Viewing affirmative mentions of binding of CEL (H. sapiens) in T cells

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Bottema et al. (2010)cellT-cellInteraction of T-cell and antigen presenting cell co-stimulatory genes in childhood IgE.
Castrejon et al. (2010)cellT-cellAntigen-specific T cells are involved in the pathogenesis; however, the nature of the antigen interacting with specific T-cell receptors is not fully defined.
Dieudonné et al. (2010)cellT-cellT-cell factors (TCF) bind to this sequence in vivo.
Kosmrlj et al. (2009)cellT-cellT-cell activation requires sufficiently strong binding of T-cell receptors on their surface to short peptides (p) derived from foreign proteins, which are bound to major histocompatibility gene products (displayed on antigen-presenting cells).
Prasad et al. (2009)cellT lymphocytesT lymphocytes play a key role in adaptive immunity and are activated by interactions of their T cell receptors (TCR) with peptides (p) derived from antigenic proteins bound to MHC gene products.
Driessens et al. (2009)DCT-cellIn conclusion, vaccines associating DC and GM-CSF-secreting tumor cells induce high therapeutic effect in mice with preexisting renal cell carcinoma that are correlated to the induction of specific CD8 and CD4+ T-cell responses.
Atamas and Bell (2009)cellT cellNumerous biological interactions, such as interactions between T cell receptors or antibodies with antigens, interactions between enzymes and substrates, or interactions between predators and prey are often not strictly specific.
Luo et al. (2008)cellT cellDuring the interaction of T cell and antigen presenting cell, a highly organized structure is formed at the interface of the two cells, where cholesterol and sphingolipids are enriched, and form a liquid ordered phase that facilitates the signaling proteins on and off.
Frankild et al. (2008)cellT cellThe emerging realization in the field is that T cell receptors (TcR) recognize multiple distinct ligands.
Oizumi et al. (2008)cellT-cellSuppression of CD8 T-cell expansion by established tumors is independent of tumor-associated expression of the antigen that is recognized by the CD8-T-cell receptor.
Dasgupta et al. (2008)cellT cellWhile authors have focused on the downstream events of the specific immune response and suggested modification of protein therapeutics to eliminate epitopes that interact with B cell receptors, T cell receptors, or MHCII molecules, the mechanisms underlying Ag interaction with APCs, a step upstream of immune effectors, have been grossly neglected.
Saarinen et al. (2007)cellT-cellThe mutation of Asn11 (a conserved residue that is known to be significant for T-cell-receptor binding in other superantigens) and Lys15 to Ala did not cause any decrease in the mitogenic activity of SDM.
Chen et al. (2007)cellT cellA link between immunoregulation and self-nonself discrimination has emerged from experiments showing that Qa-1-restricted CD8(+) T cells selectively down-regulate target T cells activated by the intermediate avidity of their own T cell antigen receptor-ligand interactions.
Stillman et al. (2006)cellT cellGalectin-3 binds to a complement of T cell surface glycoprotein receptors distinct from that recognized by galectin-1.
Doytchinova and Flower (2006)cellT cellDuring the process of T cell recognition, T cell receptors (TCR) interact with the central section of the bound nonamer peptide; thus only positions 4-8 were considered in the study.
Schmid et al. (2006)cellT-cellTransfection of drug-specific T-cell receptors into hybridoma cells: tools to monitor drug interaction with T-cell receptors and evaluate cross-reactivity to related compounds.
Castell and Castell (2006)cellT-cellRECENT FINDINGS: Formation and presentation of drug-protein adducts, or a direct interaction with the major histocompatibility complex/T-cell receptor complex is a necessary but not sufficient stimulus to trigger a hypersensitivity reaction.
Hsu et al. (2006)cellT-cellThe activation of T-cells is initiated by binding of T-cell receptors (TCR) with antigen epitopes.
Roy et al. (2005)cellT-cellSEs elicit the release of lethal amounts of cytokines by binding to major histocompatibility complex (MHC) class II and cross-linking susceptible T-cell receptors.
