Database : MEDLINE
Search on : Lymphocytes [Words]
References found : 454223 [refine]
Displaying: 1 .. 10   in format [Detailed]

page 1 of 45423 go to page                         

  1 / 454223 MEDLINE  
              next record last record
select
to print
Photocopy
Full text

[PMID]: 26115192
[Au] Autor:Wüthrich C; Batson S; Koralnik IJ
[Ad] Address:From the Division of Neuro-Immunology, Department of Neurology, Center for Virology and Vaccine Research, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.
[Ti] Title:Lack of Major Histocompatibility Complex Class I Upregulation and Restrictive Infection by JC Virus Hamper Detection of Neurons by T Lymphocytes in the Central Nervous System.
[So] Source:J Neuropathol Exp Neurol;74(8):791-803, 2015 Aug.
[Is] ISSN:1554-6578
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The human polyomavirus JC (JCV) infects glial cells in immunosuppressed individuals, leading to progressive multifocal leukoencephalopathy. Polyomavirus JC can also infect neurons in patients with JCV granule cell neuronopathy and JCV encephalopathy. CD8-positive T cells play a crucial role in viral containment and outcome in progressive multifocal leukoencephalopathy, but whether CD8-positive T cells can also recognize JCV-infected neurons is unclear. We used immunohistochemistry to determine the prevalence of T cells in neuron-rich areas of archival brain samples from 77 patients with JCV CNS infections and 94 control subjects. Neurons predominantly sustained a restrictive infection with expression of JCV regulatory protein T antigen (T Ag), whereas glial cells were productively infected and expressed both T Ag and the capsid protein VP1. T cells were more prevalent near JCV-infected cells with intact nuclei expressing both T Ag and VP1 compared with those expressing either protein alone. CD8-positive T cells also colocalized more with JCV-infected glial cells than with JCV-infected neurons. Major histocompatibility complex class I expression was upregulated in JCV-infected areas but could only be detected in rare neurons interspersed with infected glial cells. These results suggest that isolated neurons harboring restrictive JCV infection do not upregulate major histocompatibility complex class I and thus may escape recognition by CD8-positive T cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1097/NEN.0000000000000218

  2 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26109644
[Au] Autor:Williams JM; Bonami RH; Hulbert C; Thomas JW
[Ad] Address:Department of Pathology, Microbiology, and Immunology, Vanderbilt University, Nashville, TN 37232; and Division of Rheumatology and Immunology, Department of Medicine, Vanderbilt University, Nashville, TN 37232....
[Ti] Title:Reversing Tolerance in Isotype Switch-Competent Anti-Insulin B Lymphocytes.
[So] Source:J Immunol;195(3):853-64, 2015 Aug 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autoreactive B lymphocytes that escape central tolerance and mature in the periphery are a liability for developing autoimmunity. IgG insulin autoantibodies that predict type 1 diabetes and complicate insulin therapies indicate that mechanisms for tolerance to insulin are flawed. To examine peripheral tolerance in anti-insulin B cells, we generated C57BL/6 mice that harbor anti-insulin VDJH-125 site directed to the native IgH locus (VH125(SD)). Class switch-competent anti-insulin B cells fail to produce IgG Abs following T cell-dependent immunization of VH125(SD) mice with heterologous insulin, and they exhibit markedly impaired proliferation to anti-CD40 plus insulin in vitro. In contrast, costimulation with LPS plus insulin drives robust anti-insulin B cell proliferation. Furthermore, VH125(SD) mice produce both IgM and IgG2a anti-insulin Abs following immunization with insulin conjugated to type 1 T cell-independent Brucella abortus ring test Ag (BRT). Anti-insulin B cells undergo clonal expansion in vivo and emerge as IgM(+) and IgM(-) GL7(+)Fas(+) germinal center (GC) B cells following immunization with insulin-BRT, but not BRT alone. Analysis of Igκ genes in VH125(SD) mice immunized with insulin-BRT reveals that anti-insulin Vκ from the preimmune repertoire is selected into GCs. These data demonstrate that class switch-competent anti-insulin B cells remain functionally silent in T cell-dependent immune responses, yet these B cells are vulnerable to reversal of anergy following combined BCR/TLR engagement that promotes Ag-specific GC responses and Ab production. Environmental factors that lead to infection and inflammation could play a critical yet underappreciated role in driving loss of tolerance and promoting autoimmune disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1403114

