Viewing affirmative mentions of gene expression of HLA-DRB1 (H. sapiens) in T cells

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Auger et al. (1998)HLA-DRB1T cellThis may cause abnormal trafficking of HLA-DRB1*0401 in B cells and/or abnormal T cell responses to bacterial and human 70 kD heat shock proteins in people who express HLA-DRB1*0401.
MacDonald and Spencer (1990)HLA-DRT cellExperimental studies have shown that T cell activation in human intestinal lamina propria in vitro produces an increase in crypt cell proliferation, villous atrophy, increased HLA-DR expression on enterocytes, increased intraepithelial lymphocyte numbers, and, phenotypically, macrophage activation.
Volpé (1988)HLA-DRT lymphocytesPresentation of the antigen by the thyroid cell via HLA-DR expression on its membrane does occur as a result of interferon gamma production by T lymphocytes.
McMillan et al. (1981)HLA DRT cellsEvidence is accumulating that HLA DR positivity may be expressed by activated T cells.
Mizrachi et al. (1982)DRwT lymphocytesThe results indicated that: 1) compared with peripheral blood, the expression of the major histocompatibility gene products is enhanced by adenoid lymphocytes; 2) adenoid T lymphocytes express DRw antigens.
Spinola et al. (1994)HLA-DRT cellsKeratinocytes and T cells expressed HLA-DR, consistent with a delayed-type hypersensitivity response.
Valnes et al. (1990)HLA-DRT cellCorrelation analyses showed a positive relation between the epithelial expression of HLA-DR and the intraepithelial as well as the lamina propria density of T cell.
Valnes et al. (1990)HLA-DRT cellsThese results suggest a biological link between T cells, aberrant HLA-DR expression, and gastritis, although the pathogenic importance of this relation is unknown.
Saha et al. (1999)HLA-DRT-cellParasite exposed T-cell blasts had a reduced surface expression of HLA-DR and were lysed by the sorted CD56+ cells.
Tsakalos et al. (1984)HLA-DRT-cellThe abilities of human monocytes differentially expressing HLA-DR and of lipopolysaccharide (LPS) to influence T-cell colony responses were investigated.
Edelstam and Karlsson-Parra (1996)HLA-DRT-lymphocytesIn some biopsies from sactosalpinx, the HLA-DR expression was found completely to cover the columnar epithelial cells and was associated with a heavy infiltration of T-lymphocytes.
Demidem et al. (1986)HLA-DRT lymphocytesThese studies present evidence that when human epidermal cells are grown in culture, they loose both the ability to stimulate the proliferation of allogeneic T lymphocytes in vitro and their expression of HLA-DR and T6 antigens.
Younes et al. (1991)HLA-DRT lymphocytesThe lack of HLA-DR and IL-2R expression by CMV-infected T lymphocytes may be one of the mechanism by which CMV causes immunosuppression.
Rizova et al. (1994)HLA-DRT lymphocytesAntigen presentation involves the interaction between the class II molecules of MHC (HLA-DR) expressed by LC and T receptor of CD4+ T lymphocytes.
Hirata et al. (1986)HLA-DRT cellsOnly small numbers of lamina propria T cells expressed HLA-DR in both control and disease tissues.
Rönnblom et al. (1986)HLA-DRT lymphocyteIntralesional T lymphocyte phenotypes and HLA-DR expression in Melkersson-Rosenthal syndrome.
Jansson et al. (1984)HLA-DRT lymphocyteIntrathyroidal HLA-DR expression and T lymphocyte phenotypes in Graves' thyrotoxicosis, Hashimoto's thyroiditis and nodular colloid goitre.
Sumiyoshi et al. (1999)HLA-DRT cellIn areas of dysplasia and intraepithelial carcinoma, T cell infiltration was significantly increased at the sites of HLA-DR antigen expression (P<0.01).
Gascón et al. (1984)HLA-DRT cellsThe role of chronic antigenic stimulation was studied by measurement of HLA-DR expression on T cells.
Hoffman et al. (2001)HLA-DRT-lymphocytesFive of the six patients showed an increased percentage of activated T-lymphocytes based on the expression of HLA-DR at 24 h of treatment when compared to the admission percentage of activation (P<.05).
