Viewing negative mentions of binding in T cells

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Fukuma et al. (1990)thyroglobulinthyroglobulinT cellsHeat denatured thyroglobulin (with which thyroglobulin autoantibodies do not interact) did not stimulate proliferation and this observation, together with the ability of T cells from some patients to respond to intact thyroglobulin in the absence of LDC, indicated that thyroglobulin-specific B cells may be involved in antigen presentation.
Schrambach et al. (2007)MHCTCRT cellsNon-conventional MHC class I MIC molecules interact not with the TCR, but with NKG2D, a C-type lectin activatory receptor present on most NK, gammadelta and CD8(+) alphabeta T cells.
Schott and Ploegh (2002)CD8class IT cellsMouse MHC class I tetramers that are unable to bind to CD8 reveal the need for CD8 engagement in order to activate naive CD8 T cells.
Yoshinaga et al. (1999)CD28-B7ICOST cellsICOS and B7RP-I do not interact with proteins in the CD28-B7 pathway, and B7RP-1 co-stimulates T cells in vitro independently of CD28.
Harel-Bellan et al. (1989)IL-2T cellsFluoresceinated IL-2 did not bind to normal resting T cells, whereas a highly significant binding was observed on PHA-activated human T cells.
Hutchings et al. (1990)CR3T cellsThe monoclonal antibody 5C6 is specific for the myelomonocytic adhesion-promoting type-3 complement receptor (CR3 or CD11b/CD18) and does not bind to T cells.
Correa et al. (2003)MUC1T cellsIn contrast, resting T cells did not bind MUC1-specific monoclonal antibodies (mAbs), nor was MUC1 mRNA detectable by reverse transcription-polymerase chain reaction (RT-PCR) or Northern blot analysis in these cells.
Burns and Littlefield (1989)MBPT-cellOne myelin-reactive T-cell clone did not recognize MBP or the major myelin lipids but responded to delipidated myelin proteins suggesting that this clone recognized another myelin protein antigen.
Cohly et al. (1988)myoglobinT-cellIn proliferative assays, the T-cell clone responded to apomyoglobin but did not recognize native myoglobin or any of the synthetic peptides corresponding to the six T sites of myoglobin.
Osband et al. (1980)albuminT cellsFluoresceinated human albumin alone (FHA), not conjugated to histamine, does not bind to T cells.
Barber et al. (2006)PD-L1T-cellHere we report that PD-1 (programmed death 1; also known as Pdcd1) was selectively upregulated by the exhausted T cells, and that in vivo administration of antibodies that blocked the interaction of this inhibitory receptor with its ligand, PD-L1 (also known as B7-H1), enhanced T-cell responses.
Horton et al. (1998)MHC-peptideT cellsThese results suggest that amoxicillin can bind directly to performed MHC-peptide complexes and need not necessarily involve the processing of haptenated self carrier proteins before recognition of the conjugate by amoxicillin-specific T cells.
Jin et al. (2004)CD4T cellCD4 and Nef could be cross-linked by a chemical cross-linker, 3,3-dithiobis[sulfosuccinimidyl-propionate], in control T cell membranes, but not in PMA-treated T cell membrane, suggesting that CD4 and Nef interacted with each other in T cells, and the phosphorylation disrupted the CD4-Nef interaction.
Mostaghel et al. (1998)CD4T cellsSurprisingly, we find that CD4+ T cells from the class II mutant mice, having been selected in the absence of a productive class II-CD4 interaction, fail to functionally engage CD4 even when subsequently provided with a wild-type class II ligand.
Santori et al. (2004)TCRT cellsThe preference for distinct TCR contacts depends on neither the affinity/avidity of TCR engagement (except in the most extreme ranges), nor the maturity of engaged T cells.
Schwarz et al. (1996)ILAT-cellThese results suggest that ILA may act by cross-linking its ligand and thereby inhibit T-cell proliferation.
Sandor et al. (1990)IgAT cellT cell populations that did not constitutively express IgA receptors failed to bind IgA after prolonged incubation with oligomeric IgA suggesting that if such cells can express IgA receptors they require other signals to induce their expression.
Sandor et al. (1990)IgAT cellsConsistent with this possibility is the finding that resting splenic T cells did not bind IgA but their activation with Con A or mAb anti-T3 resulted in high level expression of IgA receptors.
Matsuzawa et al. (2002)FasT cellsTaken together with the fact that DN T cells massively express Fas ligand (FasL), this study implied that FasL overexpressed on DN cells may be involved in the accumulation of DN T cells in LN, LN atrophy and wasting syndrome, and that lprcg Fas, which can bind to Fas ligand but not transduce apoptosis signal into cells, may modulate these pathological conditions by interfering with the binding of FasL to Fas.
