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  1 / 4328 MEDLINE  
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PMID:29412476
Autor:Bakela K; Dimakopoulou M; Batsou P; Manidakis N; Athanassakis I
Endereço:Laboratory of Immunology, Department of Biology, University of Crete, Heraklion, Crete, Greece.
Título:Soluble MHC class II-driven therapy for a systemic lupus erythematosus murine experimental in vitro and in vivo model.
Fonte:Scand J Immunol; 87(3), 2018 Mar.
ISSN:1365-3083
País de publicação:England
Idioma:eng
Resumo:Taking into consideration the multiparametric nature of systemic lupus erythematosus (SLE), the severity and variability of symptoms and the lack of effective therapeutic approaches, this study took advantage of the recently described role of soluble major histocompatibility complex class II (sMHCII) molecules in maintaining tolerance to the organism and attempted to apply sMHCII proteins as a treatment to murine SLE experimental models in vitro as well as in vivo. After breaking tolerance to DNA in vitro, which was accompanied by development of specific anti-dsDNA antibodies, syngeneic or allogeneic sMHCII molecules, purified from healthy mouse serum, could significantly reduce the specific antibody levels and drive the system towards immunosuppression, as assessed by specific marker analysis on T cells and cytokine production by flow cytometry and ELISA, respectively. The in vivo experimental model consisted of pristane-induced SLE symptoms to BALB/c mice, which developed maximal levels of anti-dsDNA 2 months after pristane inoculation. Syngeneic or allogeneic sMHCII administration could alleviate pristane-induced symptoms, significantly decrease specific anti-dsDNA antibody production and develop immunosuppression to the host, as manifested by increase of CD4 + CTLA-4 +  and CD4 + CD25 +  cell populations in the spleen. Thus, the results presented in this study introduced the ability of sMHCII proteins to suppress specific autoantigen response, opening new areas of research and offering novel therapeutic approaches to SLE with expanding features to other autoimmune diseases.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antibodies, Antinuclear); 0 (Autoantigens); 0 (CD4 Antigens); 0 (CTLA-4 Antigen); 0 (Histocompatibility Antigens Class II); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Terpenes); 26HZV48DT1 (pristane); 9007-49-2 (DNA)


  2 / 4328 MEDLINE  
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PMID:29363337
Autor:Patti F; Chisari CG; D'Amico E; Zappia M
Endereço:a Department "GF Ingrassia", Section of Neurosciences, Multiple Sclerosis Center , University of Catania , Catania , Italy.
Título:Pharmacokinetic drug evaluation of daclizumab for the treatment of relapsing-remitting multiple sclerosis.
Fonte:Expert Opin Drug Metab Toxicol; 14(3):341-352, 2018 Mar.
ISSN:1744-7607
País de publicação:England
Idioma:eng
Resumo:INTRODUCTION: Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system. Despite the availability of several disease-modifying therapies for relapsing MS, there is a need for highly efficacious targeted therapy with a favorable benefit-risk profile and a high level of treatment adherence. Daclizumab is a humanized monoclonal antibody directed against CD25, the α subunit of the high-affinity interleukin 2 (IL-2) receptor, that reversibly modulates IL-2 signaling. Areas covered: Daclizumab blocks the activation and expansion of autoreactive T cells that plays a role in the immune pathogenesis of MS. As its modulatory effects on the immune system, daclizumab's potential for use in MS was tested extensively showing a high efficacy in reducing relapse rate, disability progression and the number and volume of gadolinium-enhancing lesions on brain magnetic resonance imaging. Moreover, phase II and III trials showed a favorable pharmacokinetic (PK) profile with slow clearance, linear pharmacokinetics at doses above 100 mg and high subcutaneous bioavailability, not influenced by age, sex or other clinical parameters. Expert opinion: Among the new emerging drugs for MS, daclizumab also, thanks to a favorable PK profile, may represent an interesting and promising therapeutic option in the wide MS therapies armamentarium.
Tipo de publicação: JOURNAL ARTICLE; REVIEW
Nome de substância:0 (Antibodies, Monoclonal, Humanized); 0 (IL2RA protein, human); 0 (Immunoglobulin G); 0 (Immunosuppressive Agents); 0 (Interleukin-2 Receptor alpha Subunit); CUJ2MVI71Y (daclizumab)