Mustafa et al. (1999)HLA-DRB1T cellsMajor histocompatibility complex restriction analysis showed that presentation of 9 of the 12 peptides to T cells were restricted by one of the 2 HLA-DR molecules expressed from self HLA-DRB1 genes, whereas 3 peptides with sequences completely identical between the M. leprae and M. tuberculosis HSP65 were presented to T cells by multiple HLA-DR molecules: peptide (aa 61 to 75) was presented by HLA-DR1, -DR2, and -DR7, peptide (aa 141 to 155) was presented by HLA-DR2, -DR7, and -DR53, whereas both HLA-DR2 and -DR4 (Dw4 and Dw14) were able to present peptide (aa 501 to 515) to T cells.
Börgermann et al. (2007)HLA-DRT-lymphocytesNeither HLA-DR expression on B- and T-lymphocytes nor the effects of GM-CSF in cardiac surgical patients have been studied before.
Börgermann et al. (2007)HLA-DRT-cellsIn contrast, HLA-DR expression on T-cells was unchanged, whereas HLA-DR expression on B-cells did not decrease before the 2nd day after CPB (152 +/- 3 MCF vs. 170 +/- 2 MCF preoperatively, P < 0.001).
Tabibzadeh et al. (1993)HLA-DRT cellsT cells bound to the ECC1 cells, and became activated as indicated by the expression of interleukin (IL)-2 receptor and HLA-DR molecules.
Tabibzadeh et al. (1993)HLA-DRT cellsA focal HLA-DR expression became apparent in the ECC1 cells adjacent to the T cells.
Biancotto et al. (2008)HLA-DRT cellsIn these tissues, apoptosis was selectively increased in T cells expressing CD25/HLA-DR and p24gag but not in cells expressing either of these markers alone.
Sadanaga et al. (1994)HLA-DRT-cellT-cell infiltration was significantly recognized at the area of HLA-DR antigen expression at the sites of both intraepithelial carcinoma and tumor invasion.
Chu et al. (1983)DR5T cellMonocytes that expressed either one of the two maternal DR antigens (HLA-DR3 and DR5) could support the proliferation of the patient's T cell lines in response to TT antigen.
Maloney et al. (1995)HLA-DRT cellHTLV-I seropositivity was associated with an increase in the mean percentage of CD4 cells expressing HLA-DR, a marker for T cell activation (P = .02).
Suciu-Foca et al. (1982)HLA-DRT cellsWe have demonstrated that activation of AMLR by allosensitized T cells is determined by the expression of the idiotype receptor for the stimulating HLA-DR alloantigen.
Balbi et al. (1993)HLA-DRT-cellWe investigated the effects of the cytokines released in cultures with TMD, on the expression of human leucocyte antigen-DR (HLA-DR) antigens by alveolar macrophages (AM) and the T-cell proliferation induced in autologous mixed leucocyte reaction (AMLR) cultures or by T-cell mitogens.
Jendro et al. (1991)HLA-DRT lymphocytesThe expression and secretion of HLA-DR by T lymphocytes is greatly enhanced in the presence of macrophages indicating that the production of HLA-DR molecules might be regulated and controlled through factors derived from antigen-presenting cells.
Saifuddin et al. (1998)HLA-DRT-cellTransfer of host T-cell membrane HLA-DR and CD25 to target cells by human retroviruses.
Roncalli et al. (1988)HLA-DRT lymphocytesThis study suggests that several phenotypes of intraepithelial dendritic cells are present in the transformation zone and that endocervical columnar cells and keratinocytes of squamous metaplasia express HLA-DR products; the latter finding may be related to the presence of intraepithelial and stromal T lymphocytes.
Miyawaki et al. (1984)HLA-DRT cellsAlthough cord blood T cells showed only weak expression of HLA-DR antigens on PWM stimulation, IFN-gamma could enhance HLA-DR expression of PWM-stimulated cord blood T cells to levels comparable to those of adult ones.
Miyawaki et al. (1984)HLA-DRT cellsA similar, but slight, increase in HLA-DR expression was inducible in PWM-stimulated adult T cells by the addition of IFN-gamma, but at higher doses.
Miyawaki et al. (1984)HLA-DrT cellsThis increased expression of HLA-Dr antigens on PWM-stimulated T cells was almost completely abolished by both acid treatment of IFN-gamma and neutralization of IFN-gamma with specific antiserum.
Miyawaki et al. (1984)HLA-DRT cellsIn contrast to IFN-gamma, neither recombinant IFN-alpha nor IFN-beta showed any effect on HLA-DR expression of PWM-stimulated T cells.
Miyawaki et al. (1984)HLA-DRT cellsThese results suggested a possible function of IFN-gamma that might modulate HLA-DR expression ability of T cells in their activation process.
