin-6R. In contrast, signaling to B cells by the virally encoded oncogenic protein latent membrane protein 1 is promoted by TNFR-associated factor 3. An important B cell-specific role for TNFR-associated factor 3 is the inhibition of homeostatic survival, directly relevant to the common occurrence of TNFR-associated factor 3 mutations in human B cell malignancies. TNFR-associated factor 3 was recently found to be a resident nuclear protein in B cells, where it interacts with and inhibits gene expression mediated by the cAMP response element-binding protein transcription complex, including expression of the prosurvival protein myeloid leukemia cell differentiation protein 1. In T lymphocytes, TNFR-associated factor 3 is required for normal signaling by the T cell antigen receptor, while inhibiting signaling by the interleukin-2 receptor. Cytoplasmic TNFR -associated factor 3 restrains nuclear factor-κB2 activation in both T and B cells. Clinical implications and future directions for the study of this context-dependent signaling regulator are discussed.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Subpopulações de Linfócitos/imunologia
Linfócitos T/imunologia
Fator 3 Associado a Receptor de TNF/imunologia
[Mh] Termos MeSH secundário: Animais
Formação de Anticorpos
Antígenos CD40/imunologia
Linhagem Celular
Sobrevivência Celular
Previsões
Seres Humanos
Imunidade Inata
Camundongos
Camundongos Knockout
NF-kappa B/metabolismo
Proteínas Nucleares/imunologia
Proteína Quinase C-delta/imunologia
Complexo Receptor-CD3 de Antígeno de Linfócitos T/imunologia
Receptores de Citocinas/imunologia
Fator 3 Associado a Receptor de TNF/deficiência
Proteínas da Matriz Viral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CD40 Antigens); 0 (EBV-associated membrane antigen, Epstein-Barr virus); 0 (NF-kappa B); 0 (Nuclear Proteins); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Receptors, Cytokine); 0 (TNF Receptor-Associated Factor 3); 0 (TRAF3 protein, human); 0 (Viral Matrix Proteins); EC 2.7.1.- (Prkcd protein, mouse); EC 2.7.11.13 (Protein Kinase C-delta)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171121
[Lr] Data última revisão:
171121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160508
[St] Status:MEDLINE


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[PMID]:26997265
[Au] Autor:Natarajan A; Nadarajah V; Felsovalyi K; Wang W; Jeyachandran VR; Wasson RA; Cardozo T; Bracken C; Krogsgaard M
[Ad] Endereço:Laura and Isaac Perlmutter Cancer Center, New York University School of Medicine, New York, NY 10016, USA.
[Ti] Título:Structural Model of the Extracellular Assembly of the TCR-CD3 Complex.
[So] Source:Cell Rep;14(12):2833-45, 2016 Mar 29.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antigen recognition of peptide-major histocompatibility complexes (pMHCs) by T cells, a key step in initiating adaptive immune responses, is performed by the T cell receptor (TCR) bound to CD3 heterodimers. However, the biophysical basis of the transmission of TCR-CD3 extracellular interaction into a productive intracellular signaling sequence remains incomplete. Here we used nuclear magnetic resonance (NMR) spectroscopy combined with mutational analysis and computational docking to derive a structural model of the extracellular TCR-CD3 assembly. In the inactivated state, CD3γε interacts with the helix 3 and helix 4-F strand regions of the TCR Cß subunit, whereas CD3δε interacts with the F and C strand regions of the TCR Cα subunit in this model, placing the CD3 subunits on opposing sides of the TCR. This work identifies the molecular contacts between the TCR and CD3 subunits, identifying a physical basis for transmitting an activating signal through the complex.
[Mh] Termos MeSH primário: Complexo CD3/química
Modelos Moleculares
Complexo Receptor-CD3 de Antígeno de Linfócitos T/química
Receptores de Antígenos de Linfócitos T/química
[Mh] Termos MeSH secundário: Complexo CD3/genética
Complexo CD3/metabolismo
Seres Humanos
Mutagênese Sítio-Dirigida
Ressonância Magnética Nuclear Biomolecular
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Estrutura Terciária de Proteína
Complexo Receptor-CD3 de Antígeno de Linfócitos T/metabolismo
Receptores de Antígenos de Linfócitos T/genética
Receptores de Antígenos de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (CD3 Complex); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160322
[St] Status:MEDLINE


