Viewing negative mentions of gene expression of HLA-E (H. sapiens) in T cells

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Document Target Regulator Anatomy Sentence
Morandi et al. (2009)MHCT cellNK cell recognition of cells that do not express or express low amounts of MHC class I molecules results not only in direct killing of target cells but also in the generation of specific T cell responses consequent to the induction of dendritic cell (DC) activation.
Yoong and Adams (1998)MHCT-cellThe absence of autologous tumour-specific cytolytic T-cell (CTL) activity may be due to the poor immunogenicity of colorectal tumour cells, which we found expressed only low levels of MHC I antigens and CD54 and failed to express MHC II antigens or the co-stimulatory molecules CD80, CD86 or CD106.
Chou (1993)MHCT-cellUnlike IBM, there is no abnormal sarcolemmal expression of MHC-I antigen in IBMD as a sign of T-cell-mediated cytotoxicity causing myofibre destruction.
Schnabl et al. (1990)MHCT lymphocytesThe 90/45 kD LA45 proteins thus appear to be non-beta 2m-associated MHC class I alpha chains that are selectively expressed by activated but not by resting human T lymphocytes.
Hayashi et al. (1988)MHCT-cellThis phenotype marks the suppressor-cytotoxic subset. (2) These cells do not express the natural killer cell marker NKH-1, which is present on a subset of CD8-positive cells in peripheral blood. (3) The infiltrating cell expresses class I (HLA A, B, C), but not class II (DR and DQ), major histocompatibility complex (MHC) molecules. (4) Other T-cell surface molecules, including the activation antigens interleukin-2 receptor, Ta1, and T11-3, as well as the marker 2H4, are largely not expressed. (5) Endothelial cells express both class I and class II MHC molecules and the 4B4 molecule in both MS and control tissue. (6) Astrocytes within the vicinity of MS lesions are predominantly class II MHC-negative.
Dukhanina et al. (2010)MHCT-cellParticularly, we show that a protein broadly known for its protective functions such as Hsp70 can make a tumoricidal "binary weapon" with another nontoxic protein Tag7 (PGRP-S); that the same Hsp70, a ubiquitous intracellular chaperone, when expressed on the MHC-negative tumor cell surface, can itself be the hallmark of immune evasion rather than a primordial MHC substitute; that a device functionally equivalent to the T-cell receptor (Tag7-Centered Recognizer) can be assembled of components in no way related to the classical pathways of T-cell-mediated immunity, and operate where the orthodox immunosurveillance fails; and that one and the same protein Mts1 (S100A4) under different circumstances may work as "reactive armor" of a tumor cell against humoral agents and as a vital part of the T-cell machinery aimed against immunoevasive cells, i.e., perform both prometastatic and antimetastatic functions.
Nisbet-Brown et al. (1987)MHCT cellsIn addition to T cells that recognized TT in association with donor class II MHC antigens, we found clones that simultaneously expressed self-restricted antigen recognition and alloreactivity, and clones with specificity for antigen in the context of MHC antigens not expressed by the T-cell donor.
Janjanin et al. (2008)MHCT cellsT-MPCs did not express class II major histocompatibility (MHC) antigens, and in a similar but less pronounced manner compared with BM-MPCs, T-MPCs were immunosuppressive, inhibiting the proliferation of T cells stimulated by allogeneic T cells or by non-specific mitogenic stimuli via an indoleamine 2,3-dioxygenase-dependent mechanism.
Holzer et al. (1997)MHCT cellsFurthermore, presenting either SEA or SEAD227A to MHC class II-negative mononuclear cells by MHC class II-negative tumour cells did not result in significant blast formation of T cells, up-regulation of CD25 or cytokine release.
Li Pira et al. (2010)MHCT-cellIf a second peptide with the same MHC binding capacity is present, it can replace the cleavable peptide and generate a new MM with a different specificity (i.e. recognized by another T-cell receptor differing for fine specificity but not for MHC restriction).
Szekeres-Bartho (2002)MHCT cellsSince polymorphic MHC is absent from the trophoblast, presentation of fetally derived antigens is unlikely to be MHC restricted. gamma/delta T cells recognize a distinct group of ligands with a smaller receptor repertoire than alpha/beta T cells.