Zajonc et al. (2005)cellT cellComparison of the binding of altered lipid ligands to CD1d and T cell receptors suggested that the differential T helper type 1-like and T helper type 2-like properties of natural killer T cells may originate largely from differences in their 'loading' in different cell types and hence in their tissue distribution in vivo.
Garcia and Adams (2005)cellT cellWhile snapshots of T cell receptors bound to their peptide-MHC ligands appear to have defined a general interaction or "docking" solution, many of the most fundamental structural questions in antigen recognition lack detailed answers and thus pose exciting experimental challenges for the future.
Seiberling et al. (2005)cellT-cellFirst, it briefly describes SAgs, focusing on how they interact with the immune system by binding to T-cell receptors (TCR) and major histocompatibility complex (MHC) class II molecules.
Sigal (2005)cellT-cellOn the other hand, "salutary autoimmunity" occurs in the interaction of immune systems with themselves or other immune pathways as part of control or recognition mechanisms, eg, idiotype network, epitope-MHC complex binding with B- or T-cell antigen receptors.
Engler et al. (2004)cellT cellDrugs can interact with T cell receptors (TCR) after binding to peptide-MHC structures.
Seibl et al. (2004)cellT-cellThey affect apoptotic pathways and dendritic cell maturation, and interact with B-cell receptors in priming T-cell responses to host-derived DNA.
Pichler (2004)cellT-cellIn addition to the hapten concept, some drugs can bind directly to T-cell receptors and stimulate them.
Cook et al. (2004)cellT-cellPreliminary findings from comparisons of wild-type, CD40 ligand knock-out, and CD28 knock-out C57BL/6 mice strongly support the suggestion of a critical role for T-cell-antigen-presenting cell interactions in the immune alterations observed in chronic ethanol abuse.
Krueger et al. (2004)cellT cellTetramers bind to T cell receptors (TCR) that recognize the MHC molecule/peptide combination with high specificity.
Nika et al. (2004)cellT-cellPhosphorylation at Ser-23 is also increased in a transient manner upon T-cell antigen receptor ligation.
Miyake (2003)cellT cellAdaptive immunity generally refers to the ability of lymphocytes to recognize microbial, viral and fungal proteins via T cell receptors and antibodies.
von Haller et al. (2003)cellT cellLipid rafts were prepared according to standard protocols from Jurkat T cells stimulated via T cell receptor/CD28 cross-linking and from control (unstimulated) cells.
Piñon et al. (2003)cellT-cellHuman T-cell leukemia virus type 1 envelope glycoprotein gp46 interacts with cell surface heparan sulfate proteoglycans.
Barrett et al. (2003)cellT cellFactors that modify immune reconstitution include immunosuppression, GVHD, the cytokine milieu and poorly-defined homeostatic mechanisms which encourage irregular T cell expansions driven by immunodominant T cell-antigen interactions.
Dudásová and Chovanec (2003)cellT cellB and T lymphocytes recognize foreign antigen through specialized receptors: the immunoglobulins and the T cell receptors, respectively.
Amoura et al. (2003)cellT cellInflammatory chemokines control lymphocyte traffic through their interaction with T cell chemokine receptors.
Britschgi et al. (2003)cellT-cellThis led us to an other new concept: the pharmacological interaction of drugs with immunological receptors, namely the MHC and T-cell receptors.
Paolucci et al. (2003)cellT lymphocytesWe report here that after exposure to DETA-NO, DCs exhibit a significantly increased ability to activate T lymphocytes stimulated by mycobacterial antigens, Staphylococcus aureus Cowen strain B, allo-antigens, or cross-linking of the CD3-T cell receptor complex.
Reiser et al. (2002)cellT cellA T cell receptor CDR3beta loop undergoes conformational changes of unprecedented magnitude upon binding to a peptide/MHC class I complex.