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[PMID]:26363782
[Au] Autor:Arndt T; Wedekind D; Jörns A; Tsiavaliaris G; Cuppen E; Hedrich HJ; Lenzen S
[Ad] Endereço:Institute of Clinical Biochemistry, Hannover Medical School, 30623, Hannover, Germany.
[Ti] Título:A novel Dock8 gene mutation confers diabetogenic susceptibility in the LEW.1AR1/Ztm-iddm rat, an animal model of human type 1 diabetes.
[So] Source:Diabetologia;58(12):2800-9, 2015 Dec.
[Is] ISSN:1432-0428
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:AIMS/HYPOTHESIS: The LEW.1AR1-iddm rat, an animal model of human type 1 diabetes, arose through a spontaneous mutation within the inbred strain LEW.1AR1. A susceptibility locus (Iddm8) on rat chromosome 1 (RNO1) has been identified previously, which is accompanied by autoimmune diabetes and the additional phenotype of a variable CD3(+) T cell frequency. METHODS: In the present study we characterised the Iddm8 region on RNO1 in backcross strains using the genetically divergent Brown Norway (BN) and Paris (PAR) rats. Candidate genes of the Iddm8 region were sequenced for mutation analysis. RESULTS: The Iddm8 region could be subdivided by single nucleotide polymorphism (SNP) analyses. In the first region, a mutation in exon 44 of the Dock8 gene was identified resulting in an amino acid exchange in the protein from glutamine to glutamate. This exchange is unique for the LEW.1AR1-iddm rat. In the second region, a SNP was detected in exon 11 of the Vwa2 gene with an exchange from arginine to tryptophan. This SNP is also present in other rat strains. CONCLUSIONS/INTERPRETATION: The Dock8 mutation gave rise to a new type 1 diabetes rat model with very close similarity to type 1 diabetes in humans, providing a deepened insight into the impact of genes involved in diabetes development.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 1/genética
Fatores de Troca do Nucleotídeo Guanina/genética
Mutação
[Mh] Termos MeSH secundário: Alelos
Substituição de Aminoácidos
Animais
Modelos Animais de Doenças
Suscetibilidade a Doenças
Éxons/genética
Seres Humanos
Células Matadoras Naturais
Modelos Moleculares
Polimorfismo de Nucleotídeo Único
Ratos
Ratos Endogâmicos Lew
Complexo Receptor-CD3 de Antígeno de Linfócitos T/genética
Fator de von Willebrand/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dock8 protein, rat); 0 (Guanine Nucleotide Exchange Factors); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (von Willebrand Factor)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150914
[St] Status:MEDLINE
[do] DOI:10.1007/s00125-015-3757-7


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[PMID]:26360253
[Au] Autor:Ramesh M; Simchoni N; Hamm D; Cunningham-Rundles C
[Ad] Endereço:Montefiore Medical Center, Bronx, NY, United States.
[Ti] Título:High-throughput sequencing reveals an altered T cell repertoire in X-linked agammaglobulinemia.
[So] Source:Clin Immunol;161(2):190-6, 2015 Dec.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To examine the T cell receptor structure in the absence of B cells, the TCR ß CDR3 was sequenced from DNA of 15 X-linked agammaglobulinemia (XLA) subjects and 18 male controls, using the Illumina HiSeq platform and the ImmunoSEQ analyzer. V gene usage and the V-J combinations, derived from both productive and non-productive sequences, were significantly different between XLA samples and controls. Although the CDR3 length was similar for XLA and control samples, the CDR3 region of the XLA T cell receptor contained significantly fewer deletions and insertions in V, D, and J gene segments, differences intrinsic to the V(D)J recombination process and not due to peripheral T cell selection. XLA CDR3s demonstrated fewer charged amino acid residues, more sharing of CDR3 sequences, and almost completely lacked a population of highly modified Vß gene segments found in control DNA, suggesting both a skewed and contracted T cell repertoire in XLA.
[Mh] Termos MeSH primário: Agamaglobulinemia/genética
Doenças Genéticas Ligadas ao Cromossomo X/genética
Receptores de Antígenos de Linfócitos T/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Linfócitos B/metabolismo
Estudos de Casos e Controles
Criança
Pré-Escolar
DNA/genética
Sequenciamento de Nucleotídeos em Larga Escala/métodos
Seres Humanos
Região Variável de Imunoglobulina/genética
Lactente
Masculino
Meia-Idade
Complexo Receptor-CD3 de Antígeno de Linfócitos T/genética
Linfócitos T/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Immunoglobulin Variable Region); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Receptors, Antigen, T-Cell); 9007-49-2 (DNA)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150912
[St] Status:MEDLINE