Kuroki and Maenaka (2007)MHCT cellAt the maternal-fetal interface, trophoblasts do not express major classical MHC class I molecules (MHCI), HLA-A and -B, to prevent normal T cell responses.
Kuroki and Maenaka (2007)MHCT cellAt the maternal-fetal interface, trophoblasts do not express major classical MHC class I molecules (MHCI), HLA-A and -B, to prevent normal T cell responses.
Martin (1993)MHCT cellsThus, the lymphokines and MHC class II-specific cytotoxic T cells generated by CD4 cells were relatively ineffective for enhancing engraftment, possibly reflecting the fact that the host T cells that contain effectors responsible for causing rejection do not express MHC class II antigens.
Hewitt and Feldmann (1989)MHCT cellNo Ag or IL-2 from the propagation procedure was carried over into assays and two-color fluorescence-activated cell sorter analysis of each clone detected no contaminating cells with the phenotype of monocytes, macrophages or B cells; in each T cell clone, all cells expressing MHC class II Ag co-expressed CD3.
Serreze et al. (1994)MHCT-cellsThese NOD-B2mnull mice do not express cell surface MHC class I molecules or produce detectable levels of CD8+ T-cells and are diabetes and insulitis resistant.
Chang et al. (1995)MHCT cellsIt has long been a puzzle that MHC class II molecules are expressed in human T cells after activation but not in mouse T cells; this expression is believed to play a role in the cell mediated immune response.
Thompson et al. (2008)MHCT cellsBecause the vaccine cells do not express the MHC II-associated invariant chain (Ii), we hypothesized that they will present endogenously synthesized tumor peptides that are not presented by professional Ii(+) antigen presenting cells (APC) and will therefore overcome tolerance to activate CD4(+) T cells.
Gowrishankar et al. (2010)MHCT cellsVZV antigen-positive neurons did not express detectable major histocompatibility complex (MHC) class I, nor did CD8(+) T cells surround infected neurons, suggesting that mechanisms of immune control may not be dependent on direct contact.
Boyle et al. (2001)MHCT cellsWe demonstrate that CD4(+) T cells capable of recognizing B27 can be isolated from humans by coculture with the MHC class II-negative cell line T2 transfected with B27.
Ingulli (2008)MHCT cellsWhen the donor and recipient differ, for example, at the MHC class I level, cytotoxic CD8 T cells specific for donor peptides bound to recipient MHC class I molecules (indirect pathway) would be unable to kill parenchymal cells of the graft because the graft cells express donor and not recipient MHC class I molecules.
Fox et al. (2009)MHCT cellBecause the APCs used for these experiments do not express MHC class II molecules on the cell surface and have reduced MHC class I expression [36], they should not stimulate marked alloreactive responses from the peripheral blood T cell populations of most donors.
Marrack et al. (1990)MHCT cellStaphylococcal enterotoxin-mediated weight loss is MHC dependent, and is almost absent in animals expressing MHC class II molecules, which, complexed with SEB, are poor T cell stimulants.
Jeras et al. (2010)MHCT cellThis statement is even more convincing as CD4+ T cell help is required for the onset and/or maintenance of the CD8+ T cell memory, closely related to increased in vivo survival of CTLs as well as for enhancing the cellular immunity against tumors lacking MHC class II expression.
Geiger et al. (2005)MHCT cellsFurthermore, if the vaccine cell is the direct APC for T cell stimulation, responses are limited to CD8+ T cells because the RCC cells do not express MHC class II molecules.
Krishnan et al. (2008)MHCT-cellTransgenic (Tg) mice expressing HLA class I alleles and lacking murine MHC class I represent a useful model for the pre-clinical evaluation of human vaccines, which focus on induction of CD8(+) T-cell responses.
Serreze et al. (2008)MHCT cellsWhen expressed in NOD, but not C57BL/6 (B6) genetic background mice, the common class I variants encoded by the H2g7 MHC haplotype aberrantly lose the ability to mediate the thymic deletion of autoreactive CD8+ T cells contributing to type 1 diabetes (T1D).