Zal et al. (2002)cellT cellInhibition of T cell receptor-coreceptor interactions by antagonist ligands visualized by live FRET imaging of the T-hybridoma immunological synapse.
Poser et al. (2002)cellT-cellDetailed analysis revealed binding of T-cell factor family transcription factors to the repressor element.
Fournel and Muller (2002)cellT-cellIn this review, we briefly summarize these results and describe recent findings on the characterization of histone T-cell epitopes recognized by CD4(+) cells from different strains of lupus mice.
Pichler (2001)cellT cellsRecent studies suggest that drugs might also bind in a non-covalent form to MHC-peptide complexes and T cell receptors, and are thereby able to stimulate T cells.
Ge et al. (2001)cellT cellDependence of lymphopenia-induced T cell proliferation on the abundance of peptide/ MHC epitopes and strength of their interaction with T cell receptors.
Regner (2001)cellT-cellCross-reactivity in T-cell antigen recognition.
Van Den Berg et al. (2001)cellT cellThe binding between MHC/peptides and T cell receptors (TCRs) has a low affinity and is highly degenerate.
Bauer et al. (2001)cellT cellFirst, T cell receptor/CD3 ligation was sufficient to induce activation as well as plasma membrane recruitment of PKC theta.
Roy et al. (2001)NFATT-cellMorphine-induced nuclear factor of activated T-cell (NFAT) binding was assayed with the electromobility shift assay in Jurkat T cells.
Roumier et al. (2001)cellT cellDynamic interactions between membrane and cytoskeleton components are crucial for T cell antigen recognition and subsequent cellular activation.
Qadri and Ward (2001)cellT cellThe molecular nature of the interaction of T cell receptors (TCR) with alloligands is not well understood.
Yang et al. (2000)cellT-cellThis interaction with T-cell-specific transcription factors indicates an important immunomodulatory role for PPARgamma in T lymphocytes and could suggest a previously unrecognized clinical potential for PPARgamma ligands as immunotherapeutic drugs to treat T-cell-mediated diseases by targeting IL-2 gene expression.
Papageorgiou and Acharya (2000)cellT cellSuperantigens are highly potent immune stimulators with a unique ability to interact simultaneously with MHC class II molecules and T cell receptors, forming a trimolecular complex that induces profound T-cell proliferation and massive cytokine production.
Grossman and Paul (2000)cellT cellSelf-tolerance: context dependent tuning of T cell antigen recognition.
Anderson et al. (2000)cellT cellIf cross-reactivity is "focused," then in an immune response to a foreign antigen all T cell receptors that recognize the foreign antigen will cross-react with a specific autoantigenic peptide.
Horwitz (2000)cellT-cellHighly immunosuppressive, nonchemotherapeutic agents that inhibit graft rejection or GVHD by blocking the critical costimulatory component of the T-cell receptor-antigen interaction are beginning to emerge and may be ideal for SCT of nonmalignant diseases.
Schweitzer et al. (2000)cellT-cellFlow cytometric analysis of peptide binding to major histocampatibility complex class I for hepatitis C virus core T-cell epitopes.
Yagüe et al. (2000)cellT-cellThe dimethyl-Arg residue was located in a central position of the peptide, amenable to interacting with T-cell receptors, and most other residues in the middle region of the peptide were Gly.
McHeyzer-Williams et al. (2000)cellT cellAntigen-specific immunity develops through a series of intercellular information exchanges organized around cognate T cell receptor-peptide/MHC interactions.
Cai and Kohwi-Shigematsu (1999)cellT cellUsing this method, we monitored single-copy loci using a short, 509-bp DNA sequence that binds in vivo to the T cell factor SATB1 within T cell nuclei, high-salt-extracted nuclei (histone-depleted nuclei generating "halos" with distended chromatin loops), and the nuclear matrix, before and after T cell activation.
Kasibhatla et al. (1999)cellT-cellThe POU domain protein T-cell factor beta1 (TCFbeta1), which binds octamer and octamer-related sequences, is a potent transactivator.
