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[PMID]:28550073
[Au] Autor:Schneider C; Wunderlich G; Bleistein J; Fink GR; Deckert M; Brunn A; Lehmann HC
[Ad] Endereço:Department of Neurology, University of Cologne, Köln, Germany.
[Ti] Título:Lymphocyte antigens targetable by monoclonal antibodies in non-systemic vasculitic neuropathy.
[So] Source:J Neurol Neurosurg Psychiatry;88(9):756-760, 2017 Sep.
[Is] ISSN:1468-330X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To identify the most relevant antigens for monoclonal antibodies in lymphocytic infiltrates in non-systemic vasculitic neuropathy (NSVN). BACKGROUND: Current immunosuppressive treatment for NSVN is insufficient. Monoclonal antibodies might be a treatment option, but the expression profile for targetable antigens on lymphocytic infiltrates in NSVN is unknown. METHODS: Sural nerve biopsies from a cohort of patients with NSVN were immunohistochemically studied for the expression of potential candidate antigens in perivascular and intramural lymphocytic infiltrates and correlated with neurological and electrophysiological parameters. 20 patients with treatment naïve NSVN and 5 patients with idiopathic axonal neuropathy were included. RESULTS: The CD52, BAFF and CD49d antigens were expressed in epineurial, perivascular or intramural lymphocytes of all (20/20) patients. CD52 was most prominently expressed in 21.49% of all inflammatory infiltrates. BAFF and CD49d were detected in 11.25% and 10.99% of these lymphocytes, respectively. The CD20, CD25 and CD126 antigens were found less frequently and at low levels only (CD20: 10/20 patients, 5.84% of lymphocytes; CD25: 17/20 patients, 5.22% of lymphocytes; CD126: 3/20 patients, 0.15% of lymphocytes). CONCLUSION: This is the first study in NSVN that identifies antigens expressed by pathogenic lymphocytes, which are potential targets for future monoclonal antibody treatment. Our data suggest that NSVN is amenable to monoclonal antibodies and, moreover, that targeting CD52 may be particularly promising. Our results strongly warrant future clinical trials in NSVN with monoclonal antibodies.
[Mh] Termos MeSH primário: Anticorpos Monoclonais
Doenças do Sistema Nervoso Periférico/patologia
Nervo Sural/patologia
[Mh] Termos MeSH secundário: Idoso
Antígenos CD/análise
Antígenos de Neoplasias/análise
Fator Ativador de Células B/análise
Antígeno CD52
Glicoproteínas/análise
Seres Humanos
Inflamação/patologia
Integrina alfa4/análise
Meia-Idade
Estudos Retrospectivos
Vasculite/complicações
Vasculite/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (B-Cell Activating Factor); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins); 0 (TNFSF13B protein, human); 143198-26-9 (Integrin alpha4)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.1136/jnnp-2017-315878


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[PMID]:28404636
[Au] Autor:Cleary KLS; Chan HTC; James S; Glennie MJ; Cragg MS
[Ad] Endereço:Antibody and Vaccine Group, Cancer Sciences Unit, Faculty of Medicine, University of Southampton, Southampton General Hospital, Southampton SO16 6YD, United Kingdom.
[Ti] Título:Antibody Distance from the Cell Membrane Regulates Antibody Effector Mechanisms.