Life et al. (1993)HSP60T cellsThe GroEL specific T cells did not respond to heat shocked human cells; this suggests (but does not prove) that they do not crossreact with human HSP60.
Guyot et al. (1996)CD2T-cellWe demonstrate that CD2 receptor engagement, but not CD3 crosslinking, induces apoptosis in lymphocytes transformed by human T-cell lymphotrophic virus type I (HTLV-I).
Nicolas and Thivolet (1989)IgET cellsAlternatively, Langerhans cells from normal individuals do not bind IgE molecules and are ineffective in stimulation of allergen specific T cells.
Shirakawa et al. (2006)DNAM-1T cellsHere, we show that, although the TCR-mediated signal induced the serine phosphorylation of DNAM-1, DNAM-1 did not associate with lipid rafts in CD4+ T cells derived from mice deficient in LFA-1 expression, indicating that lipid raft recruitment of DNAM-1 depends on LFA-1 expression.
Zhang et al. (2004)Oct-2HIV-1 LTRT cellsOur studies demonstrate that Oct-1 and Oct-2 fail to bind to the HIV-1 LTR and have no effect on HIV-1 transcription in primary human CD4 T cells.
Reich et al. (2000)CD95T cellsThis report demonstrates that neither TNF receptor-ligand interactions nor CD95 was required for down-regulation of LCMV-specific CD8 T cells following acute LCMV infection in vivo.
Smith and Potter (1998)CD8T cellsAlloreactive T cells that do not require TCR and CD8 coengagement are present in naive mice and contribute to graft rejection.
Knollmann et al. (1997)CD4T-lymphocyteThese three features showed no association with CD4(+)-T-lymphocyte count or CDC category.
Zhang et al. (2004)Oct-1HIV-1 LTRT cellsOur studies demonstrate that Oct-1 and Oct-2 fail to bind to the HIV-1 LTR and have no effect on HIV-1 transcription in primary human CD4 T cells.
Evans et al. (1977)TH1T-cellA heterologous antihuman T-cell serum (anti-TH1), raised against purified peripheral T cells, and absorbed with an autologous Ig+ line, was shown to bind specifically to T- but not to B-lymphoid cells by both a complement-dependent cytotoxic assay and indirect immunofluorescence.
Bardos et al. (2003)CD4T cellsThe CD4+CD25- T cells, which did not bind to magnetic beads, were collected from the flow through the washing steps (purity >98%).
Tan et al. (1993)BB1CD28T cellsSecondary T cell proliferative responses to specific alloantigen were inhibited by addition to the primary culture of monovalent Fab fragments of anti-CD28 monoclonal antibody (mAb) 9.3, which block interaction of CD28 with B7/BB1 without activating T cells.
Vijayan et al. (2005)CD95T cellsIn this model, islet grafts from C3H mice that carry the lpr mutation, and therefore lack the ability to undergo apoptosis through CD95-CD95L interaction, were completely protected when grafted in autoimmune diabetic mice despite periinsulitis (infiltration of T cells) which however did not progress to islet destruction.
Charo et al. (2001)hsp65T cellsInterestingly, T cells specific for this epitope did not recognize the corresponding human hsp65 homologue, probably due to structural differences as revealed by modeling studies.
Killeen et al. (1993)CD4T cellIn vivo experiments show that, whereas helper T cell development is impaired in CD4-deficient mice, high level expression of a transgenic CD4 that cannot bind lck rescues development of this T cell subset.
Nevala and Wettstein (1997)CTT-1CTLsCTT-1 was recognized by B6 CTLs specific for these inbred strains, except for the LP and 129 strains that stimulated CTL specific for the CTT-8 peptide expressed by these two strains.
Caputo et al. (2010)DQ8T celltTG-catalyzed deamidation of specific glutamine residues within naturally digested gluten peptides generates negatively charged amino acid residues that bind with an increased affinity to the HLA-DQ2/DQ8 molecules, thus potentiating T cell activation.
Beck et al. (2010)tumor-specific antigensT cellsIn contrast to antigen-specific alphabeta-T cells (adaptive immune system), gammadelta-T cells can recognize and lyse malignantly transformed cells almost immediately upon encounter in a manner that does not require the recognition of tumor-specific antigens (innate immune system).