  3 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 26053123
[Au] Autor:Blaho VA; Galvani S; Engelbrecht E; Liu C; Swendeman SL; Kono M; Proia RL; Steinman L; Han MH; Hla T
[Ad] Address:1] Center for Vascular Biology, Department of Pathology and Laboratory Medicine, Weill Medical College of Cornell University, New York, New York 10065, USA [2] Brain and Mind Research Institute, Weill Medical College of Cornell University, New York, New York 10065, USA....
[Ti] Title:HDL-bound sphingosine-1-phosphate restrains lymphopoiesis and neuroinflammation.
[So] Source:Nature;523(7560):342-6, 2015 Jul 16.
[Is] ISSN:1476-4687
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Lipid mediators influence immunity in myriad ways. For example, circulating sphingosine-1-phosphate (S1P) is a key regulator of lymphocyte egress. Although the majority of plasma S1P is bound to apolipoprotein M (ApoM) in the high-density lipoprotein (HDL) particle, the immunological functions of the ApoM-S1P complex are unknown. Here we show that ApoM-S1P is dispensable for lymphocyte trafficking yet restrains lymphopoiesis by activating the S1P1 receptor on bone marrow lymphocyte progenitors. Mice that lacked ApoM (Apom(-/-)) had increased proliferation of Lin(-) Sca-1(+) cKit(+) haematopoietic progenitor cells (LSKs) and common lymphoid progenitors (CLPs) in bone marrow. Pharmacological activation or genetic overexpression of S1P1 suppressed LSK and CLP cell proliferation in vivo. ApoM was stably associated with bone marrow CLPs, which showed active S1P1 signalling in vivo. Moreover, ApoM-bound S1P, but not albumin-bound S1P, inhibited lymphopoiesis in vitro. Upon immune stimulation, Apom(-/-) mice developed more severe experimental autoimmune encephalomyelitis, characterized by increased lymphocytes in the central nervous system and breakdown of the blood-brain barrier. Thus, the ApoM-S1P-S1P1 signalling axis restrains the lymphocyte compartment and, subsequently, adaptive immune responses. Unique biological functions imparted by specific S1P chaperones could be exploited for novel therapeutic opportunities.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/nature14462

  4 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25995259
[Au] Autor:Gombos RB; Kolodkin-Gal D; Eslamizar L; Owuor JO; Mazzola E; Gonzalez AM; Korioth-Schmitz B; Gelman RS; Montefiori DC; Haynes BF; Schmitz JE
[Ad] Address:Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA rgombos@outlook.com....
[Ti] Title:Inhibitory Effect of Individual or Combinations of Broadly Neutralizing Antibodies and Antiviral Reagents against Cell-Free and Cell-to-Cell HIV-1 Transmission.
[So] Source:J Virol;89(15):7813-28, 2015 Aug 1.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: To date, most therapeutic and vaccine candidates for human immunodeficiency virus type 1 (HIV-1) are evaluated preclinically for efficacy against cell-free viral challenges. However, cell-associated HIV-1 is suggested to be a major contributor to sexual transmission by mucosal routes. To determine if neutralizing antibodies or inhibitors block cell-free and cell-associated virus transmission of diverse HIV-1 strains with different efficiencies, we tested 12 different antibodies and five inhibitors against four green fluorescent protein (GFP)-labeled HIV-1 envelope (Env) variants from transmitted/founder (T/F) or chronic infection isolates. We evaluated antibody/inhibitor-mediated virus neutralization using either TZM-bl target cells, in which infectivity was determined by virus-driven luciferase expression, or A3R5 lymphoblastoid target cells, in which infectivity was evaluated by GFP expression. In both the TZM-bl and A3R5 assays, cell-free virus or infected CD4(+) lymphocytes were used as targets for neutralization. We further hypothesized that the combined use of specific neutralizing antibodies targeting HIV-1 Env would more effectively prevent cell-associated virus transmission than the use of individual antibodies. The tested antibody combinations included two gp120-directed antibodies, VRC01 and PG9, or VRC01 with the gp41-directed antibody 10E8. Our results demonstrated that cell-associated virus was less sensitive to neutralizing antibodies and inhibitors, particularly using the A3R5 neutralization assay, and the potencies of these neutralizing agents differed among Env variants. A combination of different neutralizing antibodies that target specific sites on gp120 led to a significant reduction in cell-associated virus transmission. These assays will help identify ideal combinations of broadly neutralizing antibodies to use for passive preventive antibody administration and further characterize targets for the most effective neutralizing antibodies/inhibitors. IMPORTANCE: Prevention of the transmission of human immunodeficiency virus type 1 (HIV-1) remains a prominent goal of HIV research. The relative contribution of HIV-1 within an infected cell versus cell-free HIV-1 to virus transmission remains debated. It has been suggested that cell-associated virus is more efficient at transmitting HIV-1 and more difficult to neutralize than cell-free virus. Several broadly neutralizing antibodies and retroviral inhibitors are currently being studied as potential therapies against HIV-1 transmission. The present study demonstrates a decrease in neutralizing antibody and inhibitor efficiencies against cell-associated compared to cell-free HIV-1 transmission among different strains of HIV-1. We also observed a significant reduction in virus transmission using a combination of two different neutralizing antibodies that target specific sites on the outermost region of HIV-1, the virus envelope. Therefore, our findings support the use of antibody combinations against both cell-free and cell-associated virus in future candidate therapy regimens.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1128/JVI.00783-15

