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  1 / 8813 MEDLINE  
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[PMID]:29422654
[Au] Autor:Marcou Q; Mora T; Walczak AM
[Ad] Endereço:Laboratoire de Physique Théorique, CNRS, Sorbonne Université and École Normale Supérieure (PSL), 24, Rue Lhomond, 75005, Paris, France.
[Ti] Título:High-throughput immune repertoire analysis with IGoR.
[So] Source:Nat Commun;9(1):561, 2018 02 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:High-throughput immune repertoire sequencing is promising to lead to new statistical diagnostic tools for medicine and biology. Successful implementations of these methods require a correct characterization, analysis, and interpretation of these data sets. We present IGoR (Inference and Generation Of Repertoires)-a comprehensive tool that takes B or T cell receptor sequence reads and quantitatively characterizes the statistics of receptor generation from both cDNA and gDNA. It probabilistically annotates sequences and its modular structure can be used to investigate models of increasing biological complexity for different organisms. For B cells, IGoR returns the hypermutation statistics, which we use to reveal co-localization of hypermutations along the sequence. We demonstrate that IGoR outperforms existing tools in accuracy and estimate the sample sizes needed for reliable repertoire characterization.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos B/genética
Receptores de Antígenos de Linfócitos T/genética
Software
Linfócitos T/imunologia
Recombinação V(D)J
[Mh] Termos MeSH secundário: Linfócitos B/citologia
Sequência de Bases
Benchmarking
DNA Complementar/genética
DNA Complementar/imunologia
Expressão Gênica
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Imunidade Inata
Anotação de Sequência Molecular
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Linfócitos T/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180210
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02832-w


  2 / 8813 MEDLINE  
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[PMID]:29386429
[Au] Autor:Uno K
[Ad] Endereço:Faculty of Pharmacy, Chiba Institute of Science.
[Ti] Título:[Pathogenic Mechanism and Diagnostic Testing for Drug Allergies].
[So] Source:Yakugaku Zasshi;138(2):151-167, 2018.
[Is] ISSN:1347-5231
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo: Three stages of the pathogenic mechanism of drug allergies can be considered: antigen formation, immune reaction and inflammation/disorder reaction. Drugs are thought to form 4 types of antigens: drug only, polymers, drug-carrier conjugates, and metabolite-carrier complexes. Antigens are recognized by B cell receptors and T cell receptors. Helper T cells (Th) are differentiated into four subsets, namely, Th1, Th2, Th17 and regulatory T cells (Treg). Th1 produces interleukin (IL)-2 and interferon (IFN)-γ, and activates macrophages and cytotoxic T cells (Tc). Macrophages induce type IV allergies, and Tc lead to serious type IV allergies. On the other hand, Th2 produces IL-4, IL-5, and IL-6, etc., and activates B cells. B cells produce IgE antibodies, and the IgE antibody affects mast cells and induces type I allergies. Activated eosinophil leads to the chronic state of type I allergy. Diagnostic testing for allergenic drugs is necessary for patients with drug allergies. Because in vivo diagnostic tests for allergenic drugs are associated with a risk and burden to the patient, in vitro allergy tests are recommended to identify allergenic drugs. In allergy tests performed in vitro, cytological tests are more effective than serological tests, and the leukocyte migration test (LMT) presently has the highest efficacy. An LMT-chamber is better than LMT-agarose in terms of usability and sensitivity, and it can detect about 80% of allergenic drugs.
[Mh] Termos MeSH primário: Ensaios de Migração de Leucócitos
Hipersensibilidade a Drogas/diagnóstico
Hipersensibilidade a Drogas/imunologia
[Mh] Termos MeSH secundário: Antígenos/imunologia
Linfócitos B/imunologia
Citocinas/metabolismo
Eosinófilos/imunologia
Seres Humanos
Imunoglobulina E
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos T/imunologia
Sensibilidade e Especificidade
Subpopulações de Linfócitos T/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antigens); 0 (Cytokines); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1248/yakushi.17-00174-1


  3 / 8813 MEDLINE  
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[PMID]:28747344
[Au] Autor:Burbage M; Keppler SJ; Montaner B; Mattila PK; Batista FD
[Ad] Endereço:Lymphocyte Interaction Laboratory, Francis Crick Institute, London NW1 1AT, United Kingdom.