Pellet et al. (1999)cellT-cellMIC molecules belong to the immunoglobulin superfamily, are encoded within the MHC region and are recognized by gamma/delta T-cell receptors.
Porcelli and Modlin (1999)cellT cellStructural, biochemical, and biophysical studies support the view that CD1 proteins bind the hydrophobic alkyl portions of these antigens directly and position the polar or hydrophilic head groups of bound lipids and glycolipids for highly specific interactions with T cell antigen receptors.
Wild et al. (1999)cellT cellDependence of T cell antigen recognition on the dimensions of an accessory receptor-ligand complex.
Wild et al. (1999)cellT cellAlthough the interaction of CD2 on T cells with wild-type or shortened forms of CD48 on APCs enhances T cell antigen recognition, the interaction of CD2 with elongated forms of CD48 is strongly inhibitory.
Seko et al. (1998)cellT-cellFor antigen-specific T-cell activation to occur, it is necessary for T cells to receive a costimulatory signal provided by costimulatory molecules expressed on antigen-presenting cells (APCs) as well as the main signal provided by binding of T-cell receptors to the antigen.
Bongioanni et al. (1998)cellT-cellT-cell interleukin-6 receptor binding in patients with myasthenia gravis.
Li et al. (1998)cellT-cellStructure-function studies of T-cell receptor-superantigen interactions.
Mazzaro et al. (1998)cellT-cellIn addition, the human T-cell lymphotrophic virus family members have also been recognized as possible aetiologic agents for several lymphomas, such as cutaneous T-cell lymphomas, T-cell leukaemia and T-cell hairy cell leukaemia.
Steward et al. (1997)cellT-cellProduction and characterization of a new monoclonal antibody effective in recognizing the CD3 T-cell associated antigen in formalin-fixed embedded tissue.
Musci et al. (1997)cellT cellAdditionally, our studies suggest that surface expression of HCP in T cells may provide a means to identify phosphotyrosine-containing proteins that are required for coupling signaling pathways initiated by ligation of the T cell Ag receptor.
Mannie (1997)cellT cellThis model is based on the assumption that thymic interactions of T cell antigen receptors with self major histocompatibility complex ligands may vary in efficacy.
Varadhachary et al. (1997)cellT cellHuman T cell clones were analyzed for their susceptibility to activation-induced cell death (AICD) in response to CD3/T cell receptor ligation.
McMichael and Phillips (1997)cellT cellMutant virus can escape by several different routes, including failure of the mutated peptide to bind to the presenting HLA molecule and altered interactions with T cell receptors (TCR), including antagonism.
Reich et al. (1997)cellT-cellLigand-specific oligomerization of T-cell receptor molecules.
Reich et al. (1997)cellT cellsT cells initiate many immune responses through the interaction of their T-cell antigen receptors (TCR) with antigenic peptides bound to major histocompatibility complex (MHC) molecules.
Roussel et al. (1997)cellT-cellBacterial superantigens are small proteins that have a very potent stimulatory effect on T lymphocytes through their ability to bind to both MHC class II molecules and T-cell receptors.
Porter and Hogg (1997)cellT cellSimilar inhibition is also seen when T cells are exposed to mAb 24, which stabilizes LFA-1 in an active state after triggering integrin function through divalent cation Mg2+, PdBu, or T cell receptor/ CD3 complex (TCR/CD3) cross-linking.
von Bonin et al. (1996)cellT cellHowever, the molecular details of hapten interactions with T cell receptors (TCR) are poorly understood.
Schmid-Antomarchi et al. (1996)cellT cellThese results contribute to understand better the control that HIV may exert on its own replication or on T cell apoptosis by modulating the activation status of its target cells through its interaction with T cell surface CD4 molecules.
Kaufmann (1996)cellT-cellT lymphocytes recognize specific ligands by clonally distributed T-cell receptors (TCR).