  5 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 26011633
[Au] Autor:van der Meer E; van Oers K
[Ad] Address:Department of Animal Ecology, Netherlands Institute of Ecology (NIOO-KNAW), Wageningen, The Netherlands; Cheetah Conservation Project Zimbabwe, Victoria Falls, Zimbabwe.
[Ti] Title:Gender and Personality Differences in Response to Social Stressors in Great Tits (Parus major).
[So] Source:PLoS One;10(5):e0127984, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In response to stressors, animals can increase the activity of the hypothalamic-pituitary-adrenocortical axis, resulting in elevated glucocorticoid concentrations. An increase in glucocorticoids results in an increase in heterophils and a decrease in lymphocytes, which ratio (H/L-ratio) is an indicator of stress in birds. The physiological response to a stressor can depend on individual characteristics, like dominance rank, sex and personality. Although the isolated effects of these characteristics on the response to a stressor have been well studied, little is known about the response in relation to a combination of these characteristics. In this study we investigate the relationship between social stress, dominance rank, sex and exploratory behaviour as a validated operational measure of personality in great tits (Parus major). Great tits show consistent individual differences in behaviour and physiology in response to stressors, and exploratory behaviour can be classified as fast or slow exploring. We group-housed four birds, two fast and two slow explorers, of the same sex that were previously singly housed, in an aviary and compared the H/L-ratio, lymphocyte and heterophil count before and after group housing. After experiencing the social context all birds increased their H/L-ratio and heterophil count. Females showed a stronger increase in H/L-ratio and heterophil count than males, which seemed to be related to a higher number of agonistic interactions compared to males. Dominance rank and exploration type did not affect the H/L-ratio or heterophil count. Contrary to our expectations, all birds increased their lymphocyte count. However, this increase was slower for fast than for slow explorers. Our study suggests that personality and sex related differences, but not dominance rank, are associated with changes in an individual's physiological response due to a social context.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150617
[Lr] Last revision date:150617
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0127984

  6 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 25992777
[Au] Autor:Chen M; McReynolds N; Campbell EC; Mazilu M; Barbosa J; Dholakia K; Powis SJ
[Ad] Address:SUPA, School of Physics and Astronomy, University of St Andrews, Fife, KY16 9SS, United Kingdom....
[Ti] Title:The use of wavelength modulated Raman spectroscopy in label-free identification of T lymphocyte subsets, natural killer cells and dendritic cells.
[So] Source:PLoS One;10(5):e0125158, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Determining the identity of cells of the immune system usually involves destructive fixation and chemical staining, or labeling with fluorescently labeled antibodies recognising specific cell surface markers. Completely label-free identification would be a significant advantage in conditions where untouched cells are a priority. We demonstrate here the use of Wavelength Modulated Raman Spectroscopy, to achieve label-free identification of purified, unfixed and untouched populations of major immune cell subsets isolated from healthy human donors. Using this technique we have been able to distinguish between CD4(+) T lymphocytes, CD8(+) T lymphocytes and CD56(+) Natural Killer cells at specificities of up to 96%. Additionally, we have been able to distinguish between CD303(+) plasmacytoid and CD1c(+) myeloid dendritic cell subsets, the key initiator and regulatory cells of many immune responses. This demonstrates the ability to identify unperturbed cells of the immune system, and opens novel opportunities to analyse immunological systems and to develop fully label-free diagnostic technologies.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1505
[Cu] Class update date: 150530
[Lr] Last revision date:150530
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0125158