[So] Source:J Immunol;198(10):3999-4011, 2017 May 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunotherapy using mAbs, such as rituximab, is an established means of treating hematological malignancies. Abs can elicit a number of mechanisms to delete target cells, including complement-dependent cytotoxicity, Ab-dependent cellular cytotoxicity, and Ab-dependent cellular phagocytosis. The inherent properties of the target molecule help to define which of these mechanisms are more important for efficacy. However, it is often unclear why mAb binding to different epitopes within the same target elicits different levels of therapeutic activity. To specifically address whether distance from the target cell membrane influences the aforementioned effector mechanisms, a panel of fusion proteins consisting of a CD20 or CD52 epitope attached to various CD137 scaffold molecules was generated. The CD137 scaffold was modified through the removal or addition of cysteine-rich extracellular domains to produce a panel of chimeric molecules that held the target epitope at different distances along the protein. It was shown that complement-dependent cytotoxicity and Ab-dependent cellular cytotoxicity favored a membrane-proximal epitope, whereas Ab-dependent cellular phagocytosis favored an epitope positioned further away. These findings were confirmed using reagents targeting the membrane-proximal or -distal domains of CD137 itself before investigating these properties in vivo, where a clear difference in the splenic clearance of transfected tumor cells was observed. Together, this work demonstrates how altering the position of the Ab epitope is able to change the effector mechanisms engaged and facilitates the selection of mAbs designed to delete target cells through specific effector mechanisms and provide more effective therapeutic agents.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/imunologia
Citotoxicidade Celular Dependente de Anticorpos
Membrana Celular/imunologia
Epitopos/imunologia
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/genética
Anticorpos Monoclonais Murinos/imunologia
Antígenos CD/genética
Antígenos CD/imunologia
Antígenos CD20/genética
Antígenos CD20/imunologia
Antígenos de Neoplasias/genética
Antígenos de Neoplasias/imunologia
Antígeno CD52
Linhagem Celular Tumoral
Glicoproteínas/genética
Glicoproteínas/imunologia
Seres Humanos
Imunoterapia
Camundongos
Fagocitose
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/genética
Membro 9 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Murine-Derived); 0 (Antigens, CD); 0 (Antigens, CD20); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Epitopes); 0 (Glycoproteins); 0 (Tumor Necrosis Factor Receptor Superfamily, Member 9)
[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:170414
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601473


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[PMID]:28122892
[Au] Autor:Ishizawa K; Fukuhara N; Nakaseko C; Chiba S; Ogura M; Okamoto A; Sunaga Y; Tobinai K
[Ad] Endereço:Department of Hematology and Rheumatology, Tohoku University Graduate School of Medicine, Sendai, Miyagi kishizaw@med.id.yamagata-u.ac.jp.
[Ti] Título:Safety, efficacy and pharmacokinetics of humanized anti-CD52 monoclonal antibody alemtuzumab in Japanese patients with relapsed or refractory B-cell chronic lymphocytic leukemia.
[So] Source:Jpn J Clin Oncol;47(1):54-60, 2017 Jan.
[Is] ISSN:1465-3621
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To evaluate the safety, efficacy and pharmacokinetics of alemtuzumab in Japanese patients, we conducted a phase I study in patients with relapsed or refractory B-cell chronic lymphocytic leukemia. METHODS: Six patients received alemtuzumab by intravenous infusion every other day three times a week for 12 weeks. The dose was gradually escalated on daily basis (3, 10 and then 30 mg) until the patient tolerated. The primary objective was to evaluate the safety of alemtuzumab in Japanese patients and the secondary objectives were to evaluate the overall response rate and the pharmacokinetics. RESULTS: The major treatment-emergent adverse events were anemia, neutropenia (6/6 patients each) and thrombocytopenia (5/6 patients) in hematologic adverse events, and nausea, vomiting, decreased appetite, cytomegalovirus test positive and pyrexia (4/6 patients) in non-hematologic adverse events. As serious adverse events, cytomegalovirus infection, pulmonary tuberculosis and diffuse large B-cell lymphoma were reported in 1/6 patient each. The overall response rate was 33% (95% confidence interval: 4-78) (1/6 patient each achieved complete response and partial response, respectively) and 3/6 patients had stable disease and 1/6 patient had progressive disease. The median time to response was 2.9 months. After last intravenous dosing (Week 12) of alemtuzumab 30 mg every other day three times a week, C , t , AUC and t were higher and CL and V were lower than the values observed after the first dose. CONCLUSIONS: The efficacy, safety and pharmacokinetics results observed with alemtuzumab in Japanese patients were generally similar to those reported in overseas clinical studies. Alemtuzumab at 30 mg by intravenous infusion every other day three times a week for 12 weeks should be safe and effective similarly in Japanese B-cell chronic lymphocytic leukemia patients. CLINICAL TRIAL REGISTRATION NO: NCT00923182.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Antígenos CD/imunologia
Antígenos de Neoplasias/imunologia
Glicoproteínas/imunologia
Leucemia Linfocítica Crônica de Células B/tratamento farmacológico
[Mh] Termos MeSH secundário: Adulto
Idoso
Alemtuzumab
Anticorpos Monoclonais Humanizados/efeitos adversos
Anticorpos Monoclonais Humanizados/farmacocinética
Área Sob a Curva
Grupo com Ancestrais do Continente Asiático
Antígeno CD52
Esquema de Medicação
Feminino
Febre/etiologia
Meia-Vida
Seres Humanos
Japão
Masculino
Meia-Idade
Recidiva Local de Neoplasia
Neutropenia/etiologia
Curva ROC
Indução de Remissão
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins); 3A189DH42V (Alemtuzumab)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170127
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1093/jjco/hyw146


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[PMID]:28087077
[Au] Autor:Pant AB; Wang Y; Mielcarz DW; Kasper EJ; Telesford KM; Mishra M; Haque A; Channon JY; Kasper LH; Begum-Haque S
[Ad] Endereço:Department of Microbiology/Immunology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA.