Gabrielli et al. (2009)b-VHCDR3T cellsThe results showed that the peptide receptive cells were PM; conversely, DC, PMN and T cells did not show any significant interaction with b-VHCDR3 (Fig. 1C).
Scholzen et al. (2009)iRBCsT cellsFoxp3 expression in CD4 T cells was not induced when purified T cells as opposed to whole PBMCs were co-cultured with iRBCs, demonstrating that induction of Foxp3+ CD4 T cells is not due to a direct interaction of T cells with iRBCs but dependent on other cells present in the co-culture system (Figure 5A).
Liu et al. (2009)tumor-specific antigensT cellsBACKGROUND AND AIMS: gammadelta-T cells can recognize and kill malignant cells, particularly those of epithelial origin, through mechanisms which do not require the recognition of tumor-specific antigens (innate immune response).
De Silva and Moss (2008)wild type VACVT lymphocytesIn contrast, wild type VACV is unable to bind to and enter resting T lymphocytes [45].
Hestvik et al. (2008)myelin proteinsT cellNo cross reactivity with myelin proteins was detected in GA-reactive T cell lines or clones from CSF.
Damsker et al. (2007)heparan sulfate receptorsT cellsFurthermore, we show that unlike resting CD4+ T cells, the cyclophilin-mediated migration of activated T cells does not require interaction with heparan sulfate receptors but instead, is dependent on CD147 interaction alone.
Schlosser et al. (2007)HLA-AT lymphocytesThe resulting cleavage products fail to bind to HLA-A(*)0201 and are not recognized by T lymphocytes.
Zhao et al. (2006)cellT cellBut there has been no direct evidence showing the engagement of gammadelta T cell receptors (TCR) of the induced cells with MICA.
de Haan et al. (2005)WTT cellsFurthermore, T cells specific for the modified peptides did not cross recognize the WT peptide.
Cobb and Kasper (2005)cellT-cellAdaptive immune responses have long been considered the "territory" of antigenic proteins, whereas carbohydrates are characterized as T-cell-independent antigens that are not typically recognized by the complete adaptive machinery.
Arce et al. (2005)T14IT cellsBlockade of GM(1) on the surface of CD8(+) T cells by LT-IIa(T14I), a mutant that binds only to GM(1) but does not induce apoptosis, did not inhibit induction of apoptosis by LT-IIa.
Sugahara et al. (2004)MAT-cellInterestingly, mice immunized with the whole MA mounted strong CD4+ T-cell responses to the identified Th epitope, whereas mice immunized with mutant MA proteins that were not bound to the plasma membrane failed to mount efficient CD4+ T-cell responses, despite the presence of the Th epitope.
Fallarino et al. (2003)FasT cellT cell apoptosis was observed at relatively low concentrations of kynurenines, did not require Fas/Fas ligand interactions and was associated with the activation of casapase-8 and the release of cytochrome c from mitochondria.
Fallarino et al. (2002)FasT cellT cell apoptosis was observed at relatively low concentrations of kynurenines, did not require Fas/Fas ligand interactions, and was associated with the activation of caspase-8 and the release of cytochrome c from mitochondria.
Richardson et al. (2002)TatT-cellAlternatively, Tat specific CD8+ T-cell responses may not appropriately recognize infected cells in vivo in this model.
Deaglio et al. (2001)CD31T cellsResults are as follows: 1) LP T cells express an enzymatically active form of CD38, characterized by a modified ratio between cyclase and hydrolase functions; 2) LP T cells do not mobilize Ca2+ upon CD38 ligation, as seen in PB T cells (this condition is due to a lack in activation of PLC- g, constantly observed in PB T lymphocytes); 3) The early steps of CD38 signaling involve activation of lck, syk, and LAT; 4) Late events include synthesis and release of IL-2, IL-4, IL-5, IL-10, IFN-g and GM-CSF; 5) The uniqueness of the CD38 pathway in LP T cells is not caused by impaired interactions with the CD31 ligand.
Dong et al. (2000)HLA-DR4Dw4T cellThe degradation product is resistant to further cleavage, accumulates in the culture supernatant, and does not bind to HLA-DR4Dw4 or stimulate T cell reactivity.
Hausser et al. (1999)thetaT cellsIn T cells, the 14-3-3tau isoform has been shown to associate with protein kinase C theta and to negatively regulate interleukin-2 secretion.
Portolés et al. (1999)CD3T lymphocytesAntibody-induced CD3-CD4 coligation inhibits TCR/CD3 activation in the absence of costimulatory signals in normal mouse CD4(+) T lymphocytes.