  7 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 25993480
[Au] Autor:Figueroa-Vega N; Moreno-Frías C; Malacara JM
[Ad] Address:Department of Medical Sciences, University of Guanajuato, León campus, León, Gto., México.
[Ti] Title:Alterations in adhesion molecules, pro-inflammatory cytokines and cell-derived microparticles contribute to intima-media thickness and symptoms in postmenopausal women.
[So] Source:PLoS One;10(5):e0120990, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Menopause, the cessation of menses, occurs with estrogens decline, low-grade inflammation, and impaired endothelial function, contributing to atherosclerotic risk. Intima-media thickness (IMT) is an early subclinical biomarker of atherosclerosis. Inflammation may have a role on symptoms: hot flashes, anxiety, and depressive mood, which also are related to endothelial dysfunction, increased IMT and cardiovascular risk. In this study we compared several inflammatory markers in early vs. late postmenopausal women and studied the association of IMT and symptoms with these markers in the full sample. In a cross-sectional design including 60 women (53.1 ± 4.4 years old) at early and late postmenopause, we evaluated the expression of CD62L, ICAM-1, PSGL-1, CD11b, CD11c, and IL-8R on PBMC by flow cytometry. Serum soluble ICAM-1, sVCAM-1, sCD62E, sCD62P, CXCL8, IL-1ß, IL-6, and TNF-α levels were quantified by ELISA. Plasma levels of microparticles (MPs) were determined by FACS. Finally, carotid intima-media thickness (IMT) was measured by ultrasound. We observed that ICAM-1 expression by lymphocytes and serum sVCAM-1 levels were augmented at late postmenopause. Late postmenopause women with severe hot flashes had increased expression of CD62L and IL-8R on neutrophils. By multivariate analysis, the carotid IMT was strongly associated with membrane-bound TNF-α, CD11b expression, Annexin V(+) CD3(+) MPs, LPS-induced NO production, HDL-cholesterol and age. Depressive mood was associated negatively with PSGL-1 and positively with LPS-induced NO. Finally, Log(AMH) levels were associated with carotid IMT, IL-8R expression and time since menopause. IMT and depressive mood were the main clinical features related to vascular inflammation. Aging, hormonal changes and obesity were also related to endothelial dysfunction. These findings provide further evidence for a link between estrogen deficiency and low-grade inflammation in endothelial impairment in mature women.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1505
[Cu] Class update date: 150530
[Lr] Last revision date:150530
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0120990

  8 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
PubMed Central Full text
Full text