[Ti] Título:Alteration of CD39+Foxp3+ CD4 T cell and cytokine levels in EAE/MS following anti-CD52 treatment.
[So] Source:J Neuroimmunol;303:22-30, 2017 Feb 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:While examining the therapeutic value of anti-CD52 antibody against EAE/MS, we identified a unique subset of CD39+ Tregs in repopulating GALT tissues, a major lymphoid reservoir, which was accompanied by amelioration of disease. Furthermore, anti-CD52 treatment leads to increased expression of BDNF, IL-10, and SMAD3 in the brains of EAE mice. This condition is associated with suppression of IL-17, a critical inflammatory factor in EAE/MS progression. Additionally, we found elevated levels of CD4+CD39+ Tregs in PBMCs of RRMS patients treated with humanized anti-CD52 mAb. Thus, anti-CD52 can affect multiple immune mediated pathways involved in the pathogenesis of EAE/MS.
[Mh] Termos MeSH primário: Anticorpos Monoclonais/uso terapêutico
Antígenos CD/metabolismo
Antígenos de Neoplasias/metabolismo
Apirase/metabolismo
Linfócitos T CD4-Positivos/metabolismo
Citocinas/metabolismo
Encefalomielite Autoimune Experimental/metabolismo
Fatores de Transcrição Forkhead/metabolismo
Glicoproteínas/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos Monoclonais/farmacologia
Antígenos CD/imunologia
Antígenos de Neoplasias/imunologia
Apirase/imunologia
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Antígeno CD52
Citocinas/imunologia
Encefalomielite Autoimune Experimental/tratamento farmacológico
Encefalomielite Autoimune Experimental/imunologia
Fatores de Transcrição Forkhead/imunologia
Glicoproteínas/antagonistas & inibidores
Glicoproteínas/imunologia
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Esclerose Múltipla/tratamento farmacológico
Esclerose Múltipla/imunologia
Esclerose Múltipla/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Cytokines); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Glycoproteins); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE


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[PMID]:28085915
[Au] Autor:Viklicky O; Hruba P; Tomiuk S; Schmitz S; Gerstmayer B; Sawitzki B; Miqueu P; Mrazova P; Tycova I; Svobodova E; Honsova E; Janssen U; Volk HD; Reinke P
[Ad] Endereço:Department of Nephrology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
[Ti] Título:Sequential Targeting of CD52 and TNF Allows Early Minimization Therapy in Kidney Transplantation: From a Biomarker to Targeting in a Proof-Of-Concept Trial.
[So] Source:PLoS One;12(1):e0169624, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: There is high medical need for safe long-term immunosuppression monotherapy in kidney transplantation. Selective targeting of post-transplant alloantigen-(re)activated effector-T cells by anti-TNF antibodies after global T cell depletion may allow safe drug minimization, however, it is unsolved what might be the best maintenance monotherapy. METHODS: In this open, prospective observational single-centre trial, 20 primary deceased donor kidney transplant recipients received 2x20 mg Alemtuzumab (d0/d1) followed by 5 mg/kg Infliximab (d2). For 14 days all patients received only tacrolimus, then they were allocated to either receive tacrolimus (TAC, n = 13) or sirolimus (SIR, n = 7) monotherapy, respectively. Protocol biopsies and extensive immune monitoring were performed and patients were followed-up for 60 months. RESULTS: TAC-monotherapy resulted in excellent graft survival (5yr 92%, 95%CI: 56.6-98.9) and function, normal histology, and no proteinuria. Immune monitoring revealed low intragraft inflammation (urinary IP-10) and hints for the development of operational tolerance signature in the TAC- but not SIR-group. Remarkably, the TAC-monotherapy was successful in all five presensitized (ELISPOT+) patients. However, recruitment into SIR-arm was stopped (after n = 7) because of high incidence of proteinuria and acute/chronic rejection in biopsies. No opportunistic infections occurred during follow-up. CONCLUSIONS: In conclusion, our novel fast-track TAC-monotherapy protocol is likely to be safe and preliminary results indicated an excellent 5-year outcome, however, a full-scale study will be needed to confirm our findings. TRIAL REGISTRATION: EudraCT Number: 2006-003110-18.
