Viewing affirmative mentions of gene expression of Mhc (D. melanogaster) in T cells

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Obst et al. (2000)MHCT cellsIn consequence, allorestricted, peptide-specific T cells (that are of interest for clinical applications) are easier to obtain if T cells and target cells express related MHC molecules.
Picus et al. (1985)MHCCTLIn this system, we have shown that tolerance to foreign MHC determinants was not, of itself, sufficient to facilitate the generation of CTL specific for target cells expressing those foreign MHC determinants.
De Vries et al. (2003)MHCT cellsTo induce an effective immune response, these cells should not only express high levels of MHC and costimulatory molecules but also migrate into the lymph nodes to interact with naïve T cells.
Miyasaka et al. (1990)MHCT cellsCells obtained from the thymic lymphatics or lymphatic emigrants were found to have distinct features different from peripheral T cells in terms of their surface morphology and expression of the MHC antigens.
Miyasaka et al. (1990)MHCT cellsVenous emigrants were also slightly different from peripheral T cells in MHC expression.
Marrack et al. (1988)MHCT cellsIn addition, development in the thymus picks out T cells to mature if their receptors will be restricted for antigen recognition in association with self MHC alleles expressed on thymus epithelial cells.
Germain (1995)MHCT cellTo elicit suitable T cell responses vaccines must, therefore, contain proteins or peptides derived from the organism against which protection is desired, the pathogen-derived peptides must be capable of interacting with the allelic forms of the MHC molecules expressed in the vaccinated individuals, and the vaccine components must be delivered in a manner that ensures they are made available for binding to the MHC molecules on appropriate antigen-presenting cells.
Liu and Zheng (2001)MHCT cellsIn contrast, both the inductive and the effector phases of MHC class II-restricted T cells are independent of MHC class II expression on tumors.
Geha and Rosen (1989)MHCT cellsThese T cells could potentially participate in a secondary immune response because they were shown to recognize TT presented by recipient fibroblasts induced to express class II MHC molecules following treatment with IFN-gamma.
Matsui et al. (1986)MHCT cellComparison of MHC antigen expression on PHA- and MLC-induced T cell lines with that on T and B lymphoblastoid cell lines by cell cycle dependency.
Matsui et al. (1986)MHCT cellsAlthough it is well known that the expression of major histocompatibility complex (MHC) antigens on the surface of lymphoblastoid cell lines are cell cycle dependent, the way in which the MHC antigen expression on activated T cells varies with cell cycle phase has not previously been described.
Matsui et al. (1986)MHCT cellsUsing 11 lymphoblastoid cell lines from malignant and nonmalignant tissues (B cells, T cells, and myeloid cells) and five activated T cell lines (two cell lines activated by phytohemagglutinin and three alloreactive T cell clones), MHC antigen expression was quantitatively studied by dual-beam flow cytometry.
Rodenko et al. (2006)MHCT-cellHere we describe in-depth procedures for the high-throughput production of peptide-MHC (pMHC) complexes by MHC exchange, the analysis of peptide exchange efficiency by ELISA and the parallel production of MHC tetramers for T-cell detection.
Goulder and Watkins (2008)MHCT-cellThe well-described association between the expression of particular MHC class I molecules and successful containment of HIV or, in the macaque model, SIV replication provide a valuable starting point from which to evaluate more precisely what might constitute effective CD8(+) T-cell responses.
Shao et al. (2007)MHCT cellsIt is speculated that like many biological responses this is a two-edge sword - namely, the expression of modest levels of MHC molecules may inhibit the activation of invading T cells, whereas overexpression of these molecules may promote activation of autoimmune T cells, enhancing the inflammatory cascade, thus leading to tissue damage.
Parham (1989)MHCT lymphocytesTheories rationalizing major histocompatibility complex (MHC) class I polymorphism and the high frequency of alloreactive T lymphocytes initiated the search for expression of genetically inappropriate MHC class I molecules by tumour cells.
Ada and Rose (1988)MHCT-cellBased on the premise that quantitative aspects are of paramount importance, we suggest that T-cell activity, MHC expression, and self-peptide binding determine the initiation of autoimmune responses.