[Ti] Título:The Small Rho GTPase TC10 Modulates B Cell Immune Responses.
[So] Source:J Immunol;199(5):1682-1695, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rho family GTPases regulate diverse cellular events, such as cell motility, polarity, and vesicle traffic. Although a wealth of data exists on the canonical Rho GTPases RhoA, Rac1, and Cdc42, several other family members remain poorly studied. In B cells, we recently demonstrated a critical role for Cdc42 in plasma cell differentiation. In this study, we focus on a close homolog of Cdc42, TC10 (also known as RhoQ), and investigate its physiological role in B cells. By generating a TC10-deficient mouse model, we show that despite reduced total B cell numbers, B cell development in these mice occurs normally through distinct developmental stages. Upon immunization, IgM levels were reduced and, upon viral infection, germinal center responses were defective in TC10-deficient mice. BCR signaling was mildly affected, whereas cell migration remained normal in TC10-deficient B cells. Furthermore, by generating a TC10/Cdc42 double knockout mouse model, we found that TC10 can compensate for the lack of Cdc42 in TLR-induced cell activation and proliferation, so the two proteins play partly redundant roles. Taken together, by combining in vivo and in vitro analysis using TC10-deficient mice, we define the poorly studied Rho GTPase TC10 as an immunomodulatory molecule playing a role in physiological B cell responses.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Infecções por Orthomyxoviridae/imunologia
Vaccinia/imunologia
Proteína cdc42 de Ligação ao GTP/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Proliferação Celular
Células Cultivadas
Centro Germinativo/imunologia
Imunomodulação
Ativação Linfocitária
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Receptores de Antígenos de Linfócitos B/metabolismo
Transdução de Sinais
Proteína cdc42 de Ligação ao GTP/genética
Proteínas rho de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cdc42 protein, mouse); 0 (Receptors, Antigen, B-Cell); EC 3.6.1.- (Rhoq protein, mouse); EC 3.6.5.2 (cdc42 GTP-Binding Protein); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602167


  4 / 8813 MEDLINE  
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[PMID]:29199989
[Au] Autor:Collins BC; Nakahara H; Acharya S; Cooper MD; Herrin BR; Wilson IA
[Ad] Endereço:Department of Integrative Structural and Computational Biology and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
[Ti] Título:Crystal structure of an anti-idiotype variable lymphocyte receptor.
[So] Source:Acta Crystallogr F Struct Biol Commun;73(Pt 12):682-687, 2017 Dec 01.
[Is] ISSN:2053-230X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Variable lymphocyte receptors (VLRs), the leucine-rich repeat (LRR)-based antigen receptors of jawless fish, have great utility in a wide variety of biochemical and biological applications, similar to classical Ig-based antibodies. VLR-based reagents may be particularly useful when traditional antibodies are not available. An anti-idiotype lamprey VLR, VLR39, has previously been identified that recognizes the heavy-chain CDR3 of the B-cell receptor (BCR) of a leukemic clone from a patient with chronic lymphocytic leukemia (CLL). VLR39 was used successfully to track the re-emergence of this clone in the patient following chemotherapy. Here, the crystal structure of VLR39 is presented at 1.5 Šresolution and compared with those of other protein-specific VLRs. VLR39 adopts a curved solenoid fold and exhibits substantial structural similarity to other protein-binding VLRs. VLR39 has a short LRRCT loop that protrudes outwards away from the concave face and is similar to those of its protein-specific VLR counterparts. Analysis of the VLR39-BCR interaction by size-exclusion chromatography and biolayer interferometry using the scFv version of the BCR confirms that VLR39 recognizes the BCR Fv region. Such VLR-based reagents may be useful for identifying and monitoring leukemia in CLL patients and in other clinical diagnostic assays.