Seo et al. (2002)HLA-DRT cellsCryopreserved Langerhans cells expressed high levels of HLA-DR and CD1a antigens and stimulated autologous T cells to an extent almost identical to that obtained from fresh Langerhans cells.
Igarashi et al. (1987)HLA-DRT cellDifferential expression of HLA-DR allospecificities on antigen specific T cell clones.
Kestens et al. (1992)HLA-DRT-lymphocyteSimultaneous expression of HLA-DR and CD38 within the CD8 T-lymphocyte compartment increased from 8% in controls to 49% in asymptomatic HIV-infected subjects (P less than 0.005).
Kestens et al. (1992)HLA-DRT-lymphocytesCONCLUSION: There is a stage-associated pattern of HLA-DR and CD38 expression on CD8 T-lymphocytes during HIV infection; specific phenotypic patterns may have functional correlates in the host response to the virus.
Shakoor (2003)HLA-DRT-lymphocytesOBJECTIVE: Immune activation often associated with human immunodeficiency virus (HIV) infection is characterized by increasing number of peripheral blood T-lymphocytes expressing HLA-DR molecule.
Shakoor (2003)HLA-DRT-lymphocytesOver a period of 2-5 years the percentage of T-lymphocytes, expressing HLA-DR molecule was found to have decreased significantly (P < or =0.0001) in all the patients most probably as a result of antiretroviral therapy.
Ko et al. (1979)HLA-DRT cellsWhen the specificities of the Ia antigens on T-cell blasts were examined with alloantiserums, it was evident that the T blasts expressed similar HLA-DR determinants to those on B cells from the same donor; occasional minor differences between stimulated T cells and autologous B-cell lines or fresh B cells were encountered.
Kaweski et al. (1981)DRwT cellsThese results indicated that DRw antigens are present in the subpopulation of T cells which may expand in the response to Con-A stimulation.
Matsuzaki et al. (1989)HLA-DRT cellsThe reduced responses of cord T cells were due to their lower efficiency in activating the cellular events in T cell activation and proliferation phase, because cord T cells have significantly less ability than adult T cells to express IL-2 receptor as well as HLA-DR and produce IL-2 molecules, thereby inducing proliferation.
Turesson et al. (2005)DRB1T cellsThe association between HLA-DRB1 genotypes and RA disease severity, including ExRA, has been interpreted as reflecting the importance of T cells in the pathogenesis of RA [26].
Li et al. (1998)DRB1T cellsHLA-DR-matched normal donors' T cells were cultured with peptide-pulsed artificial antigen-presenting cells (CHO cells cotransfected with genes for HLA-DRB1*0401 and CD80 and coexpressing high levels of both human molecules).
Zhang et al. (2006)HLA-DRT cellOBJECTIVE: The study was designed to investigate the changes in CD(69), CD(25) and HLA-DR expressions in peripheral blood T cell in Kawasaki disease (KD).
Zhang et al. (2006)HLA-DRT cellMETHODS: The authors detected CD(69), CD(25) and HLA-DR expressions in peripheral blood T cell by using flow cytometry.
Thorsby et al. (1983)HLA-DRT cellsAlloantisera to DR specificities shared between antigen presenting cells (APC) and T cells displayed a strong inhibitory activity: alloantisera to HLA-DR specificities expressed only by APC or the T cell donor displayed lower or no inhibitory activity.
Wollman et al. (1980)HLA-DRT lymphocytes[Kinetics of the appearance of HLA-DR antigens on human alloactivated T lymphocytes and the demonstration of new antigenic determinants].
Pawelec et al. (1982)HLA-DRT lymphocytesAlloactivated long-term cultured human T lymphocytes express both HLA-DR and SB antigens but lack lymphocyte stimulation capacity.
Pawelec et al. (1982)HLA-DRT lymphocytesThese data show that the activated T lymphocytes which express both HLA-DR and SB antigens are by themselves unable to stimulate lymphocyte proliferation.
Ramagopalan et al. (2009)DRB1T cellsGiven the results of this study, variable expression of HLA-DRB1 could affect central deletion of autoreactive T cells.
Rastogi et al. (2007)DRB1T cellsUsing MHC tetramers, HA-specific CD4(+) T cells were detected among 25.0% (3 of 12) and 42.9% (6 of 14) of cord blood specimens possessing DRB1*0101 and DRB1*0401 HLA types, respectively, and were detected even when the DRB1 HLA type was inherited from the father.