  3 / 4328 MEDLINE  
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PMID:28457753
Autor:Sadovnik I; Herrmann H; Eisenwort G; Blatt K; Hoermann G; Mueller N; Sperr WR; Valent P
Endereço:Department of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, Vienna, Austria.
Título:Expression of CD25 on leukemic stem cells in BCR-ABL1 CML: Potential diagnostic value and functional implications.
Fonte:Exp Hematol; 51:17-24, 2017 07.
ISSN:1873-2399
País de publicação:Netherlands
Idioma:eng
Resumo:Chronic myeloid leukemia (CML) is a stem cell-derived leukemia in which neoplastic cells exhibit the Philadelphia chromosome and the related oncoprotein BCR-ABL1. The disease is characterized by an accumulation of myeloid precursor cells in the peripheral blood and bone marrow (BM). A small fraction of neoplastic cells in the CML clone supposedly exhibits self-renewal and thus long-term disease-propagating ability. However, so far, little is known about the phenotype, function, and target expression profiles of these leukemic stem cells (LSCs). Recent data suggest that CML LSCs aberrantly express the interleukin-2 receptor alpha chain CD25. Whereas normal CD34 /CD38 BM stem cells display only low amounts of CD25 or lack CD25 altogether, CD34 /CD38 LSCs express CD25 strongly in more than 90% of all patients with untreated CML. As a result, CD25 can be used to identify and quantify CML LSCs. In addition, it has been shown that CD25 serves as a negative growth regulator of CML LSCs. Here, we review the value of CD25 as a novel marker and potential drug target in CML LSCs.
Tipo de publicação: JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de substância:0 (Antigens, CD34); 0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)


  4 / 4328 MEDLINE  
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PMID:29261670
Autor:Jeffery HC; McDowell P; Lutz P; Wawman RE; Roberts S; Bagnall C; Birtwistle J; Adams DH; Oo YH
Endereço:Centre for Liver Research and National Institute for Health Research Birmingham Biomedical Research Centre, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, United Kingdom.
Título:Human intrahepatic ILC2 are IL-13positive amphiregulinpositive and their frequency correlates with model of end stage liver disease score.
Fonte:PLoS One; 12(12):e0188649, 2017.
ISSN:1932-6203
País de publicação:United States
Idioma:eng
Resumo:INTRODUCTION: Innate lymphoid cells (ILC) have been implicated in the initiation of inflammation and fibrosis in mice. However, ILC have not been characterized in inflamed human liver tissue. METHODS: Human intrahepatic lymphocytes were isolated by mechanical digestion and phenotyped by flow cytometry. Conditioned medium from cultures of primary human biliary epithelial cells, stellate cells, fibroblasts and inflamed human liver tissue was used to model the effects of the inflammatory liver environment of ILC phenotype and function. RESULTS: All three ILC subsets were present in the human liver, with the ILC1 (CRTH2negCD117neg) subset constituting around 70% of intrahepatic ILCs. Both NCRpos (NKp44+) and NCRneg ILC3 (CRTH2negCD117pos) subsets were also detected. ILC2 (CRTH2pos) frequency correlated with disease severity measured by model of end stage liver disease (MELD) scoring leading us to study this subset in more detail. ILC2 displayed a tissue resident CD69+ CD161++ phenotype and expressed chemokine receptor CCR6 allowing them to respond to CCL20 secreted by cholangiocytes and stellate cells. ILC2 expressed integrins VLA-5 and VLA-6 and the IL-2 and IL-7 cytokine receptors CD25 and CD127 although IL-2 and IL-7 were barely detectable in inflamed liver tissue. Although biliary epithelial cells secrete IL-33, intrahepatic ILC2 had low expression of the ST2 receptor. Intrahepatic ILC2 secreted the immunoregulatory and repair cytokines IL-13 and amphiregulin. CONCLUSIONS: Intrahepatic ILC2 express receptors allowing them to be recruited to bile ducts in inflamed portal tracts. Their frequencies increased with worsening liver function. Their secretion of IL-13 and amphiregulin suggests they may be recruited to promote resolution and repair and thereby they may contribute to ongoing fibrogenesis in liver disease.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Amphiregulin); 0 (Integrins); 0 (Interleukin-13); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-7); 0 (NK Cell Lectin-Like Receptor Subfamily B); 0 (Receptors, Chemokine); 0 (Receptors, Immunologic); 0 (Receptors, Prostaglandin); 0 (prostaglandin D2 receptor)