Burakova et al. (1997)mouse homing receptorsT cellsCONCLUSIONS: The different homing patterns exhibited by the T and B lymphocytes indicate that the homing receptors on human B cells might be cross-reactive with their mouse counterparts, in contrast to the human T cells, which seem to be unable to interact with the mouse homing receptors.
Griffith and Pusey (1997)HLA genesT-cellIn most T-cell-dependent autoimmune diseases there are clear positive and/or negative associations with HLA genes.
Chen and Dierich (1996)mAb 4E10T cellsWe demonstrated by flow cytometry that mAb 2F5 could block gp41-binding to human cell lines H9 (T cells), Raji and U937, but the control mAb 4E10 that recognizes another region of gp41 (amino acids 686-728) and can not inhibit HIV infection, did not block this binding.
Hansen (1995)major histocompatibility antigensT-cellHowever, endometrial lymphocytes are distinct in many respects from lymphoid cells at peripheral sites; one major subpopulation expresses the gamma delta T-cell receptor and may not recognize major histocompatibility antigens.
Raab et al. (1994)p59fynT cellsNo binding between p59fyn(T) and CD5 was detected in T cells.
Raab et al. (1994)TT cellsNo binding between p59fyn(T) and CD5 was detected in T cells.
Claësson and Nissen (1994)beta 2mT-cellThree T lymphomas and one IL-2-dependent T-cell line (HT-1) bound substantial amounts of h beta 2m, whereas P815 mastocytoma cells, an Abelson virus-infected pre-B cell line (ABLS-8), X63 B-lymphoma cells and YAC cells did not bind h beta 2m.
Tanaka et al. (1993)T-cell integrinsT-cellAdhesion requires not only integrin ligands on the endothelium, but also activation signals because T-cell integrins cannot bind well until they are activated.
Berkowitz and Braunstein (1992)MHCT cellsThese results sharply contrast with observations made in the analysis of Ag-specific T cells and lead to the suggestion that a subset of alloreactive T cells are not peptide specific and can directly recognize MHC polymorphisms.
Cherrie et al. (1992)major histocompatibility complex phenotypeT cellsRecognition was major histocompatibility complex class I restricted, but no association between major histocompatibility complex phenotype and protein specificity of T cells was seen.
Arvin (1992)VZV proteinsT cellsProliferation or cytotoxicity assays, done under limiting dilution conditions to estimate responder cell frequencies, indicate no preferential recognition of VZV proteins by human T cells.
Stiemer et al. (1992)Other S-antigen peptidesT-cellOther S-antigen peptides with homologies to epitope S2 and peptides exhibiting the pathogenic and T-cell proliferation inducing sites did not bind these mAbs.
Hillert et al. (1991)cellT cellNo association with germline T cell receptor beta-chain gene alleles or haplotypes in Swedish patients with multiple sclerosis.
Harding et al. (1991)class II major histocompatibility complex moleculesT-cellPolysaccharides do not appear to bind to class II major histocompatibility complex molecules, which explains the T-cell independence of polysaccharide antigens.
Braun and Arnold (1991)Myf proteinsT cellsCombinations of Myf proteins with one another and with lyl-1, and HLH protein from human T cells, do not bind to DNA in vitro.
Kabelitz et al. (1990)hsp 65T cellsEstablished clones of mycobacteria-reactive gamma/delta+ T cells specifically recognized mycobacteria, but neither PPD nor hsp 65.
Davis et al. (1990)CD3 complexT cellThese findings suggested that the interaction between fibronectin and its receptor transduced a signal to the T cell and did not merely stabilize the interaction between anti-CD3 and the CD3 complex.
Cruz and Bergstresser (1990)MHCT cellsThe seminal observation made 30 years ago that T cells do not discriminate between native and denatured proteins, whereas B cells generally do, can now be explained by the fact that T cells never see antigens in their native conformation and that intact proteins cannot associate simultaneously with MHC molecules and the TCR.
Vandebriel et al. (1989)anti-kappa/lambda L chain antibodiesT cellImmunochemical studies showed that both factors have a molecular mass between 45 and 90 kDa and bind to the mAb 14-30 (directed against specific T cell factors), but not to anti-kappa/lambda L chain antibodies.
Sakai et al. (1989)major histocompatibility complex proteinsT cellsPrevention of experimental encephalomyelitis with peptides that block interaction of T cells with major histocompatibility complex proteins.
Ciccone et al. (1988)WT31 mAbT lymphocytesThe resulting populations were CD2+4-8- expressed variable proportions of CD3+ cells (40-90%), and did not react with the WT31 mAb, which is specific for a framework determinant of the alpha/beta heterodimer that serves as receptor for antigen on most human T lymphocytes.