Eljaafari et al. (1992)HLA-DRT cellsOur results further establish that human activated T cells expressing HLA-DR molecules can present Ag to and be lysed by CD4+ HLA-DR restricted CTLs.
Eljaafari et al. (1992)HLA-DRTTCsHowever, we find that in our model: (a) TTCs are able to present artificially processed peptidic fragments of Ag, but not the corresponding natural Ag in the context of class II determinants, even if they can process whole virus in the context of class I determinants; (b) TTCs must express high density of HLA-DR molecules on their membrane; (c) preincubation of TTCs with high concentrations of peptide is required; and (d) interestingly enough, addition of free peptide at similar concentration during the cytolytic assay to replace TTC preincubation inhibits TTC lysis by at least two different mechanisms, i.e., cold-target inhibition in which CTLs serve as their own cold targets and inhibition at the effector cell level.
Volpé (1991)HLA-DRT lymphocytesPresentation of the antigen by the thyroid cell via HLA-DR expression on its cell membrane does occur as a result of IFN-gamma production by T lymphocytes.
Ito et al. (1993)DRB1T cellsThe study implied that gene products of DRB1*0406, DQA1*0301, and/or DQB1*0302 may be involved in the presentation of human insulin to T cells.
Ito et al. (1993)DRB1T cellsUsing DRB1*0406-transfected L cells as APC, we confirmed that these T cells clones recognize human insulin in the context of gene products of DRB1*0406.
Ito et al. (1993)DRB1T cellsOur recent study indicated that all the insulin autoimmune syndrome (IAS) patients had specific HLA class II alleles, the DRB1*0406, DQA1*0301, and DQB1*0302, which allowed T cells to proliferate when autologous APC were exposed to human insulin.
Boorstein et al. (1994)HLA-DRT-lymphocyteAberrant cellular expression of HLA-DR and intercellular adhesion molecule-1 (ICAM-1), both of which are necessary for optimal antigen-induced T-lymphocyte responses, is present in lesions of HSK, but little is known concerning endogenous cytokines that may inhibit HLA-DR or ICAM-I expression in human disease.
Uibo and Lernmark (2008)DRB1T cellsAnalyses of T cells with HLA DRB1 0401-tetramers with GAD65-specific peptides as well as of anti-idiotypic GAD65 autoantibodies suggest that GAD65 autoreactivity is common.
Masewicz et al. (2001)DRB1T cellThe majority of T cell responses were restricted by DRB1 molecules; however, DRB4 restricted responses were also observed.
Geisler et al. (1990)anti-HLA-DRT-cellWe have analysed the capacity of HUT.78 cells (1) to stimulate HLA-DR-specific T-cell lines or clones and (2) to be induced to synthesize IL-2 by anti-HLA-DR monoclonal antibodies.
McGeer et al. (1987)HLA-DRT-lymphocytesHLA-DR is a class II cell surface glycoprotein of the human histocompatibility complex usually expressed on the surface of cells that are simultaneously presenting foreign antigen to T-lymphocytes.
Sellebjerg et al. (2000)HLA-DRT-cellsTreatment resulted in a decrease in the concentration of myelin basic protein, a decrease in the serum concentration of immunoglobulin G (IgG) and intrathecal IgG synthesis, an increase in the cerebrospinal fluid concentration of transforming growth factor-beta1, and changes in the expression of CD25, CD26, and human leukocyte antigen-DR (HLA-DR) on CD4 T-cells.
Santoli et al. (1986)HLA-DRT cellImmunofluorescence analysis performed with a panel of monoclonal antibodies (mAb) specific for HLA-DR or -DQ antigens did not reveal any significant difference in the expression of HLA-DR antigens but revealed reduced expression of HLA-DQ antigens on two out of four T cell lines tested.
Jalleh et al. (1993)HLA-DRT-lymphocytesAs expression of major histocompatibility (MHC) antigens is a prerequisite for organ specific autoimmunity, the expression of HLA class I (beta 2-microglobulin) and class II (HLA-DR) determinants have been analysed, together with the presence of T-lymphocytes, in 93 patients (64 men and 29 women, mean age 40.6 years) having an operation for chronic pancreatitis.
Fujita et al. (1998)HLA-DRB1T cellThe DRB1*1401-restricted T cell clone specific for p193-204 killed a B lymphoblastoid cell line homozygous for HLA-DRB1*1401 when the cell line was pre-pulsed with p53 protein as well as peptide.