[Mh] Termos MeSH primário: Glicoproteínas/antagonistas & inibidores
Rejeição de Enxerto/tratamento farmacológico
Imunossupressores/uso terapêutico
Transplante de Rim/efeitos adversos
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
Antígenos CD
Antígenos de Neoplasias
Biomarcadores/metabolismo
Antígeno CD52
Feminino
Perfilação da Expressão Gênica
Rejeição de Enxerto/etiologia
Seres Humanos
Masculino
Meia-Idade
Monitorização Imunológica
Estudos Prospectivos
Sirolimo/uso terapêutico
Tacrolimo/uso terapêutico
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins); 0 (Immunosuppressive Agents); 0 (Tumor Necrosis Factor-alpha); W36ZG6FT64 (Sirolimus); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0169624


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[PMID]:27925187
[Au] Autor:von Kutzleben S; Pryce G; Giovannoni G; Baker D
[Ad] Endereço:Neuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, London, UK.
[Ti] Título:Depletion of CD52-positive cells inhibits the development of central nervous system autoimmune disease, but deletes an immune-tolerance promoting CD8 T-cell population. Implications for secondary autoimmunity of alemtuzumab in multiple sclerosis.
[So] Source:Immunology;150(4):444-455, 2017 Apr.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The objective was to determine whether CD52 lymphocyte depletion can act to promote immunological tolerance induction by way of intravenous antigen administration such that it could be used to either improve efficiency of multiple sclerosis (MS) inhibition or inhibit secondary autoimmunities that may occur following alemtuzumab use in MS. Relapsing experimental autoimmune encephalomyelitis was induced in ABH mice and immune cell depletion was therapeutically applied using mouse CD52 or CD4 (in conjunction with CD8 or CD20) depleting monoclonal antibodies. Immunological unresponsiveness was then subsequently induced using intravenous central nervous system antigens and responses were assessed clinically. A dose-response of CD4 monoclonal antibody depletion indicated that the 60-70% functional CD4 T-cell depletion achieved in perceived failed trials in MS was perhaps too low to even stop disease in animals. However, more marked (~75-90%) physical depletion of CD4 T cells by CD4 and CD52 depleting antibodies inhibited relapsing disease. Surprisingly, in contrast to CD4 depletion, CD52 depletion blocked robust immunological unresponsiveness through a mechanism involving CD8 T cells. Although efficacy was related to the level of CD4 T-cell depletion, the observations that CD52 depletion of CD19 B cells was less marked in lymphoid organs than in the blood provides a rationale for the rapid B-cell hyper-repopulation that occurs following alemtuzumab administration in MS. That B cells repopulate in the relative absence of T-cell regulatory mechanisms that promote immune tolerance may account for the secondary B-cell autoimmunities, which occur following alemtuzumab treatment of MS.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Linfócitos B/imunologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Encefalomielite Autoimune Experimental/terapia
Esclerose Múltipla/terapia
[Mh] Termos MeSH secundário: Alemtuzumab
Animais
Antígenos CD/imunologia
Antígenos CD/metabolismo
Antígenos de Neoplasias/imunologia
Antígenos de Neoplasias/metabolismo
Autoimunidade
Antígeno CD52
Linfócitos T CD8-Positivos/imunologia
Células Cultivadas
Encefalomielite Autoimune Experimental/imunologia
Feminino
Glicoproteínas/imunologia
Glicoproteínas/metabolismo
Seres Humanos
Tolerância Imunológica
Depleção Linfocítica
Masculino
Camundongos
Camundongos Biozzi
Esclerose Múltipla/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins); 3A189DH42V (Alemtuzumab)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12696


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[PMID]:27480387
[Au] Autor:Boysen J; Nelson M; Magzoub G; Maiti GP; Sinha S; Goswami M; Vesely SK; Shanafelt TD; Kay NE; Ghosh AK
[Ad] Endereço:Division of Hematology, Mayo Clinic, Rochester, MN, USA.
[Ti] Título:Dynamics of microvesicle generation in B-cell chronic lymphocytic leukemia: implication in disease progression.
