Disease relevance of Cd276

• B7-H3-deficient mice developed experimental autoimmune encephalomyelitis several days earlier than their wild-type littermates, and accumulated higher concentrations of autoantibodies to DNA [1].
• Preferential dependence of autoantibody production in murine lupus on CD86 costimulatory molecule [2].
• Attenuation of experimental autoimmune myocarditis by blocking activated T cells through inducible costimulatory molecule pathway [3].

High impact information on Cd276

• B7-H3 inhibited T cell proliferation mediated by antibody to T cell receptor or allogeneic antigen-presenting cells [1].
• B7-H3-deficient mice developed more severe airway inflammation than did wild-type mice in conditions in which T helper cells differentiated toward type 1 (T(H)1) rather than type 2 (T(H)2) [1].
• In addition to causing abnormal MHC expression, the ds nucleic acids increase the expression of genes necessary for antigen processing and presentation: proteasome proteins (e.g., LMP2), transporters of antigen peptides; invariant chain, HLA-DM, and the costimulatory molecule B7 [4].
• We found that a tumor cell line derived from one such tumor expresses the T-cell costimulatory molecule B7-1, the expression of which is normally restricted to antigen-presenting cells [5].
• Pneumocystis cell wall beta-glucans induce dendritic cell costimulatory molecule expression and inflammatory activation through a Fas-Fas ligand mechanism [6].

Biological context of Cd276

• Additionally, B7-1 costimulatory molecule expression and lymphocyte-specific apoptosis were examined [7].

Anatomical context of Cd276

• Moreover, feeding Hsp65/SBTI resulted in a lower number of both spleen and mesenteric lymph node (MLN) cells expressing the costimulatory molecule CD80 (B7-1) [8].
• In this study, we sought to investigate the regulation of costimulatory molecule expression on primary microglia and microglial cell line, BV-2, by pituitary adenylyl cyclase-activating polypeptide (PACAP) and vasoactive intestinal peptide (VIP), potent anti-inflammatory neuropeptides [9].
• Although the mechanisms are not clear, the induction of tolerance to grafted spleens seems to rely mainly on blockage of expression of the costimulatory molecule CD86, by interleukin-10, leading to enhanced apoptosis of allospecific T cells by immature and tolerogenic dendritic cells [10].

Associations of Cd276 with chemical compounds

• Reduction of 1-methyl-1-nitrosourea-induced tumor burden with DNA vaccines encoding mutated ras epitopes and the costimulatory molecule B7.1 [11].

Analytical, diagnostic and therapeutic context of Cd276

• We investigated the in vivo function of the B7 family member B7-H3 (also known as B7RP-2) by gene targeting [1].
• NF-kappaB binding activities, costimulatory molecule (CD40, CD80, CD86) surface expression, IL-12 protein expression and allostimulatory capacity of DCs were measured with electrophoretic mobility shift assay (EMSA), flow cytometry, Western blotting, and mixed lymphocyte reaction (MLR), respectively [12].
• Local or short-term systemic costimulatory molecule blockade prolongs rat corneal allograft survival [13].

References