viewpointCostimulation of T cells for tumor immunity
References (24)
- et al.
Adv. Cancer Res.
(1969) Adv. Cancer Res.
(1992)Adv. Immunol.
(1991)- et al.
Adv. Immunol.
(1992) Cell
(1991)- et al.
Curr. Opin. Immunol.
(1992) - et al.
Cell
(1992) Cell
(1992)- et al.
- et al.
Nature
(1991)
Science
Cited by (345)
CAR-T cells: Early successes in blood cancer and challenges in solid tumors
2021, Acta Pharmaceutica Sinica BReview of immune checkpoint inhibitors in immuno-oncology
2021, Advances in PharmacologyCitation Excerpt :The binding of the MHC:peptide complex to a TCR is the first step in activating a naive T cell. To be fully functional the T cell requires a second signal (Fig. 1) (Chen, Linsley, & Hellstrom, 1993; Hellstrom, Hellstrom, Linsley, & Chen, 1993). The interaction between CD28 on a T cell with CD80 and CD86 on an APC is termed the “co-stimulatory” pathway.
Autoantibodies as diagnostic and prognostic cancer biomarker: Detection techniques and approaches
2019, Biosensors and BioelectronicsCitation Excerpt :Melanoma antigens are usually expressed in the male testicular cells. Additional mechanisms associated with autoantibodies inhibitions are i) downregulation of antigen presenting cell, MHC class I molecules (Hofbauer et al., 2005) ii) lack of expression of co-stimulatory molecules on the tumor cells (Chen et al., 1993) iii) tumors producing immunosuppressive factors like TGF-, IL-10 and VEGF (Kusmartsev and Gabrilovich, 2006). The immunogenicity of a tumor depends on several factors that may be variable even among tumors of a similar type.
Critical role of transcription factor PU.1 in the expression of CD80 and CD86 on dendritic cells
2011, BloodCitation Excerpt :In the present study, we succeeded in both the suppression and induction of CD80 and CD86 expression by targeting a single transcription factor. One crucial role of CD80 and CD86 is the costimulation of the T-cell response and the induction of T cell–mediated immunity, such as the rejection of tumors.52,53 Conversely, their other crucial role is to block the development of several autoimmune diseases or to induce donor-specific tolerance to allografts by abrogation of CD28/B7 signals.47-50
Psoriasis patients generate increased serum levels of autoantibodies to tumor necrosis factor-α and interferon-α
2009, Journal of Dermatological ScienceCitation Excerpt :TNF-α dependent inhibition of neutral red uptake of 4 × 104 U937 cells/well was studied in the absence of blocking Abs and in the presence of commercial anti-TNF-α Abs (TNF-alpha/TNFSF1A, R&D), and Abs purified from the three psoriatic patients (1 μg/ml of each Ab). Since the levels of IFN-α correlate with increased inhibition of T-cell growth, the ability of anti-IFN-α auto Abs purified from three psoriatic patients with high titers to prevent IFN-α induced inhibition of normal T-cells proliferation was examined [16]. Anti-CD3ɛ mAb (BD Biosciences) was immobilized to a 96-well plate (2 μg/ml, 50 μl/well) for 1 h at 37 °C.