| Document |
Target |
Regulator |
Anatomy |
Sentence |
| Liu et al. (1998) | CTLA-4 | | T cells | But patients with SLE had significantly increased percentages of CTLA-4-positive T cells compared with normal controls, implying at least that there was no apparent defective expression of CTLA-4 molecule in human lupus. |
| Schlotmann et al. (2000) | CTLA-4 | | T cells | After initiation of antiplasmodial treatment, it returned to control values within a few days. gammadelta T cells, which also are implicated in the pathogenesis of human malaria, did not express CTLA-4. |
| Xerri et al. (1997) | CTLA4 | | T-cell | CTLA4 was present in neoplastic cells from most (10/11) T-cell malignancies, except for anaplastic and lymphoblastic subtypes (0/4). |
| Newland et al. (2004) | CTLA4 | | T cell | CTLA4 (CD152) is a transmembrane molecule expressed on activated T cells and functions as a negative regulator of T cell activation upon binding to the costimulatory molecules CD80/86. |
| Perkins et al. (1996) | CTLA4 | | T cell | The CTLA4 molecule is not expressed on resting T cells, but is induced after the initial steps of T cell activation. |
| Boulougouris et al. (1998) | CTLA-4 | | T cells | In the absence of intracellular calcium elevation, CTLA-4 was not expressed at the cell surface, and CD80 acted positively as a costimulator of T cells, via CD28. |
| Kuiper et al. (1995) | CTLA-4 | | T cells | Purified B cells did not express CTLA-4 when mitogenically activated with alpha IgM and CD40 Ab, but did express the molecule when cultured in the presence of membranes from activated T cells, which suggests that induction of CTLA-4 expression on B cells was dependent on direct cell-cell contact of B lymphocytes and activated T cells. |
| Lozanoska-Ochser et al. (2008) | CTLA-4Ig | | T cell | Identical results were obtained for T cell adhesion using either CTLA-4 blocking mAb or CTLA-4Ig (abatacept), indicating CTLA-4 as the T cell ligand for these CD86-mediated effects. |
| Freeman et al. (1992) | CTLA-4 | | T cells | CD28 was detected in resting T cells, whereas CTLA-4 was not. |
| Hoffmann et al. (2006) | CTLA-4 | | T-cell | Further analysis revealed that these cells originate from CD45RA+ naive cells within the CD4+ CD25high T-cell compartment, as only this subpopulation homogeneously expressed CD62L, CCR7, cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), and forkhead box P3 (FOXP3), produced no inflammatory cytokines and maintained robust suppressive activity after expansion. |
| Pfoertner et al. (2006) | CTLA4 | | T cells | Furthermore, CD25 as well as other TReg cell molecules (for instance, GITR and CTLA4) are not expressed on all CD4+ T cells with regulatory function [15]. |
| Zaunders et al. (2006) | CTLA-4 | | T cells | The majority of these initial vaccinia virus-specific CD4+ T cells were CD127+ and produced interleukin-2 (IL-2) but not CTLA-4 in response to restimulation in vitro. |
| Elrefaei et al. (2009) | CTLA-4 | | T cells | and IL-10 positive CD8+ T cells did not express CTLA-4. |
| Joosten et al. (2010) | CTLA4 | | T-cells | As mentioned above, the HLA-E/peptide specific T-cells also expressed several markers that have been associated with human CD8+ Tregs, notably CD25 and LAG-3 in the absence of CD127 [32], although they did not express FoxP3, GITR and CTLA4 (Figure 3). |
| Damle et al. (1994) | CTLA-4 | | T cells | Resting CD4+ T cells express CD28 but not CTLA-4 on their surface. |
| Elrefaei et al. (2009) | CTLA-4 | | T cells | TGF-beta and IL-10 positive CD8+ T cells did not express CTLA-4. |
| Elrefaei et al. (2010) | CTLA-4 | | T cells | Interestingly, HIV-specific TGF-beta-positive CD4(+) T cells did not substantially express CTLA-4. |
| Kato et al. (2001) | CTLA-4 | | T cells | The CD28(-)CD4(+) T cells did not express detectable levels of CD25, CD69, V(alpha)24, or CTLA-4 but expressed heterogeneous amounts of CD45 RA on the surface. |
| Wan et al. (2006) | CTLA-4 | | T cells | In this study, initial analysis of costimulatory molecules led to the unexpected observation that, in addition to CD80, several negative regulators (e.g., CTLA-4, programmed death-1 (PD-1), and PD ligand-1) were overexpressed in synovial T cells and macrophages derived from RA patients as opposed to controls. |
| Jaffar et al. (1999) | CTLA-4 | | T cells | FACS analysis revealed that stimulated asthmatic bronchial tissue was comprised of CD4+ T cells that expressed surface CD28 (75. 3%) but little CTLA-4 (4.0%). |
| Ahmadzadeh et al. (2009) | CTLA-4 | | T cells | PD-1(+) TIL expressed CTLA-4 and Ki-67, markers that were not expressed by PD-1(-) TIL and T cells in the normal tissues and PBL. |
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