Inghirami et al. (1988)alpha immunoglobulin heavy chainsT lymphocytesBiotinylated EBV efficiently bound to all B lymphocytes, including those bearing surface mu, delta, gamma, and alpha immunoglobulin heavy chains or the surface CD5 (Leu-1) marker, but not to T lymphocytes, natural killer cells, or monocytes.
McDuffie et al. (1988)MHC moleculesT cellWe conclude that clonal deletion events during thymic development may be initiated by T cell precursor interactions with MHC molecules against which the mature clones display no measurable reactivity.
Sterkers et al. (1987)HLA moleculesT cellThis regulation of IL-2 receptor expression by AC was specific of adherent cells, did not involve Fc receptors, was impaired when AC were metabolically inactivated and did not require T cell-AC interaction via LFA1, CD4, or HLA molecules.
Spits et al. (1986)target antigenT-cellFurthermore, T-cell receptor and target antigen cannot interact unless there is conjugate formation.
Lakey et al. (1986)L3T4T cellsThus, either Ia does not bind L3T4 or, if it does, I-Ek must be a sufficient ligand for L3T4 for T cells that recognize their antigen in the context of I-Ek.
Chizzolini and Perrin (1986)Plasmodium berghei antigenT cellThese clones secreted IL 2 in response to M.Ag. 4) Differential patterns of reactivity to native M.Ag, heat-stable antigens, and heat-precipitated antigens were exhibited by T cell clones, and the tested clones did not recognize Plasmodium berghei antigen.
Thomas (1985)protein antigensT cellsIn addition, T cells that interact with class II MHC antigens do not bind foreign protein antigens in their native form, but seem to recognize only proteolytic peptide fragments as the relevant antigen.
Youngren et al. (1984)RD114V proteinsT-cellNo binding was seen to human T-cell leukemia virus, bovine leukemia virus, equine infectious anemia virus, or RD114V proteins, however.
Boldt et al. (1984)OKT4/anti-Leu3a reagentsT lymphocytesBaboon T lymphocytes did not react with the OKT3/anti-Leu4 or OKT4/anti-Leu3a reagents which detect, respectively, Tp19-29 and Tp55, major surface glycoproteins on human T lymphocytes.
Shaut et al. (1983)DRT cellsThis lack of cross-reactivity suggests that mouse T cells primed toward Ia determinants do not regularly recognize cross-reacting determinants of DR or D-associated antigens expressed on human PBLs.
Shaut et al. (1983)D-associated antigensT cellsThis lack of cross-reactivity suggests that mouse T cells primed toward Ia determinants do not regularly recognize cross-reacting determinants of DR or D-associated antigens expressed on human PBLs.
Delovitch et al. (1982)host I-A antigensT cellsBy contrast, donor T cells that either bind or do not bind host I-A antigens display no H-2-restricted interaction and help both donor and host immune B cells.
van de Griend et al. (1982)OKT3T lymphocytesThe first subpopulation accounts for about 70% of the total T gamma cell population, does not bind OKT3 (a monoclonal antibody directed against an antigen present on most T lymphocytes), and displays strong killer (K) cell and natural killer (NK) cell activity.
Tsudo et al. (1982)Ia-like antigenT cellsIn the mixed lymphocyte culture, the expression of Ia-like antigen on allo-activated T cells was also inhibited by anti-Tac antibody, although the antibody does not recognize Ia-like antigen.
Semenzato et al. (1982)OKT-11 monoclonal antibodyT-cellIn the second, E-rosette formation was found to be independent of both surface immunoglobulins and the classic E-rosette receptor since the leukemic cells were recognized neither by the OKT-11 monoclonal antibody nor by other markers specific to T-cell lineage.
Steinman et al. (1979)surface Ig and T-cell antigensT-cellDCs, however, lacked surface Ig and T-cell antigens, and did not bind or interiorize opsonized erythrocytes.
Tachibana et al. (2000)gp120CD4T cellIn this report, coreceptor functions of mutant human CD4 molecules, which have no or reduced affinity to an HIV envelope protein, gp120, were assessed in a murine T cell receptor/class II MHC recognition system.
Page et al. (1997)IL-7RT cellsFurthermore, IL-7R:gamma c chain association correlates with the expression of JAK-3 in T cells, but not in transfected COS-7 cells.
Sharma et al. (1997)hsp60T-cellT-cell recognition of H. pylori hsp60 was found in both infected and uninfected subjects, and there was no recognition of human hsp60.