[Mh] Termos MeSH primário: Receptores de Antígenos/química
Receptores de Antígenos/imunologia
[Mh] Termos MeSH secundário: Cromatografia em Gel
Cristalografia por Raios X
Epitopos/metabolismo
Seres Humanos
Modelos Moleculares
Conformação Proteica
Receptores de Antígenos/genética
Receptores de Antígenos/metabolismo
Receptores de Antígenos de Linfócitos B/química
Receptores de Antígenos de Linfócitos B/imunologia
Receptores de Antígenos de Linfócitos B/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epitopes); 0 (Receptors, Antigen); 0 (Receptors, Antigen, B-Cell); 0 (Recombinant Proteins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1107/S2053230X1701620X


  5 / 8813 MEDLINE  
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[PMID]:28461109
[Au] Autor:Amrouche K; Jamin C
[Ad] Endereço:UMR 1227, Lymphocytes B et Autoimmunité, Université de Brest, INSERM, Brest, France; LabEx IGO "Immunotherapy, Graft, Oncology", Brest, France.
[Ti] Título:Influence of drug molecules on regulatory B cells.
[So] Source:Clin Immunol;184:1-10, 2017 11.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:By their suppressive functions, regulatory B (Breg) cells are considered as key elements in the control and development of various disease states. Many signals can induce Bregs in vivo and in vitro and often from heterogeneous populations. Several specific signals delivered in a timely immunological context contribute to the establishment of Bregs. These are endogenous and physiological signals or stimuli, widely discussed in the literature participating in the establishment of an effective immune response. However, exogenous signals, much less clearly identified can also be considered as Bregs inducers. These extrinsic signals are capable of directly or indirectly influencing the suppressive capacity of Bregs, but also their expansion and functional restoration in its absence. Faced with the excitement generated by the development of processes favoring the expansion of Bregs in mice for therapeutic purposes, the challenge today is to extrapolate such approaches in humans. This perspective may already be in effect.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Linfócitos B Reguladores/efeitos dos fármacos
Imunossupressores/farmacologia
Vitaminas/farmacologia
[Mh] Termos MeSH secundário: Corticosteroides/farmacologia
Animais
Anticorpos Monoclonais Humanizados/farmacologia
Fator Ativador de Células B/imunologia
Linfócitos B Reguladores/imunologia
Antígenos CD40/imunologia
Citocinas/imunologia
Seres Humanos
Metotrexato/farmacologia
Ácido Micofenólico/farmacologia
Pirróis/farmacologia
Quinazolinas/farmacologia
Receptores de Antígenos de Linfócitos B/imunologia
Semaforinas/farmacologia
Sirolimo/farmacologia
Receptores Toll-Like/imunologia
Tretinoína/farmacologia
Vitamina D/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Antibodies, Monoclonal, Humanized); 0 (Antineoplastic Agents); 0 (B-Cell Activating Factor); 0 (CD40 Antigens); 0 (Cytokines); 0 (Immunosuppressive Agents); 0 (Pyrroles); 0 (Quinazolines); 0 (Receptors, Antigen, B-Cell); 0 (Semaphorins); 0 (Toll-Like Receptors); 0 (Vitamins); 1406-16-2 (Vitamin D); 5688UTC01R (Tretinoin); 7I279E1NZ8 (sotrastaurin); HU9DX48N0T (Mycophenolic Acid); I031V2H011 (tocilizumab); W36ZG6FT64 (Sirolimus); YL5FZ2Y5U1 (Methotrexate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  6 / 8813 MEDLINE  
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[PMID]:28468967
[Au] Autor:Keller B; Stumpf I; Strohmeier V; Usadel S; Verhoeyen E; Eibel H; Warnatz K
[Ad] Endereço:Center for Chronic Immunodeficiency, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany.
[Ti] Título:High SYK Expression Drives Constitutive Activation of CD21 B Cells.