[PMID]: 25992581
[Au] Autor:Squires JE; Shivakumar P; Mourya R; Bessho K; Walters S; Bezerra JA
[Ad] Address:Department of Pediatrics of the University of Cincinnati College of Medicine, the Division of Gastroenterology, Hepatology and Nutrition and the Pediatric Liver Care Center of Cincinnati Children's Hospital Medical Center; Cincinnati, Ohio, United States of America....
[Ti] Title:Natural killer cells promote long-term hepatobiliary inflammation in a low-dose rotavirus model of experimental biliary atresia.
[So] Source:PLoS One;10(5):e0127191, 2015.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Biliary atresia is a rapidly progressive obstructive cholangiopathy of infants. Mechanistic studies in the mouse model of Rhesus rotavirus (RRV)-induced biliary atresia have linked the importance of effector lymphocytes to the pathogenesis of extrahepatic bile duct (EHBD) injury and obstruction in experimental biliary atresia; however, studies of the progressive liver injury have been limited by early death of newborn mice. Here, we aimed to determine 1) if a lower inoculum of RRV induces obstruction of EHBDs while allowing for ongoing liver inflammation, and 2) if NK cells regulate intrahepatic injury. The administration of 0.25 x 10(6) fluorescence forming units of RRV induced an obstructive extrahepatic cholangiopathy, but allowed for restoration of the duct epithelium, increased survival, and the development of a progressive intrahepatic inflammatory injury with molecular and cellular signatures equivalent to the traditional infectious model. Investigating the mechanisms of liver injury, we found that NK cell depletion at the onset of jaundice decreased liver inflammation, suppressed the expression of fibrosis and inflammation/immunity genes, lowered plasma ALT and bilirubin and improved survival. CONCLUSIONS: Lower inoculation of RRV-induced progressive liver injury and fibrosis via NK cells. These findings point to the potential use of NK cell-depleting strategies to block progression of liver disease in biliary atresia.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1505
[Cu] Class update date: 150530
[Lr] Last revision date:150530
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1371/journal.pone.0127191

  9 / 454223 MEDLINE  
              first record previous record next record last record
select
to print
Photocopy
Full text

[PMID]: 25799995
[Au] Autor:Chen Z; Shojaee S; Buchner M; Geng H; Lee JW; Klemm L; Titz B; Graeber TG; Park E; Tan YX; Satterthwaite A; Paietta E; Hunger SP; Willman CL; Melnick A; Loh ML; Jung JU; Coligan JE; Bolland S; Mak TW; Limnander A; Jumaa H; Reth M; Weiss A; Lowell CA; Müschen M
[Ad] Address:Department of Laboratory Medicine, University of California, San Francisco, California 94143, USA....
[Ti] Title:Signalling thresholds and negative B-cell selection in acute lymphoblastic leukaemia.
[So] Source:Nature;521(7552):357-61, 2015 May 21.
[Is] ISSN:1476-4687
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:B cells are selected for an intermediate level of B-cell antigen receptor (BCR) signalling strength: attenuation below minimum (for example, non-functional BCR) or hyperactivation above maximum (for example, self-reactive BCR) thresholds of signalling strength causes negative selection. In ∼25% of cases, acute lymphoblastic leukaemia (ALL) cells carry the oncogenic BCR-ABL1 tyrosine kinase (Philadelphia chromosome positive), which mimics constitutively active pre-BCR signalling. Current therapeutic approaches are largely focused on the development of more potent tyrosine kinase inhibitors to suppress oncogenic signalling below a minimum threshold for survival. We tested the hypothesis that targeted hyperactivation--above a maximum threshold--will engage a deletional checkpoint for removal of self-reactive B cells and selectively kill ALL cells. Here we find, by testing various components of proximal pre-BCR signalling in mouse BCR-ABL1 cells, that an incremental increase of Syk tyrosine kinase activity was required and sufficient to induce cell death. Hyperactive Syk was functionally equivalent to acute activation of a self-reactive BCR on ALL cells. Despite oncogenic transformation, this basic mechanism of negative selection was still functional in ALL cells. Unlike normal pre-B cells, patient-derived ALL cells express the inhibitory receptors PECAM1, CD300A and LAIR1 at high levels. Genetic studies revealed that Pecam1, Cd300a and Lair1 are critical to calibrate oncogenic signalling strength through recruitment of the inhibitory phosphatases Ptpn6 (ref. 7) and Inpp5d (ref. 8). Using a novel small-molecule inhibitor of INPP5D (also known as SHIP1), we demonstrated that pharmacological hyperactivation of SYK and engagement of negative B-cell selection represents a promising new strategy to overcome drug resistance in human ALL.
[Mh] MeSH terms primary: B-Lymphocytes/metabolism
B-Lymphocytes/pathology
Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism
Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology
Signal Transduction
[Mh] MeSH terms secundary: Amino Acid Motifs/genetics
Animals
Antigens, CD/metabolism
Antigens, CD31/metabolism
B-Lymphocytes/drug effects
Cell Death/drug effects
Cell Line, Tumor
Cell Transformation, Neoplastic
Disease Models, Animal
Drug Resistance, Neoplasm/drug effects
Enzyme Activation/drug effects
Female
Fusion Proteins, bcr-abl/genetics
Gene Deletion
Humans
Intracellular Signaling Peptides and Proteins/agonists
Intracellular Signaling Peptides and Proteins/metabolism
Mice
Mice, Inbred NOD
Mice, SCID
Phosphoric Monoester Hydrolases/antagonists & inhibitors
Phosphoric Monoester Hydrolases/metabolism
Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug therapy
Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics
Precursor Cells, B-Lymphoid/drug effects
Precursor Cells, B-Lymphoid/metabolism
Precursor Cells, B-Lymphoid/pathology
Protein Tyrosine Phosphatase, Non-Receptor Type 6/deficiency
Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics
Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism
Protein-Tyrosine Kinases/metabolism
Receptors, Antigen, B-Cell/deficiency
Receptors, Antigen, B-Cell/genetics
Receptors, Antigen, B-Cell/metabolism
Receptors, Immunologic/genetics
Receptors, Immunologic/metabolism
Signal Transduction/drug effects
Tyrosine/metabolism
Xenograft Model Antitumor Assays
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antigens, CD); 0 (Antigens, CD31); 0 (CD300A protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (Receptors, Antigen, B-Cell); 0 (Receptors, Immunologic); 0 (leukocyte-associated immunoglobulin-like receptor 1); 42HK56048U (Tyrosine); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (Syk kinase); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.1.3.- (Phosphoric Monoester Hydrolases); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 6); EC 3.1.3.48 (Ptpn6 protein, mouse); EC 3.1.3.56 (inositol-polyphosphate 5-phosphatase)
[Em] Entry month:1507
[Cu] Class update date: 150718
[Lr] Last revision date:150718
[Js] Journal subset:IM
[Da] Date of entry for processing:150521
[St] Status:MEDLINE
[do] DOI:10.1038/nature14231