Whisler et al. (1996)cellT cellAge-related reductions in the activation of mitogen-activated protein kinases p44mapk/ERK1 and p42mapk/ERK2 in human T cells stimulated via ligation of the T cell receptor complex.
Sebzda et al. (1996)cellT cellThese studies demonstrate that (a) peptides that induce efficient positive selection at high concentrations are not exclusively antagonists; (b) some agonists do not promote clonal deletion; (c) positive selection requires a unique T cell receptor-peptide-major histocompatibility complex interaction; and (d) interactions with selecting peptides during T cell ontogeny may define the functional reactivity of mature T cells.
Huard et al. (1996)cellT cellThese functional studies indicate that T cell MHC class II molecules down-regulate T cell proliferation following LAG-3 binding and suggest a role for LAG-3 in the control of the CD4+ T cell response.
Nagai et al. (1996)cellT-cellThe T-cell repertoire shaped by HTLV-I infection included T-cells which recognized HTLV-I-infected T-cell antigens as well as spinal cord antigen in particular.
Whittaker (1996)cellT-cellEach T cell expresses a unique membrane bound T-cell antigen receptor (TCR) which combines with specific antigenic peptides and major histocompatibility complex molecules.
Faris et al. (1996)cellT cellWhereas extracellular signal-regulated kinase is activated by T cell receptor/CD3 ligation alone, activation of JNK requires co-stimulation by the CD28 receptor.
Garcia et al. (1996)cellT-cellT-cell antigen receptors (TCR) generally interact with moderate affinity with the complex formed by major histocompatibility complex (MHC) molecules and foreign peptides.
Sei et al. (1995)cellT cellCa2+ influx triggered by antigen binding to T cell receptors (TCR) is an early event in T cell activation.
Vidovi? et al. (1995)cellT cellThe observed MHC down-regulation requires a specific T cell receptor-peptide-class II interaction, a direct contact between T cell and APC, and the involvement of CD2 molecules.
Clark (1995)cellT-cellEnhanced adhesiveness and T-cell activation follow the T-cell signalling that results from crosslinking of T-cell receptors (TCR).
Foster et al. (1995)cellT cellgp120-induced programmed cell death in recently activated T cells without subsequent ligation of the T cell receptor.
Abrahmsén (1995)cellT-cellTheir ability to efficiently cross-link molecules of the major histocompatibility complex class II and T-cell receptors causes the normal antigen specificity of each receptor to be bypassed.
Onda et al. (1995)cellT cellA phage display system for detection of T cell receptor-antigen interactions.
Kallan et al. (1995)cellT cellsThus far little information is available on the beta cell antigen or antigens recognized by auto-reactive T cells.
Schafer et al. (1995)cellT cellThe 'dimer of dimers' or 'superdimer' structure led to speculation that the binding of T-cell receptors to monomeric class II molecules on the antigen presenting cell surface may affect dimerization and thus initiate signaling both in the T cell and in the antigen presenting cell.
Imbert et al. (1994)cellT-cellPervanadate synergized with signals delivered by T-cell antigen receptor engagement or by a phorbol ester to induce interleukin 2 production.
Todd et al. (1994)cellT cellsThe tolerant T cells are unable to respond to either presentation of Mls 1a on spleen cells or cross-linking anti-T cell receptor antibody in vitro.
Buday et al. (1994)cellT cellImmunoprecipitates of Sos from the lysates of T cells contain a 36-kDa protein which is phosphorylated on tyrosine residues in response to T cell receptor/CD3 cross-linking.
Faull et al. (1994)cellT cellWe further show that high affinity binding of soluble fibronectin can be induced by either differentiation of the monocytic cell line THP-1 or by cross-linking the T cell receptor complexes on the T lymphoid cell line HUT-78.
Opdenakker and Van Damme (1994)cellT-cellHere, Ghislain Opdenakker and Jo Van Damme propose the REGA-model (Remnant Epitope Generates Autoimmunity) to explain the generation of autoantigens and their interaction with the T-cell receptor complex.