[So] Source:J Immunol;198(11):4285-4292, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human CD21 B cells present with an activated phenotype and accumulate in distinct disorders connected with chronic immune stimulation. Signaling studies had revealed an increased basal phosphorylation of spleen tyrosine kinase (SYK) and phospholipase Cγ2. Additional BCR stimulation of these constitutively active cells, however, led to reduced activation of these signaling molecules and subsequently NF-κB and Ca activation. In this article, we demonstrate that high SYK expression is a common feature of CD21 B cells independent of the underlying disorder, and that this high expression is sufficient to drive constitutive phosphorylation of SYK and its immediate targets Bruton's tyrosine kinase and phospholipase Cγ2. Inhibition of SYK activity eliminated features of the constitutive activation in these cells and partly restored BCR signaling. High SYK expression is especially induced by CpG or CD40L in combination with IL-21, but not BCR stimulation, suggesting the importance of the immune-stimulatory context for the induction of this B cell phenotype. In summary, high SYK expression is a common feature of human CD21 B cells and presumably results from chronic activation in inflammatory environments present in a subgroup of patients with heterogeneous disorders like chronic infection, autoimmunity, and immunodeficiency. High SYK expression by itself drives the constitutive activation observed in these B cells, which in turn may contribute to the hyporesponsiveness upon BCR stimulation. Given the high prevalence of autoreactive clones among CD21 B cells in autoimmune disorders, the dominant role of SYK in CD21 B cells may provide a new option for therapeutic interventions in patients with expanded CD21 B cells and humoral autoimmunity.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Ativação Linfocitária
Receptores de Complemento 3d/imunologia
Quinase Syk/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Linfócitos B/fisiologia
Ligante de CD40/imunologia
Feminino
Seres Humanos
Interleucinas/farmacologia
Masculino
Meia-Idade
Oligodesoxirribonucleotídeos/imunologia
Fosfolipase C gama/metabolismo
Fosforilação
Proteínas Tirosina Quinases/metabolismo
Receptores de Antígenos de Linfócitos B/imunologia
Transdução de Sinais
Quinase Syk/antagonistas & inibidores
Quinase Syk/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CPG-oligonucleotide); 0 (Interleukins); 0 (Oligodeoxyribonucleotides); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Complement 3d); 0 (interleukin-21); 147205-72-9 (CD40 Ligand); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (SYK protein, human); EC 2.7.10.2 (Syk Kinase); EC 3.1.4.3 (Phospholipase C gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700079


  7 / 8813 MEDLINE  
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[PMID]:28462919
[Au] Autor:Slinger E; Thijssen R; Kater AP; Eldering E
[Ad] Endereço:Cancer Center Amsterdam, Department of Experimental Immunology, Academic Medical Center, Amsterdam, The Netherlands.
[Ti] Título:Targeting antigen-independent proliferation in chronic lymphocytic leukemia through differential kinase inhibition.
[So] Source:Leukemia;31(12):2601-2607, 2017 Dec.
[Is] ISSN:1476-5551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The clinical success of B-cell receptor (BCR) signaling pathway inhibitors in chronic lymphocytic leukemia (CLL) is attributed to inhibition of adhesion in and migration towards the lymph node. Proliferation of CLL cells is restricted to this protective niche, but the underlying mechanism(s) is/are not known. Treatment with BCR pathway inhibitors results in rapid reductions of total clone size, while CLL cell survival is not affected, which points towards inhibition of proliferation. In vitro, BCR stimulation does not induce proliferation of CLL, but triggering via Toll-like receptor, tumor necrosis factor or cytokine receptors does. Here, we investigated the effects of clinically applied inhibitors that target BCR signaling, in the context of proliferation triggered either via CD40L/IL-21 or after CpG stimulation. CD40L/IL-21-induced proliferation could be inhibited by idelalisib and ibrutinib. We demonstrate this was due to blockade of CD40L-induced ERK-signaling. Targeting JAKs, but not SYK, blocked CD40L/IL-21-induced proliferation. In contrast, PI3K, BTK as well as SYK inhibition prevented CpG-induced proliferation. Knockdown experiments showed that CD40L/IL-21 did not co-opt upstream BCR components such as CD79A, in contrast to CpG-induced proliferation. Our data indicate that currently applied BTK/PI3K inhibitors target antigen-independent proliferation in CLL, and suggest that targeting of JAK and/or SYK might be clinically useful.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/imunologia
Leucemia Linfocítica Crônica de Células B/imunologia
Leucemia Linfocítica Crônica de Células B/metabolismo
Fosfotransferases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Biomarcadores
Antígenos CD40/imunologia
Antígenos CD40/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Seres Humanos
Interleucinas/metabolismo
Janus Quinases/metabolismo
Leucemia Linfocítica Crônica de Células B/genética
NF-kappa B/metabolismo
Fosfotransferases/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Receptores de Antígenos de Linfócitos B/metabolismo
Fatores de Transcrição STAT/metabolismo
Transdução de Sinais/efeitos dos fármacos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (Biomarkers); 0 (CD40 Antigens); 0 (Interleukins); 0 (NF-kappa B); 0 (Protein Kinase Inhibitors); 0 (Receptors, Antigen, B-Cell); 0 (STAT Transcription Factors); 0 (interleukin-21); EC 2.7.- (Phosphotransferases); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171215
[Lr] Data última revisão:
171215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2017.129


  8 / 8813 MEDLINE  
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[PMID]:28972089
[Au] Autor:Bednar KJ; Shanina E; Ballet R; Connors EP; Duan S; Juan J; Arlian BM; Kulis MD; Butcher EC; Fung-Leung WP; Rao TS; Paulson JC; Macauley MS
[Ad] Endereço:Immunology Team, Janssen Research and Development, LLC, Raritan, NJ 08869.