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[PMID]:26342115
[Au] Autor:Paensuwan P; Ngoenkam J; Khamsri B; Preechanukul K; Sanguansermsri D; Pongcharoen S
[Ad] Endereço:Department of Microbiology and Parasitology, Faculty of Medical Science; Naresuan University, Pitsanulok 65000 Thailand.
[Ti] Título:Evidence for inducible recruitment of Wiskott-Aldrich syndrome protein to T cell receptor-CD3 complex in Jurkat T cells.
[So] Source:Asian Pac J Allergy Immunol;33(3):189-95, 2015 Sep.
[Is] ISSN:0125-877X
[Cp] País de publicação:Thailand
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The engagement of the T cell receptor (TCR)-CD3 complex induces the formation of multiple signalling complexes, which are required for actin cytoskeletal rearrangement. The Wiskott-Aldrich syndrome protein (WASp) is a key regulator of actin polymerization that is recruited to the TCR activation site. Since WASp is a binding partner of adaptor protein Nck, which is recruited directly to the TCR CD3? subunit upon TCR ligation, therefore we proposed that the direct recruitment of Nck to TCR-CD3 may also bring WASp directly to TCR-CD3. OBJECTIVE: The aim of this present study was to assess the distribution of WASp, in relation to Nck, to the TCR-CD3ε complex. METHODS: Jurkat T cells were stimulated with anti-TCR antibody and then the cell lysates were immunoprecipitated with anti-CD3 antibody before immunoblotting with antibodies specific to WASp, Nck1, Nck2, SLP-76 and CD3ε molecules. RESULTS: WASp was recruited to SLP-76 and also directly to the TCR-CD3 complex upon TCR triggering. The inducible recruitment of WASp to the TCR-CD3 complex is partially dependent of tyrosine phosphorylation. CONCLUSIONS: The present findings provide an alternative mechanism of WASp recruitment to the site of TCR activation that may be involved in recruitment of Nck.
[Mh] Termos MeSH primário: Complexo CD3/metabolismo
Complexo Receptor-CD3 de Antígeno de Linfócitos T/metabolismo
Linfócitos T/metabolismo
Proteína da Síndrome de Wiskott-Aldrich/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Complexo CD3/imunologia
Seres Humanos
Células Jurkat
Ativação Linfocitária
Proteínas Oncogênicas/metabolismo
Fosfoproteínas/metabolismo
Fosforilação
Ligação Proteica
Conformação Proteica
Transporte Proteico
Complexo Receptor-CD3 de Antígeno de Linfócitos T/imunologia
Transdução de Sinais
Linfócitos T/imunologia
Tirosina
Proteína da Síndrome de Wiskott-Aldrich/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (CD3 Complex); 0 (CD3E protein, human); 0 (Nck protein); 0 (Oncogene Proteins); 0 (Phosphoproteins); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (SLP-76 signal Transducing adaptor proteins); 0 (WAS protein, human); 0 (Wiskott-Aldrich Syndrome Protein); 42HK56048U (Tyrosine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150906
[St] Status:MEDLINE
[do] DOI:10.12932/AP0544.33.3.2015


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[PMID]:26141031
[Au] Autor:Mahasongkram K; Pata S; Chruewkamlow N; Kasinrerk W
[Ad] Endereço:Division of Clinical Immunology, Department of Medical Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai 50200, Thailand.
[Ti] Título:Identification of a T cell surface molecule using a monoclonal antibody produced by TCR/CD3 complex immunization.
[So] Source:Asian Pac J Allergy Immunol;33(2):107-16, 2015 Jun.
[Is] ISSN:0125-877X
[Cp] País de publicação:Thailand
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Several molecules are known to be involved in T-cell activation via the TCR/CD3 complex and while the mechanisms of late T cell signaling have been well characterized, the very early events are still not fully understood. OBJECTIVE: The aim of this study was to identify yet unknown molecules associated with the TCR/CD3 complex. RESULTS: To identify new molecules associated with the TCR/CD3 complex, a monoclonal antibody termed MT3 was produced by immunoprecipitated beads immunization. Colocalization of the MT3 mAb recognizing molecules with the TCR/CD3 complexes was verified by confocal microscopic analysis. The surface antigen recognized by MT3 antibody was expressed on a subpopulation of CD3+ T cells, and on both CD4+ and CD8+ lymphocytes. The antigen was also expressed on na?ve CD4+ T cells and on a subset of memory CD4+ T cells. In contrast, in the CD8 population, the majority of MT3+ cells were found in the na?ve population. The MT3 mAb recognizing molecules were also expressed on red blood cells but only in particular subjects. Similar to peripheral blood leukocytes, MT3 mAb recognizing molecules are exclusively expressed on T cell lines. CONCLUSIONS: Based on the cellular distribution patterns and confocal microscopic analysis, the MT3 mAb recognizing molecule that we investigated is proposed to be a TCR/CD3 associated molecule and might be involved in the antigen recognition of T cells.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Imunização
Ativação Linfocitária
Complexo Receptor-CD3 de Antígeno de Linfócitos T/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/metabolismo
Linhagem Celular Tumoral
Epitopos
Seres Humanos
Hibridomas
Imunoprecipitação
Camundongos Endogâmicos BALB C
Microscopia Confocal
Complexo Receptor-CD3 de Antígeno de Linfócitos T/administração & dosagem
Complexo Receptor-CD3 de Antígeno de Linfócitos T/metabolismo
Transdução de Sinais
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Epitopes); 0 (Receptor-CD3 Complex, Antigen, T-Cell)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170127
[Lr] Data última revisão:
170127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150705
[St] Status:MEDLINE
[do] DOI:10.12932/AP0538.33.2.2015