  5 / 4328 MEDLINE  
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PMID:29246441
Autor:Essig K; Hu D; Guimaraes JC; Alterauge D; Edelmann S; Raj T; Kranich J; Behrens G; Heiseke A; Floess S; Klein J; Maiser A; Marschall S; Hrabe de Angelis M; Leonhardt H; Calkhoven CF; Noessner E; Brocker T; Huehn J; Krug AB; Zavolan M; Baumjohann D; Heissmeyer V
Endereço:Institute for Immunology, Biomedical Center, Ludwig-Maximilians-Universität München, 82152 Planegg-Martinsried, Germany.
Título:Roquin Suppresses the PI3K-mTOR Signaling Pathway to Inhibit T Helper Cell Differentiation and Conversion of Treg to Tfr Cells.
Fonte:Immunity; 47(6):1067-1082.e12, 2017 Dec 19.
ISSN:1097-4180
País de publicação:United States
Idioma:eng
Resumo:Roquin proteins preclude spontaneous T cell activation and aberrant differentiation of T follicular helper (Tfh) or T helper 17 (Th17) cells. Here we showed that deletion of Roquin-encoding alleles specifically in regulatory T (Treg) cells also caused the activation of conventional T cells. Roquin-deficient Treg cells downregulated CD25, acquired a follicular Treg (Tfr) cell phenotype, and suppressed germinal center reactions but could not protect from colitis. Roquin inhibited the PI3K-mTOR signaling pathway by upregulation of Pten through interfering with miR-17∼92 binding to an overlapping cis-element in the Pten 3' UTR, and downregulated the Foxo1-specific E3 ubiquitin ligase Itch. Loss of Roquin enhanced Akt-mTOR signaling and protein synthesis, whereas inhibition of PI3K or mTOR in Roquin-deficient T cells corrected enhanced Tfh and Th17 or reduced iTreg cell differentiation. Thereby, Roquin-mediated control of PI3K-mTOR signaling prevents autoimmunity by restraining activation and differentiation of conventional T cells and specialization of Treg cells.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (MIRN17-92 microRNA, mouse); 0 (MicroRNAs); 0 (Repressor Proteins); 0 (roquin-2 protein, mouse); EC 2.3.2.26 (Itch protein, mouse); EC 2.3.2.27 (Rc3h1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.1.1 (mTOR protein, mouse); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (Pten protein, mouse)


  6 / 4328 MEDLINE  
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PMID:28942020
Autor:Lang C; Wang J; Chen L
Endereço:Department of Gastroenterology, Liaocheng People's Hospital, Liaocheng, Shandong Province 252000, China. Electronic address: cuicuilang@163.com.
Título:CD25-expressing Th17 cells mediate CD8 T cell suppression in CTLA-4 dependent mechanisms in pancreatic ductal adenocarcinoma.
Fonte:Exp Cell Res; 360(2):384-389, 2017 Nov 15.
ISSN:1090-2422
País de publicação:United States
Idioma:eng
Resumo:The tumor-associated immune response is governed by the signalling events of various regulatory molecules, one of which is the cytotoxic T lymphocyte-associated antigen 4 (CTLA-4). In conventional T cells, CTLA-4 could outcompete CD28 in binding to CD80/86 but does not produce a co-stimulatory signal, resulting in T cell anergy. CTLA-4 in regulatory T cells (Tregs) could also function in a cell-extrinsic fashion by removing CD80/CD86 from the antigen-presenting cells (APCs), thus preventing further priming of other T cells. In this study, we examined the role of CTLA-4 in CD4 T cell subsets from pancreatic cancer patients. In circulating CD4 T cells, the expression of CTLA-4 was low at baseline but was significantly upregulated following T cell stimulation. Interestingly, the CTLA-4-expressing CD4 T cells at baseline were overwhelmingly FOXP3-expressing. With the increase of T cell stimulation, the proportion of ROR gamma t-expressing CD4 T cells was progressively increased. By CD25 vs. CCR6 staining, the CD25 CCR6 and the CD25 CCR6 CD4 T cells both presented high levels of CTLA-4 expression, but only the CD25 CCR6 and the CD25 CCR6 expressed significant amounts of IL-17. When incubated with autologous CD8 T cells, the CD25 CCR6 Th17 cells presented significantly higher suppressive function than the CD25 CCR6 Th17 cells in a CTLA-4-dependent manner. Finally, the CTLA-4-expressing Th17 cells were present at higher levels in the tumor-infiltrating lymphocytes than in circulating blood. Overall, these data suggest that CTLA-4 expressing Th17 cells may present regulatory activities in pancreatic cancer patients.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (CTLA-4 Antigen); 0 (CTLA4 protein, human); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 82115-62-6 (Interferon-gamma)