  10 / 454223 MEDLINE  
              first record previous record
select
to print
Photocopy
Full text

[PMID]: 25698348
[Au] Autor:Ghosh S; Hoselton SA; Wanjara SB; Carlson J; McCarthy JB; Dorsam GP; Schuh JM
[Ad] Address:Department of Veterinary and Microbiological Sciences, North Dakota State University, Fargo, ND 58108, USA. Electronic address: Sumit.Ghosh@ndsu.edu....
[Ti] Title:Hyaluronan stimulates ex vivo B lymphocyte chemotaxis and cytokine production in a murine model of fungal allergic asthma.
[So] Source:Immunobiology;220(7):899-909, 2015 Jul.
[Is] ISSN:1878-3279
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Allergic asthma is a chronic inflammatory disease of the airways characterized by excessive eosinophilic and lymphocytic inflammation with associated changes in the extracellular matrix (ECM) resulting in airway wall remodeling. Hyaluronan (HA) is a nonsulfated glycosaminoglycan ECM component that functions as a structural cushion in its high molecular mass (HMM) but has been implicated in metastasis and other disease processes when it is degraded to smaller fragments. However, relatively little is known about the role HA in mediating inflammatory responses in allergy and asthma. In the present study, we used a murine Aspergillus fumigatus inhalational model to mimic human disease. After observing in vivo that a robust B cell recruitment followed a massive eosinophilic egress to the lumen of the allergic lung and corresponded with the detection of low molecular mass HA (LMM HA), we examined the effect of HA on B cell chemotaxis and cytokine production in the ex vivo studies. We found that LMM HA functioned through a CD44-mediated mechanism to elicit chemotaxis of B lymphocytes, while high molecular mass HA (HMM HA) had little effect. LMM HA, but not HMM HA, also elicited the production of IL-10 and TGF-ß1 in these cells. Taken together, these findings demonstrate a critical role for ECM components in mediating leukocyte migration and function which are critical to the maintenance of allergic inflammatory responses.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1505
[Cu] Class update date: 150523
[Lr] Last revision date:150523
[Js] Journal subset:IM
[St] Status:In-Process


page 1 of 45423 go to page                         
   


Refine the search
  Database : MEDLINE Advanced form   

    Search in field  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/PAHO/WHO - Latin American and Caribbean Center on Health Sciences Information