Renoux et al. (1988)MHCT lymphocytesBrain neocortex and imuthiol regulate the expression of MHC antigens on mouse T lymphocytes.
von Boehmer et al. (1983)MHCT cellsAllorestricted T cells, the existence of which was previously thought to be incompatible with the concept of complete repertoire selection by self MHC antigens, were shown to significantly cross-react on targets expressing self MHC antigens.
Jenkinson (1981)MHCT cellAs an approach to investigating the intrathymic environment, MHC antigen expression during normal thymic development and lymphopoiesis, and in the embryonic thymus of T cell-deficient nude mice, has been examined.
Borghans et al. (2003)MHCT cellThe number of different major histocompatibility (MHC) molecules expressed per individual is widely believed to represent a trade-off between maximizing the detection of foreign antigens, and minimizing the loss of T cell clones due to self-tolerance induction.
Borghans et al. (2003)MHCT cellBased on experimental parameter estimates, we show that the number of clones in the functional T cell repertoire would in fact increase if the MHC diversity within an individual were to exceed its normal value, until more than one hundred different MHC molecules would be expressed.
Cockfield et al. (1990)MHCT cellAn intact T cell compartment was not necessary for normal levels of expression; in athymic nude mice and mice with severe combined immunodeficiency disease, MHC expression was similar to or greater than that of controls.
Cockfield et al. (1990)MHCT cellsThus, although exposure to bacterial flora or other sources of endotoxin was not required for normal MHC expression, a change in flora can up-regulate expression, probably by inducing the secretion of cytokines from non-T cells.
Torgan and Daniels (2001)MHCT-cellsThe results suggest that contractile activity-dependent expression of slow MHC is mediated largely through the CN-nuclear factor of activated T-cells pathway, whereas suppression of fast MHC expression may be independent of nuclear factor of activated T-cells.
Puri et al. (1985)MHCT cellA panel of inducer T cell clones with different activation specificities and homogeneous lines of APC expressing different MHC haplotypes was used to define this ligand.
Wettstein et al. (1991)MHCT cellsA murine class II major histocompatibility complex (MHC) heterodimer, Ek, expressed as a glycan-phosphatidyl inositol-anchored chimera on Chinese Hamster Ovary cells, can present peptides, but not processed antigen to T cells.
Singer and Hodes (1982)MHCT cellThe present study has examined the possibility of TNP-Ficoll-responsive B cells recognize the MHC determinants expressed by the accessory cells with which they interact for the generation of T cell-independent responses to "high" concentrations (10(-2) micrograms/ml) of TNP-Ficoll.
McHoney et al. (2006)MHCT-cellsMonocyte class II major histocompatibility complex (MHC) expression is necessary for antigen presentation and stimulation of T-cells.
Burakoff et al. (1978)MHCT-cellWe find that early in ontogeny, prekiller activity against both trinitrophenyl (TNP)-coupled autologous MHC products and allogeneic MHC products resides in the same (Ly123(+)) T-cell pool; later in ontogeny alloreactivity is invested in Ly23 cells which, when activated, lyse TNP-coupled autologous cells as well as appropriate allogeneic target cells.
Hugo et al. (1993)MHCT-cellDuring development in the thymus, thymocytes bearing alpha beta T-cell receptors are selected to mature if the receptors they bear are able to interact in some way with major histocompatibility complex (MHC) proteins expressed on thymic stromal cells.
Finnegan et al. (1985)MHCT cellAntigen processing requirements for T cell activation: differential requirements for presentation of soluble conventional antigen vs cell surface MHC determinants.
Nicholas et al. (1987)MHCT cellsH-2-incompatible neural transplants (allografts), unlike their H-2-identical counterpart (isografts), are characterized by the presence of T cells comprising both major T-cell subsets and macrophages, and by a marked increase in the expression of both class I and class II (Ia) MHC antigens.
Burakoff et al. (1978)MHCT-cellThese results suggest the following model to account for the presence of large numbers of alloreactive T-cell clones in adult animals: continuous stimulation of Ly123 cells by autologous MHC antigens associated with foreign materials such as a virus results in the formation of Ly23 memory progeny carrying receptors that recognize MHC products that are foreign due to genetic polymorphism (alloantigens).