[Ti] Título:Human CD22 Inhibits Murine B Cell Receptor Activation in a Human CD22 Transgenic Mouse Model.
[So] Source:J Immunol;199(9):3116-3128, 2017 Nov 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CD22, a sialic acid-binding Ig-type lectin (Siglec) family member, is an inhibitory coreceptor of the BCR with established roles in health and disease. The restricted expression pattern of CD22 on B cells and most B cell lymphomas has made CD22 a therapeutic target for B cell-mediated diseases. Models to better understand how in vivo targeting of CD22 translates to human disease are needed. In this article, we report the development of a transgenic mouse expressing human CD22 (hCD22) in B cells and assess its ability to functionally substitute for murine CD22 (mCD22) for regulation of BCR signaling, Ab responses, homing, and tolerance. Expression of hCD22 on transgenic murine B cells is comparable to expression on human primary B cells, and it colocalizes with mCD22 on the cell surface. Murine B cells expressing only hCD22 have identical calcium (Ca ) flux responses to anti-IgM as mCD22-expressing wild-type B cells. Furthermore, hCD22 transgenic mice on an mCD22 background have restored levels of marginal zone B cells and Ab responses compared with deficiencies observed in CD22 mice. Consistent with these observations, hCD22 transgenic mice develop normal humoral responses in a peanut allergy oral sensitization model. Homing of B cells to Peyer's patches was partially rescued by expression of hCD22 compared with CD22 B cells, although not to wild-type levels. Notably, Siglec-engaging antigenic liposomes formulated with an hCD22 ligand were shown to prevent B cell activation, increase cell death, and induce tolerance in vivo. This hCD22 transgenic mouse will be a valuable model for investigating the function of hCD22 and preclinical studies targeting hCD22.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Hipersensibilidade a Amendoim/imunologia
Nódulos Linfáticos Agregados/imunologia
Receptores de Antígenos de Linfócitos B/imunologia
Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico/imunologia
Transdução de Sinais/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/patologia
Modelos Animais de Doenças
Seres Humanos
Ativação Linfocitária/genética
Camundongos
Camundongos Transgênicos
Hipersensibilidade a Amendoim/genética
Hipersensibilidade a Amendoim/patologia
Nódulos Linfáticos Agregados/patologia
Receptores de Antígenos de Linfócitos B/genética
Lectina 2 Semelhante a Ig de Ligação ao Ácido Siálico/genética
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD22 protein, human); 0 (Cd22 protein, mouse); 0 (Receptors, Antigen, B-Cell); 0 (Sialic Acid Binding Ig-like Lectin 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700898


  9 / 8813 MEDLINE  
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[PMID]:28953967
[Au] Autor:Obeng-Adjei N; Portugal S; Holla P; Li S; Sohn H; Ambegaonkar A; Skinner J; Bowyer G; Doumbo OK; Traore B; Pierce SK; Crompton PD
[Ad] Endereço:Malaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
[Ti] Título:Malaria-induced interferon-γ drives the expansion of Tbethi atypical memory B cells.