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[PMID]:26109064
[Au] Autor:He Y; Rangarajan S; Kerzic M; Luo M; Chen Y; Wang Q; Yin Y; Workman CJ; Vignali KM; Vignali DA; Mariuzza RA; Orban J
[Ad] Endereço:From the W. M. Keck Laboratory for Structural Biology, University of Maryland Institute for Bioscience and Biotechnology Research, Rockville, Maryland 20850, the Departments of Chemistry and Biochemistry and.
[Ti] Título:Identification of the Docking Site for CD3 on the T Cell Receptor ß Chain by Solution NMR.
[So] Source:J Biol Chem;290(32):19796-805, 2015 Aug 07.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The T cell receptor (TCR)-CD3 complex is composed of a genetically diverse αß TCR heterodimer associated noncovalently with the invariant CD3 dimers CD3ϵγ, CD3ϵδ, and CD3ζζ. The TCR mediates peptide-MHC recognition, whereas the CD3 molecules transduce activation signals to the T cell. Although much is known about downstream T cell signaling pathways, the mechanism whereby TCR engagement by peptide-MHC initiates signaling is poorly understood. A key to solving this problem is defining the spatial organization of the TCR-CD3 complex and the interactions between its subunits. We have applied solution NMR methods to identify the docking site for CD3 on the ß chain of a human autoimmune TCR. We demonstrate a low affinity but highly specific interaction between the extracellular domains of CD3 and the TCR constant ß (Cß) domain that requires both CD3ϵγ and CD3ϵδ subunits. The mainly hydrophilic docking site, comprising 9-11 solvent-accessible Cß residues, is relatively small (∼400 Å(2)), consistent with the weak interaction between TCR and CD3 extracellular domains, and devoid of glycosylation sites. The docking site is centered on the αA and αB helices of Cß, which are located at the base of the TCR. This positions CD3ϵγ and CD3ϵδ between the TCR and the T cell membrane, permitting us to distinguish among several possible models of TCR-CD3 association. We further correlate structural results from NMR with mutational data on TCR-CD3 interactions from cell-based assays.
[Mh] Termos MeSH primário: Complexo CD3/química
Subunidades Proteicas/química
Complexo Receptor-CD3 de Antígeno de Linfócitos T/química
Receptores de Antígenos de Linfócitos T alfa-beta/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Complexo CD3/genética
Complexo CD3/imunologia
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Seres Humanos
Espectroscopia de Ressonância Magnética
Simulação de Acoplamento Molecular
Dados de Sequência Molecular
Mutação
Dobramento de Proteína
Multimerização Proteica
Estrutura Secundária de Proteína
Estrutura Terciária de Proteína
Subunidades Proteicas/genética
Subunidades Proteicas/imunologia
Complexo Receptor-CD3 de Antígeno de Linfócitos T/genética
Complexo Receptor-CD3 de Antígeno de Linfócitos T/imunologia
Receptores de Antígenos de Linfócitos T alfa-beta/genética
Receptores de Antígenos de Linfócitos T alfa-beta/imunologia
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/imunologia
Linfócitos T/química
Linfócitos T/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (CD3 Complex); 0 (Protein Subunits); 0 (Receptor-CD3 Complex, Antigen, T-Cell); 0 (Receptors, Antigen, T-Cell, alpha-beta); 0 (Recombinant Proteins)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150626
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.663799



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