Duan et al. (2002)MHCT cellsHowever, there were markedly increased levels of expression of MHC class I and class II antigens, and a number of T cells infiltrating in the graft sites in both the MHC class I-deficient and wild-type groups.
Crowley et al. (2000)MHCT cellsHere, the expression of the major histocompatibility complex (MHC) class Ib T22 and the closely related T10 molecules is shown to be activation-induced, and they confer specificity to about 0.4% of the gammadelta T cells in normal mice.
Benoist and Mathis (1989)MHCT lymphocytesT lymphocytes that express the V beta 6 variable region are positively selected in the thymus by cells expressing major histocompatibility complex (MHC) class II E molecules.
van den Berg and Rand (2003)MHCT cellsWe consider the way in which antigen is presented to T cells on MHC molecules and ask how MHC peptide presentation could be optimized so as to obtain an effective and safe immune response.
Lan et al. (2002)MHCT cells[Discovery of MHC restriction in antigen recognition of T cells].
Chaturvedi et al. (1997)MHCT cellsSusceptibility loci for autoimmune diabetes such as the major histocompatability complex (MHC) may function by producing different repertoires of T cells, which could gain autoreactivity following activation, resulting in autoimmune disease.
Busch et al. (1999)MHCT cellsThese studies demonstrate the following: 1) The size of a peptide-specific T-cell response does not correlate with the amount of epitope presented by infected cells; 2) T cells specific for dominant epitopes do not, in the case of L. monocytogenes infection, inhibit responses to subdominant epitopes; 3) T cells responding to different epitopes presented by MHC class Ia molecules expand, contract and enter the memory pool synchronously; 4) Repeated in vivo expansion of antigen-specific T-cell populations results in a narrowing of their T-cell receptor repertoire and in an increase in their affinity for antigen; and 5) T cells restricted by H2-M3 MHC class Ib molecules constitute a major part of the primary response to bacterial infection, but appear to play a relatively smaller role in memory responses.
Purcell and Gorman (2004)MHCT cellThese complexes are then scrutinized by effector T cells that express clonally distributed T cell receptors with specificity for specific MHC-peptide complexes.
Bakács et al. (2001)MHCT cellsPeptides presented during a viral infection typically decrease complementarity between the structures that are the products of the major histocompatibility complex (MHC) genes (or other genes related to it) and T cells.
Dohlsten et al. (1991)MHCT-cellIn this paper, Mikael Dohlsten and colleagues present evidence suggesting that these bacterial superantigens direct T cells to eradicate MHC class-II-expressing antigen-presenting cells, thus counteracting specific T-cell functions.
Shao et al. (2007)MHCT cellsIn this paper, we hypothesize that the appearance of MHC molecules on parenchymal cells may augment the activation of invading autoreactive T cells and either exacerbate or suppress local inflammation.
Remedi et al. (2003)MHCT lymphocytesWe conclude that the development of a specific immune response could be achieved by the superexpression of MHC molecules on tumor cells or when tumor ulceration promotes APC to take up necrotic cells and tumor antigens are presented to T lymphocytes.
Araneo (1986)MHCT cellRegulation of T cell effector functions by major histocompatibility complex (MHC) gene products has been extensively researched.
Yagüe et al. (1985)MHCT cellThree independent T cell hybridomas were isolated that have identical specificities for antigen and products of the major histocompatibility complex (MHC).
Huseby et al. (2005)MHCT cellsHere we show that the pool of T cells initially positively selected in the thymus contains many T cells that are very crossreactive for peptide and MHC and that subsequent negative selection establishes the MHC-restriction and peptide specificity of peripheral T cells.
Bosshart (1999)MHCT cellsThe malignant cells in Hodgkin's disease (HD), commonly referred to as Hodgkin and Reed-Sternberg (HRS) cells, express major histocompatibility complex (MHC) class II molecules and, like "professional" antigen-presenting cells (APCs), different accessory or costimulatory molecules which can provide an additional activation signal to T cells.
Oluwole et al. (1994)MHCT-cellsThis observation suggests that donor-specific unresponsiveness can be readily achieved by IT inoculation of major histocompatibility (MHC) class I expressing donor-type resting T-cells rather than by any donor-type antigen presenting cells that express MHC class I and II molecules.