  7 / 4328 MEDLINE  
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PMID:28935468
Autor:Ma QY; Huang DY; Zhang HJ; Wang S; Chen XF
Endereço:Department of Thoracic Surgery, Huashan Hospital Affiliated to Fudan University, Shanghai, China.
Título:Function and regulation of LAG3 on CD4 CD25 T cells in non-small cell lung cancer.
Fonte:Exp Cell Res; 360(2):358-364, 2017 Nov 15.
ISSN:1090-2422
País de publicação:United States
Idioma:eng
Resumo:LAG3 is a surface molecule found on a subset of immune cells. The precise function of LAG3 appears to be context-dependent. In this study, we investigated the effect of LAG3 on CD4 CD25 T cells from non-small cell lung cancer (NSCLC) patients. We found that in the peripheral blood mononuclear cells of NSCLC patients, LAG3 was significantly increased in CD4 T cells directly ex vivo and primarily in the CD4 CD25 fraction, which was regulated by prolonged TCR stimulation and the presence of IL-27. TCR stimulation also increased CD25 expression, but not Foxp3 expression, in LAG3-expressing CD4 CD25 cells Compared to LAG3-nonexpressing CD4 CD25 cells, LAG3-expressing CD4 CD25 cells presented significantly higher levels of PD1 and TIM3, two inhibitory receptors best described in exhausted CD8 T effector cells. LAG3-expressing CD4 CD25 cells also presented impaired proliferation compared with LAG3-nonexpressing CD4 CD25 cells but could be partially rescued by inhibiting both PD1 and TIM3. Interestingly, CD8 T cells co-incubated with LAG3-expressing CD4 CD25 cells at equal cell numbers demonstrated significantly lower proliferation than CD8 T cells incubated alone. Co-culture with CD8 T cell and LAG3-expressing CD4 CD25 T cell also upregulated soluble IL-10 level in the supernatant, of which the concentration was positively correlated with the number of LAG3-expressing CD4 CD25 T cells. In addition, we found that LAG3-expressing CD4 CD25 T cells infiltrated the resected tumors and were present at higher frequencies of in metastases than in primary tumors. Taken together, these data suggest that LAG3-expressing CD4 CD25 T cells represent another regulatory immune cell type with potential to interfere with anti-tumor immunity.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antigens, CD); 0 (CD223 antigen); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit)


  8 / 4328 MEDLINE  
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PMID:28901888
Autor:Tzang BS; Liu CH; Hsu KC; Chen YH; Huang CY; Hsu TC
Endereço:1Institute of Biochemistry, Microbiology and Immunology,Chung Shan Medical University,Taichung 402,Taiwan,ROC.
Título:Effects of oral Lactobacillus administration on antioxidant activities and CD4+CD25+forkhead box P3 (FoxP3)+ T cells in NZB/W F1 mice.
Fonte:Br J Nutr; 118(5):333-342, 2017 Sep.
ISSN:1475-2662
País de publicação:England
Idioma:eng
Resumo:Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterised by a dysregulation of the immune system, which causes inflammation responses, excessive oxidative stress and a reduction in the number of cluster of differentiation (CD)4+CD25+forkhead box P3 (FoxP3)+ T cells. Supplementation with certain Lactobacillus strains has been suggested to be beneficial in the comprehensive treatment of SLE. However, little is known about the effect and mechanism of certain Lactobacillus strains on SLE. To investigate the effects of Lactobacillus on SLE, NZB/W F1 mice were orally gavaged with Lactobacillus paracasei GMNL-32 (GMNL-32), Lactobacillus reuteri GMNL-89 (GMNL-89) and L. reuteri GMNL-263 (GMNL-263). Supplementation with GMNL-32, GMNL-89 and GMNL-263 significantly increased antioxidant activity, reduced IL-6 and TNF-α levels and significantly decreased the toll-like receptors/myeloid differentiation primary response gene 88 signalling in NZB/W F1 mice. Notably, supplementation with GMNL-263, but not GMNL-32 and GMNL-89, in NZB/W F1 mice significantly increased the differentiation of CD4+CD25+FoxP3+ T cells. These findings reveal beneficial effects of GMNL-32, GMNL-89 and GMNL-263 on NZB/W F1 mice and suggest that these specific Lactobacillus strains can be used as part of a comprehensive treatment of SLE patients.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Antioxidants); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Il2ra protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-6); 0 (RNA, Messenger); 0 (Thiobarbiturates); 0 (Toll-Like Receptors); 0 (Tumor Necrosis Factor-alpha); GAN16C9B8O (Glutathione); M1YZW5SS7C (thiobarbituric acid)