Miyawaki et al. (1984)HLA-DRT lymphocytesInterferon-gamma can augment expression ability of HLA-DR antigens on pokeweed mitogen-stimulated human T lymphocytes.
Osusky et al. (1997)HLA-DRT lymphocytesRetinal pigment epithelial (RPE) cells induced to express MHC class II (HLA-DR) by incubation with interferon gamma (IFN-gamma) were investigated for their ability to present a microbial superantigen to T lymphocytes.
Parkhurst et al. (2003)HLA-DR beta 1T cellDC-888mel hybrids also presented HLA-DR beta 1*0401- and HLA-DR beta 1*0701-restricted peptides from gp100 to CD4(+) T cell populations.
Vayuvegula et al. (1990)HLA-DRT cellsParaformaldehyde-fixed monocytes pulsed with anti-CD3 MoAb induced significantly less DNA synthesis, HLA-DR expression, and CD25 antigen expression on autologous T cells as compared to responses induced by unfixed anti-CD3-pulsed monocytes.
Bosch et al. (1996)HLA-DRB1T-cellHLA DR4 (DRB1*0401) restricted T-cell line P4 and several subsequently derived clones recognized HLA-DRB1*0401 and p210b3a2-mRNA expressing blasts from an allogeneic patient with CML in blast crisis.
Mann and Sharrow (1980)DRwT lymphocytesHLA-DRw alloantigens can be detected on peripheral blood T lymphocytes.
Dudek et al. (2007)DRB1T cellT cell epitopes of the La/SSB autoantigen in humanized transgenic mice expressing the HLA class II haplotype DRB1*0301/DQB1*0201.
Vlassopoulos (2003)DRB1T-cellHepatitis B vaccination non-responders express increased levels of HLA class II alleles (T-cell immune response modulators) DRB1 01 (DR1) and DRB1 15 (DR15).
Madsen et al. (1999)DRB1T-cellIn transgenic mice, we have expressed three human components involved in T-cell recognition of an MS-relevant autoantigen presented by the HLA-DR2 molecule: DRA*0101/DRB1*1501 (HLA-DR2), an MHC class II candidate MS susceptibility genes found in individuals of European descent; a T-cell receptor (TCR) from an MS-patient-derived T-cell clone specific for the HLA-DR2 bound immunodominant myelin basic protein (MBP) 4102 peptide; and the human CD4 coreceptor.
Hermans et al. (1997)HLA-DRB1T cellsIt is interesting that MBP-reactive T cells from MS patients expressing the disease-associated HLA-DRB1*15 allele produced increased quantities of TNF alpha, a cytokine suggested to play an important role in inflammation and demyelination.
Walser-Kuntz et al. (1995)HLA-DRT cellsThe contributions of germline-encoded T cell receptor segments and of HLA-DR polymorphisms in shaping the repertoire of human CD4+ CD45RO- T cells were investigated in healthy unrelated individuals and in patients with rheumatoid arthritis, an HLA-DRB1 04-associated disease.
van Es et al. (1984)HLA-DRT lymphocytesExpression of HLA-DR on T lymphocytes following renal transplantation, and association with graft-rejection episodes and cytomegalovirus infection.
van Es et al. (1984)HLA-DRT lymphocyteThe expression of HLA-DR by T lymphocyte subpopulations recognized by monoclonal antibodies and flow cytometry was monitored in 10 normal controls, 15 patients on hemodialysis, 25 recipients of a renal allograft with stable graft function, 16 transplant recipients suffering rejection episodes, and 4 transplant recipients with cytomegalovirus (CMV)4 infection.
Endl et al. (1997)HLA-DRT lymphocytesIdentification of naturally processed T cell epitopes from glutamic acid decarboxylase presented in the context of HLA-DR alleles by T lymphocytes of recent onset IDDM patients.
Ohno et al. (1990)HLA-DRT-cellThe neoplastic cells expressed CD2, NKH-1, HLA-DR and leukocyte common antigen, but lacked other T-cell, B-cell and myeloid markers.
Perry et al. (2004)HLA-DRT cellsExpression of HLA-DR by monocytes is essential for the presentation of peptides derived from ingested microbes to CD4 positive T cells to initiate a specific immune response 3 .
Maeda et al. (1999)HLA-DRT cellsWe found that the ratio was decreased in SLE patients and that this was significantly related to expression of HLA-DR by CD8+ (but not CD4+) T cells.