Iwatani et al. (1989)MHCT cellsThis class II MHC expression is induced by interferon-gamma produced by T cells as a result of various immune responses, such as autoimmune reaction.
Iwatani et al. (1989)MHCT cellsThus, the expression of class II MHC antigens on non-lymphoid cells may serve as a peripheral mechanism for the induction and maintenance of self-tolerance in autoreactive T cells that escape negative selection in the thymus or that are specific for extrathymic tissue antigens, in a fail-safe mechanism against autoimmunity.
Schneck et al. (2001)MHC-IgT cellsMethods for constructing and detecting these MHC-Ig dimers are included along with protocols for applying their use for the quantitation of antigen-specific T cells.
Cui et al. (2006)MHCT-cellMajor histocompatibility complex (MHC)-binding peptides are essential for antigen recognition by T-cell receptors and are being explored for vaccine design.
Schuler et al. (2001)MHCT cellThe fate of T cell responses to peptide-based vaccination is subject to constraints by the major histocompatibility complex (MHC), MHC restriction.
Zhang et al. (1995)MHCT cellsThe present studies evaluated whether the autoreactive T cells participate in the induction of facilitated graft acceptance after CsA treatment by recognizing and eliminating activated allograft responsive T cells that express MHC class II determinants.
Sprent et al. (1990)MHCT cellsIn certain situations partial unresponsiveness of mature T cells can be achieved by exposing T cells to foreign MHC molecules expressed on atypical antigen-presenting cells.
Singh and Raghava (2003)MHCT-cellThe simultaneous prediction of MHC binders and proteasome cleavage sites in an antigenic sequence leads to the identification of potential T-cell epitopes.
Miller and Vadas (1977)MHCT-cellThe implications of the results are discussed in terms of (1) different T-cell subsets, (2) the mode of action of Ir genes, and (3) the possible parallel evolution of T-cell receptors for antigen and gene products of the MHC.
Gebe and Kwok (2007)MHCT cellsRecombinant MHC multimers have been produced where MHC-binding peptide antigens are either covalently or noncovalently bound to the MHC, with the latter having the advantage of the ability to use a single recombinant MHC to investigate multiple MHC-binding peptides and their interacting T cells.
Barbis et al. (1994)MHCT cellMHC class II antigen expression was compared between adult horses and foals, and the level of expression of MHC class II antigens on horse T cell subpopulations was also determined.
Barbis et al. (1994)MHCT cellDual staining for MHC class II antigens and markers for equine T cell subsets demonstrated that both EqCD4+ and EqCD8+ T cells expressed MHC class II molecules.
Finnegan et al. (1985)MHCT cellIn contrast, the same T cell clones were only minimally affected in their ability to respond to similarly chloroquine-treated APC expressing allogeneic MHC products.
Janeway et al. (1985)MHCT cellsMajor histocompatibility complex (MHC)-restricted T cells, which we have analyzed in detail, appear to recognize antigen only on the surface of cells bearing the appropriate MHC gene product.
Wanders et al. (1995)MHCT-lymphocytesThe cell composition found in the intima and media of the allogeneic vessels consisted of macrophages, T-lymphocytes, MHC class II-expressing cells, and smooth muscle cells, whereas the syngeneic grafts contained almost exclusively smooth muscle cells and macrophages.
Morris (1990)MHCT-cellThe down-regulation of major histocompatibility complex (MHC) antigen expression which occurs in tumours may be an important element in tumour progression - the increasing malignancy of tumours - which is so much a feature of cancer - if it allowed the avoidance of T-cell immunity.
Haugarvoll et al. (2008)MHCT cellsMajor histocompatibility complex (MHC) class II+ cells were detected by immunohistochemistry, and laser capture micro-dissection and subsequent RT-PCR analysis revealed expression of T-cell receptor transcripts in the investigated tissue, suggesting the presence of T cells.
Ferrone and Marincola (1995)MHCT-cellInterest in the characterization of abnormalities in the expression of MHC class I by melanoma cells has been rekindled by the current emphasis on the application of T-cell-based immunotherapy to melanoma.
Huang et al. (1994)MHCT cellProtein transfer of preformed MHC-peptide complexes sensitizes target cells to T cell cytolysis.
