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Coexpression of CD200R-CD28 enhances function in WT1 (show CD200R1 Proteins)-specific T-cell receptor - transduced (show CD8A Proteins) human primary T cells.
the upregulation of others syncytial molecules, including LAG3 (show LAG3 Proteins), CTLA4 (show CTLA4 Proteins), CD28 and CD3 (show CD3 Proteins), assisting the formation of syncytia with APC (show APC Proteins) cells.
our data provide the first evidence of a strict link between the absence of CD28 and the expression of perforin (show PRF1 Proteins), which is likewise enhanced by the expression of NKG2D (show KLRK1 Proteins), within selected CD4 (show CD4 Proteins)(+) T cells from cervical cancer patients.
Mutation of the basic clusters in the CD28 cytoplasmic domain reduced the recruitment to the CD28-Lck (show LCK Proteins) complex of protein kinase (show CDK7 Proteins) Ctheta; (PKCtheta (show PRKCQ Proteins);), which serves as a key effector kinase in the CD28 signaling pathway.
The mutant CD28 isoforms could accelerate tumor cell growth.
CD3 (show CD3 Proteins)/28-activated T cells expanded in IL-7 (show IL7 Proteins) and IL-15 (show IL15 Proteins) produced greater expansion of memory stem T cells and central memory T cell-derived T cells compared with IL-2 (show IL2 Proteins). Our strategy provides a powerful tool to elucidate the characteristics of CAR-modified T cells, regardless of the protocol used for expansion, reveals the functional properties of each expanded T cell subset.
identified recurrent mutations in CD28 in peripheral T-cell lymphomas. Molecular modeling studies on each of these mutations suggested how these mutants result in increased affinities.
the scaffolding role of RLTPR predominates during CD28 co-stimulation and underpins the similar function of RLTPR in human and mouse T cells.
Our data show that mast cells can costimulate human CD4 (show CD4 Proteins)(+) T cells to induce strong T-cell proliferation, but that therapies aiming at disrupting the interaction of CD28 and B7 molecules do not inhibit mast cell mediated T-cell activation.
High CD28 Circulating Levels are associated with Breast Cancer.
In adoptive therapy of disseminated leukemia, CD200R (show CD200R1 Proteins)-CD28-transduced leukemia-specific CD8 (show CD8A Proteins) T cells eradicated otherwise lethal disease more efficiently than wild-type cells and bypassed the requirement for interleukin-2 (show IL2 Proteins) administration to sustain in vivo activity.
Study shows that CD28 ligation during priming endows T cells with mitochondrial capacity that is important for future T cell responses. We speculate that CD28 temporarily restricts TXNIP (show TXNIP Proteins) and miR33 expression, and this leads to a transient induction of Cpt1a (show CPT1A Proteins) and fatty acid oxidation, which are marked by characteristic changes in mitochondria shape and structure.
findings revealed a dual mechanism of monocyte and neutrophil recruitment by T cells relying on overlapping and nonoverlapping roles for the noninducible costimulatory receptor CD28 and the inflammatory cytokine TNF (show TNF Proteins)
results are consistent with a complex pathway in which CD28 is the primary driver of Treg proliferation and CTLA-4 (show CTLA4 Proteins) functions as the main brake but is also dependent on TCR signals and interactions with CD80 (show CD80 Proteins)/CD86 (show CD86 Proteins).
data suggest that mPEG PV1 (show PLVAP Proteins)-Fab (show FANCB Proteins)' acts mainly on IFN-gamma (show IFNG Proteins)-producing CD4 (show CD4 Proteins)+ T cells and emphasize that this specific CD28 blockade strategy is a potential specific and alternative tool for the treatment of autoimmune disorders in the eye.
BAFF (show TNFSF13B Proteins) upregulates CD28/B7 and CD40 (show CD40 Proteins)/CD154 (show CD40LG Proteins) expression, and promotes the interactions between T and B cells in a BAFF-R (show TNFRSF13C Proteins)-dependent manner
we report that cell-intrinsic deletion of CD28 after the peak of the primary response does not affect the establishment, maintenance, or recall of long-term memory. Thus, if given sufficient time, the progeny of primed CD8 (show CD8A Proteins)(+) T cells adapt to the absence of this costimulator.
Deletion of CD28 co-stimulatory signals exacerbates left ventricular remodeling and increases cardiac rupture after MI through prolongation of the inflammatory period and reduction of collagen fiber in the infarct scars.
The protein encoded by this gene is essential for T-cell proliferation and survival, cytokine production, and T-helper type-2 development. Several alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, T-cell-specific surface glycoprotein CD28
, CD28 antigen (Tp44)
, T-cell-specific surface glycoprotein CD28 homolog
, T-cell costimulatory molecule CD28
, cell surface protein
, costimulatory molecule B7 receptor CD28
, antigen CD28
, T-cell specific surface glycoprotein CD28
, CD28 precursor protein
, T-cell-specific surface glycoprotein CD28-like protein
, CD28 molecule L homeolog