[So] Source:Leukemia;31(2):350-360, 2017 Feb.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Previously, we reported that B-cell chronic lymphocytic leukemia (CLL) patients contained elevated levels of microvesicles (MVs). However, given the quiescent nature of CLL B-cells and the relative indolence of the disease, the dynamics of MV generation and their unique phenotypes are not clearly defined. In this study, we find that CLL B-cells generate MVs spontaneously and can be further induced by B-cell receptor-ligation. Most interestingly, CLL B-cells predominantly generate CD52 MVs, but not CD19 MVs in vitro, suggesting preferential usage of CD52 into leukemic-MVs and that the CLL plasma MV phenotypes corroborate well with the in vitro findings. Importantly, we detected increased accumulation of CD52 MVs in previously untreated CLL patients with progressive disease. Finally, sequential studies on MVs in pre- and post-therapy CLL patients demonstrate that although the plasma CD52 MV levels drop significantly after therapy in most and remain at low levels in some patients, a trend of increased accumulation of CD52 MVs was detected in majority of post-therapy CLL patients (25 of 33). In total, this study emphasizes that dynamic accumulation of CD52 MVs in plasma can be used to study CLL progression and may be a useful biomarker for patients as they progress and require therapy.
[Mh] Termos MeSH primário: Micropartículas Derivadas de Células/metabolismo
Leucemia Linfocítica Crônica de Células B/metabolismo
Leucemia Linfocítica Crônica de Células B/patologia
[Mh] Termos MeSH secundário: Antígenos CD/metabolismo
Antígenos CD19/metabolismo
Antígenos de Neoplasias/metabolismo
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linfócitos B/metabolismo
Linfócitos B/ultraestrutura
Biomarcadores
Antígeno CD52
Linhagem Celular Tumoral
Micropartículas Derivadas de Células/ultraestrutura
Progressão da Doença
Glicoproteínas/metabolismo
Seres Humanos
Imunofenotipagem
Leucemia Linfocítica Crônica de Células B/tratamento farmacológico
Tempo para o Tratamento
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, CD19); 0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160803
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2016.217


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[PMID]:27560943
[Au] Autor:Hotta R; Ohira M; Matsuura T; Muraoka I; Tryphonopoulos P; Fan J; Tekin A; Selvaggi G; Levi D; Ruiz P; Ricordi C; Vianna R; Ohdan H; Waldmann H; Tzakis AG; Nishida S
[Ad] Endereço:Division of Liver and Gastrointestinal Transplantation, Department of Surgery, University of Miami Miller School of Medicine, Miami, FL, United States of America.
[Ti] Título:CD52-Negative NK Cells Are Abundant in the Liver and Less Susceptible to Alemtuzumab Treatment.
[So] Source:PLoS One;11(8):e0161618, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: T-cell depleting strategies have become an integral part of immunosuppressive regimens in organ transplantation. Alemtuzumab is a humanized monoclonal antibody against CD52, a cell-surface antigen on several immune cells. It has been suggested that lymphocyte depletion increases the risk of serious infections. However, this has not been observed with short-term alemtuzumab treatment in an organ transplant setting. For induction therapy using alemtuzumab following liver transplantation, we found that T- and B-cell numbers declined rapidly after alemtuzumab therapy; however, the natural killer (NK) cell number was sustained. NK cells are important effectors of innate immunity. Since the effects of alemtuzumab on NK cell functions, especially those of liver NK cells, are unknown, this study aimed to investigate this in detail. METHODS: To assess the effect of alemtuzumab on NK cells, samples were obtained from 7 organ donors and examined by flow cytometry using Annexin V and propidium iodide. Phenotypical and functional differences within subsets of NK cells with different levels of CD52 expression were determined by flow cytometry and in vitro cytotoxicity assays. RESULTS: CD52 expression on NK cells was lower than that on other lymphocyte subsets. The liver contained a large number of CD52- NK cells compared with the peripheral blood. In vitro treatment of liver-derived NK cells with alemtuzumab did not result in cell death. In contrast, co-incubation with alemtuzumab induced cell death in peripheral blood mononuclear cells and non-NK cells in the liver. Furthermore, CD52- liver NK cells were more cytotoxic and produced more IFN-γ than CD52+ NK cells after cytokine activation. CONCLUSION: The liver contains a large number of CD52- NK cells. These cells are refractory to alemtuzumab and have robust activity. These findings indicate that CD52- NK cells persist and could protect against infection after alemtuzumab-based lymphocyte depletion.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Antígenos CD/metabolismo
Antígenos de Neoplasias/metabolismo
Resistência a Medicamentos
Glicoproteínas/metabolismo
Células Matadoras Naturais/efeitos dos fármacos
Fígado/citologia
[Mh] Termos MeSH secundário: Alemtuzumab
Anticorpos Monoclonais/química
Anticorpos Antineoplásicos
Complexo CD3/metabolismo
Antígeno CD52
Morte Celular
Citocinas/metabolismo
Citometria de Fluxo
Seres Humanos
Interferon gama/metabolismo
Células Matadoras Naturais/citologia
Hepatopatias/cirurgia
Transplante de Fígado
Depleção Linfocítica
Doadores de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); 0 (Antibodies, Neoplasm); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (CD3 Complex); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Cytokines); 0 (Glycoproteins); 3A189DH42V (Alemtuzumab); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160826
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0161618


  9 / 398 MEDLINE  
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[PMID]:27490409
[Au] Autor:Furukawa A; Wisel SA; Tang Q
[Ad] Endereço:Department of Surgery, University of California, San Francisco, San Francisco, CA, United States.
