costimulatory molecule

costimulatory molecule

membrane-bound or secreted product of accessory cells that is required for signal transduction.

co·stim·u·la·to·ry mol·e·cule

(kō-stim'yū-lă-tōr'ē mol'ĕ-kyūl)
Membrane-bound or secreted product of accessory cells that is required for signal transduction.
References in periodicals archive ?
Tasuku Honjo, "for their discovery of cancer therapy by inhibition of negative immune regulation." Among his most notable discoveries are the determination of the T-cell receptor structure and that CD28 is the major costimulatory molecule that allows full activation of naive T-cells and prevents anergy in T-cell clones.
Freeman, "Programmed death-1 ligand 1 interacts specifically with the B7-1 costimulatory molecule to inhibit T cell responses," Immunity, vol.
It plays a vital role in regulating T cell activation and maintaining peripheral tolerance as a core costimulatory molecule [2,3].
Paolieri et al., "B7.1 costimulatory molecule is expressed on thyroid follicular cells in Hashimoto's thyroiditis, but not in Graves' disease," The Journal of Clinical Endocrinology & Metabolism, vol.
An example of APC inhibition is the Treg expression of CTLA-4, an inhibitory receptor relative to the T cell costimulatory molecule CD28.
More and more researches demonstrated that the cognate interaction between the inducible costimulatory molecule (ICOS) and ICOS ligand (ICOSL), a member of the CD28 family, is an indispensable signaling for the activation of T cells.
CD8 protein performs the adhesive and costimulatory molecule function of the T cell receptor and can exist in a soluble form.
Other candidates for the permeability factor are cardiotrophin-like cytokine factor-1 (CLCF-1) [4] and autoantibodies against the costimulatory molecule CD40 [5].
DC maturation is critical for inducing immune responses and can be characterized by cellular morphology and selected costimulatory molecule expression, such as that of CD86, CD83, CD80, CD40, and MHC I and II.
DCs treated with adenosine 2A receptor ([A.sub.2]AR) agonists protected the kidney from ischemia/reperfusion injury through suppression of IFN-[gamma] production by NK T cells and decreased costimulatory molecule expression [31].
PVRIG and TIGIT constitute parallel immune checkpoint pathways that counteract DNAM-1, a costimulatory molecule on T cells and NK cells.