Burakoff et al. (1978)MHCCTLIn general, these studies indicate that alloaggression (as manifest by Ly23 cells in the CTL response) reflects a high degree of cross stimulation between physiologically relevant antigens, e.g., viral determinants associated with self MHC products, and biologically irrelevant allelic variants of the MHC.
Pamer et al. (1993)MHCT cellsDo nonclassical, class Ib MHC molecules present bacterial antigens to T cells?
Stefanová et al. (2002)MHCT cellsOnly those precursor T cells whose TCRs generate an adequate but not excessive signalling response to self-peptides bound to the expressed MHC proteins undergo successful maturation.
Watson et al. (2006)MHCT-cellMany colorectal tumors lose or downregulate cell surface expression of MHC class I molecules conferring resistance to T-cell-mediated attack.
McCarthy and Singer (1986)MHCT lymphocytesWe have analyzed the signals influencing the generation of major histocompatibility complex (MHC) class II allospecific cytolytic T lymphocytes (CTL) and have found that the development of these CTL is actively regulated in primary in vitro cultures by Lyt-2+ T cells triggered in response to MHC class I alloantigens.
Oluwole et al. (1994)MHCT-cellsThese results suggest that manipulation of the immune system through thymic reeducation of the developing T-cells by the deliberate introduction of foreign MHC class I cellular alloantigens has therapeutic potential in the induction of transplantation tolerance in adult animals.
Martin (1996)MHCT cellsWe propose that the expression of MHC class I molecules on donor T cells makes it possible for these cells to inactivate the host response against donor class I alloantigens through a veto mechanism, whereas the absence of MHC class II molecules on murine T cells explains why these cells cannot inactivate the host response against donor class II alloantigens.
Coady et al. (1999)MHCT cellIf these factors can be cloned, the potential exists for developing transgenic animals that cannot express MHC or peptide antigen to T cell receptors through the MHC system.
Grandjean et al. (2003)MHCT cellsHere we controlled for some of the features that differed among the earlier studies, and analyzed both the survival and expansion of naive CD4+ T cells transferred into MHC syngeneic, allogeneic, or MHC negative environments.
Dalakas (2001)MHCT cellsIn particular, we now have a better understanding of TCR gene rearrangement in endomysial T cells, regulation of MHC expression, activity of co-stimulatory molecules, and the signalling cascades activated by cytokines, chemokines and metalloproteinases.
Rawson et al. (2000)MHCT cellsThe three cell lines expressed different levels of MHC class I molecules and had different abilities to stimulate proliferation of LCMV(33-41)-specific T cells in vitro.
Zinkernagel et al. (1979)MHCT cellsThis interpretation stems from experiments with chimeras formed by lethally irradiating parental type mice and reconstituting them with F(1) stem cells: the maturing F(1) T cells expressed predominantly the restriction specificities for the recipient parental MHC type (3-8).
Huang et al. (1994)MHCT cellsMany tumours express tumour-specific antigens capable of being presented to CD8+ T cells by major histocompatibility complex (MHC) class I molecules.
Huang et al. (1994)MHCT cellsCurrent models of antigen presentation predict that the tumour cell itself should present its own MHC class I-restricted antigens to T cells.
Cockfield et al. (1989)MHCT cellsMultiple low dose streptozotocin induces systemic MHC expression in mice by triggering T cells to release IFN-gamma.
Moor et al. (1995)MHCT-cellThus the aim of the present study was to assess the rate of synthesis of MHC class I proteins in murine T-cell lymphoma cells (RMA) after treatment with 8-MOP and UVA.
Bousso (2000)MHC-peptideT-cellGeneration of MHC-peptide tetramers: a new opportunity for dissecting T-cell immune responses.
Stefanová et al. (2002)MHCT lymphocytesMajor histocompatibility complex (MHC) class I and II molecules are highly polymorphic proteins that bind and present foreign peptides to the clonally distributed alphabeta receptors (TCR) of T lymphocytes.
Ignatowicz et al. (1996)MHCT cellsT cells that mature in thymuses expressing a single MHC/peptide ligand react frequently with foreign MHC, suggesting that the repertoire of alpha beta receptors may be more biased toward reaction with MHC than was previously thought.