  9 / 4328 MEDLINE  
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PMID:28892471
Autor:Botta D; Fuller MJ; Marquez-Lago TT; Bachus H; Bradley JE; Weinmann AS; Zajac AJ; Randall TD; Lund FE; León B; Ballesteros-Tato A
Endereço:Department of Microbiology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Título:Dynamic regulation of T follicular regulatory cell responses by interleukin 2 during influenza infection.
Fonte:Nat Immunol; 18(11):1249-1260, 2017 Nov.
ISSN:1529-2916
País de publicação:United States
Idioma:eng
Resumo:Interleukin 2 (IL-2) promotes Foxp3 regulatory T (T ) cell responses, but inhibits T follicular helper (T ) cell development. However, it is not clear how IL-2 affects T follicular regulatory (T ) cells, a cell type with properties of both T and T cells. Using an influenza infection model, we found that high IL-2 concentrations at the peak of the infection prevented T cell development by a Blimp-1-dependent mechanism. However, once the immune response resolved, some T cells downregulated CD25, upregulated Bcl-6 and differentiated into T cells, which then migrated into the B cell follicles to prevent the expansion of self-reactive B cell clones. Thus, unlike its effects on conventional T cells, IL-2 inhibits T cell responses.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Interleukin-2); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Prdm1 protein, mouse); 0 (Proto-Oncogene Proteins c-bcl-6); 0 (Transcription Factors); EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)


  10 / 4328 MEDLINE  
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PMID:28866095
Autor:Sadras T; Heatley SL; Kok CH; Dang P; Galbraith KM; McClure BJ; Muskovic W; Venn NC; Moore S; Osborn M; Revesz T; Moore AS; Hughes TP; Yeung D; Sutton R; White DL
Endereço:Cancer Theme, South Australian Health & Medical Research Institute, Adelaide, SA, Australia; Discipline of Medicine, University of Adelaide, Adelaide, SA, Australia.
Título:Differential expression of MUC4, GPR110 and IL2RA defines two groups of CRLF2-rearranged acute lymphoblastic leukemia patients with distinct secondary lesions.
Fonte:Cancer Lett; 408:92-101, 2017 Nov 01.
ISSN:1872-7980
País de publicação:Ireland
Idioma:eng
Resumo:CRLF2-rearrangements (CRLF2-r) occur frequently in Ph-like B-ALL, a high-risk ALL sub-type characterized by a signaling profile similar to Ph + ALL, however accumulating evidence indicates genetic heterogeneity within CRLF2-r ALL. We performed thorough genomic characterization of 35 CRLF2-r cases (P2RY8-CRLF2 n = 18; IGH-CRLF2 n = 17). Activating JAK2 mutations were present in 34% of patients, and a CRLF2-F232C mutation was identified in an additional 17%. IKZF1 deletions were detected in 63% of cases. The majority of patients (26/35) classified as Ph-like, and these were characterized by significantly higher levels of MUC4, GPR110 and IL2RA/CD25. In addition, Ph-like CRLF2-r samples were significantly enriched for IKZF1 deletions, JAK2/CRLF2 mutations and increased expression of JAK/STAT target genes (CISH, SOCS1), suggesting that mutation-driven CRLF2/JAK2 activation is more frequent in this sub-group. Less is known about the genomics of CRLF2-r cases lacking JAK2-pathway mutations, but KRAS/NRAS mutations were identified in 4/9 non-Ph-like samples. This work highlights the heterogeneity of secondary lesions which may arise and influence intracellular-pathway activation in CRLF2-r patients, and importantly presents distinct therapeutic targets within a group of patients harboring identical primary translocations, for whom efficient directed therapies are currently lacking.
Tipo de publicação: JOURNAL ARTICLE
Nome de substância:0 (CRLF2 protein, human); 0 (GPR110 protein, human); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (MUC4 protein, human); 0 (Mucin-4); 0 (Oncogene Proteins); 0 (Receptors, Cytokine); 0 (Receptors, G-Protein-Coupled); EC 2.7.10.2 (JAK2 protein, human); EC 2.7.10.2 (Janus Kinase 2)



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