[So] Source:PLoS Pathog;13(9):e1006576, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many chronic infections, including malaria and HIV, are associated with a large expansion of CD21-CD27- 'atypical' memory B cells (MBCs) that exhibit reduced B cell receptor (BCR) signaling and effector functions. Little is known about the conditions or transcriptional regulators driving atypical MBC differentiation. Here we show that atypical MBCs in malaria-exposed individuals highly express the transcription factor T-bet, and that T-bet expression correlates inversely with BCR signaling and skews toward IgG3 class switching. Moreover, a longitudinal analysis of a subset of children suggested a correlation between the incidence of febrile malaria and the expansion of T-bethi B cells. The Th1-cytokine containing supernatants of malaria-stimulated PBMCs plus BCR cross linking induced T-bet expression in naïve B cells that was abrogated by neutralizing IFN-γ or blocking the IFN-γ receptor on B cells. Accordingly, recombinant IFN-γ plus BCR cross-linking drove T-bet expression in peripheral and tonsillar B cells. Consistent with this, Th1-polarized Tfh (Tfh-1) cells more efficiently induced T-bet expression in naïve B cells. These data provide new insight into the mechanisms underlying atypical MBC differentiation.
[Mh] Termos MeSH primário: Linfócitos B/citologia
Linfócitos B/imunologia
Diferenciação Celular/imunologia
Regulação da Expressão Gênica/imunologia
Memória Imunológica/imunologia
Interferon gama/biossíntese
Malária/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Feminino
Proteínas Fetais/metabolismo
Seres Humanos
Lactente
Malária/metabolismo
Masculino
Receptores de Antígenos de Linfócitos B/metabolismo
Proteínas com Domínio T-Box/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Fetal Proteins); 0 (Receptors, Antigen, B-Cell); 0 (T-Box Domain Proteins); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006576


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[PMID]:28924003
[Au] Autor:Greiff V; Weber CR; Palme J; Bodenhofer U; Miho E; Menzel U; Reddy ST
[Ad] Endereço:Department of Biosystems Science and Engineering, Swiss Federal Institute of Technology Zurich, CH-4058 Basel, Switzerland.
[Ti] Título:Learning the High-Dimensional Immunogenomic Features That Predict Public and Private Antibody Repertoires.
[So] Source:J Immunol;199(8):2985-2997, 2017 Oct 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have revealed that immune repertoires contain a substantial fraction of public clones, which may be defined as Ab or TCR clonal sequences shared across individuals. It has remained unclear whether public clones possess predictable sequence features that differentiate them from private clones, which are believed to be generated largely stochastically. This knowledge gap represents a lack of insight into the shaping of immune repertoire diversity. Leveraging a machine learning approach capable of capturing the high-dimensional compositional information of each clonal sequence (defined by CDR3), we detected predictive public clone and private clone-specific immunogenomic differences concentrated in CDR3's N1-D-N2 region, which allowed the prediction of public and private status with 80% accuracy in humans and mice. Our results unexpectedly demonstrate that public, as well as private, clones possess predictable high-dimensional immunogenomic features. Our support vector machine model could be trained effectively on large published datasets (3 million clonal sequences) and was sufficiently robust for public clone prediction across individuals and studies prepared with different library preparation and high-throughput sequencing protocols. In summary, we have uncovered the existence of high-dimensional immunogenomic rules that shape immune repertoire diversity in a predictable fashion. Our approach may pave the way for the construction of a comprehensive atlas of public mouse and human immune repertoires with potential applications in rational vaccine design and immunotherapeutics.
[Mh] Termos MeSH primário: Linfócitos B/fisiologia
Regiões Determinantes de Complementaridade/genética
Imunoterapia/métodos
Receptores de Antígenos de Linfócitos B/genética
Receptores de Antígenos de Linfócitos T/genética
Linfócitos T/fisiologia
Vacinas/imunologia
[Mh] Termos MeSH secundário: Animais
Diversidade de Anticorpos
Seleção Clonal Mediada por Antígeno
Células Clonais
Conjuntos de Dados como Assunto
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complementarity Determining Regions); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Antigen, T-Cell); 0 (Vaccines)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1700594



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