[Ti] Título:Impact of Immune-Modulatory Drugs on Regulatory T Cell.
[So] Source:Transplantation;100(11):2288-2300, 2016 Nov.
[Is] ISSN:1534-6080
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunosuppression strategies that selectively inhibit effector T cells while preserving and even enhancing CD4FOXP3 regulatory T cells (Treg) permit immune self-regulation and may allow minimization of immunosuppression and associated toxicities. Many immunosuppressive drugs were developed before the identity and function of Treg were appreciated. A good understanding of the interactions between Treg and immunosuppressive agents will be valuable to the effective design of more tolerable immunosuppression regimens. This review will discuss preclinical and clinical evidence regarding the influence of current and emerging immunosuppressive drugs on Treg homeostasis, stability, and function as a guideline for the selection and development of Treg-friendly immunosuppressive regimens.
[Mh] Termos MeSH primário: Imunossupressores/farmacologia
Linfócitos T Reguladores/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antígenos CD/imunologia
Antígenos de Neoplasias/imunologia
Antígeno CD52
Inibidores de Calcineurina/farmacologia
Glicoproteínas/imunologia
Homeostase
Seres Humanos
Interleucina-2/farmacologia
Subunidade alfa de Receptor de Interleucina-2/imunologia
Receptores de Interleucina-6/imunologia
Linfócitos T Reguladores/imunologia
Serina-Treonina Quinases TOR/antagonistas & inibidores
Vitamina D/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Calcineurin Inhibitors); 0 (Glycoproteins); 0 (Immunosuppressive Agents); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Receptors, Interleukin-6); 1406-16-2 (Vitamin D); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160805
[St] Status:MEDLINE
[do] DOI:10.1097/TP.0000000000001379


  10 / 398 MEDLINE  
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[PMID]:26862819
[Au] Autor:Bhowmick M; Auckbarallee F; Edgar P; Ray A; Dasgupta S
[Ad] Endereço:From the Department of Pathology, Saint James School of Medicine, Albert Lake Drive, A-I-2640, The Quarter, P.O Box 318, Anguilla, British West Indies.
[Ti] Título:Humanized Monoclonal Antibody Alemtuzumab Treatment in Transplant.
[So] Source:Exp Clin Transplant;14(1):17-21, 2016 Feb.
[Is] ISSN:2146-8427
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:Successful attenuation of allograft rejection rate is a major clinical aspect in transplant. The CD52 binding monoclonal antibody CAMPATH1 or alemtuzumab, in this aspect, shows a promise as an effective immunomodifier. This humanized monoclonal antibody efficiently depletes CD52-bearing mature B- and T lymphocytes from circulation and thereby causes transient lymphopenia, a condition for generalized immunosuppression. Alemtuzumab is an approved drug for the treatment of B cell chronic lymphocytic leukemia. However, its implication in transplant as nonsteroidal drug is a growing area of investigation. Here, we provided a brief account on alemtuzumab as an immunomodifier in allotransplant.
[Mh] Termos MeSH primário: Anticorpos Monoclonais Humanizados/uso terapêutico
Rejeição de Enxerto/prevenção & controle
Sobrevivência de Enxerto/efeitos dos fármacos
Imunossupressores/uso terapêutico
Transplante de Órgãos/efeitos adversos
[Mh] Termos MeSH secundário: Alemtuzumab
Aloenxertos
Animais
Anticorpos Monoclonais Humanizados/efeitos adversos
Antígenos CD/imunologia
Antígenos de Neoplasias/imunologia
Antígeno CD52
Glicoproteínas/imunologia
Rejeição de Enxerto/imunologia
Seres Humanos
Imunossupressores/efeitos adversos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal, Humanized); 0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (CD52 Antigen); 0 (CD52 protein, human); 0 (Glycoproteins); 0 (Immunosuppressive Agents); 3A189DH42V (Alemtuzumab)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160211
[St] Status:MEDLINE



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