• CD28
  • CD80 is a 'co-stimulatory' molecule that is part of the CD80/CD28 pathway required for activation of T lymphocytes. (medindia.net)
  • In order to try and prevent bone loss in the research mice whose ovaries were removed and determine how reactive oxygen was exerting its toxic effects, the research team treated the mice with the immunosuppressant CTLA4-Ig, which prevents the activation of T cells by blocking the binding of CD80 to CD28. (medindia.net)
  • Negative selection is the process by which the developing lymphocyte receptor repertoire rids itself of autoreactive specificities.One mechanism requires simultaneous TCR and costimulatory signals initiated by CD28.We propose that these mechanisms represent two distinct clonal deletion strategies that are differentially implemented during development depending on whether immature thymocytes encounter antigen in the thymic cortex or thymic medulla. (nih.gov)
  • CD80 (B7-1) binds both CD28 and CTLA-4 with a low affinity and very fast kinetics. (nih.gov)
  • Preliminary reports have suggested that CD80 binds CTLA-4 and CD28 with affinities (Kd values approximately 12 and approximately 200 nM, respectively) that are high when compared with other molecular interactions that contribute to T cell-APC recognition. (nih.gov)
  • In the present study, we use surface plasmon resonance to measure the affinity and kinetics of CD80 binding to CD28 and CTLA-4. (nih.gov)
  • At 37 degrees C, soluble recombinant CD80 bound to CTLA-4 and CD28 with Kd values of 0.42 and 4 microM, respectively. (nih.gov)
  • The 2D10.4 antibody reacts with human CD80, also known as B7-1, a 55 kDa type I transmembrane protein ligand for CD152 (CTLA-4) and for CD28, a co-stimulatory receptor for the T cell receptor (TCR). (vwr.com)
  • Association of the TCR of a naive T cell with MHC:antigen complex without CD28:B7 interaction results in a T cell that is anergic. (wikipedia.org)
  • More recent work has suggested that CTLA-4 may function in vivo by capturing and removing B7-1 and B7-2 from the membranes of antigen-presenting cells, thus making these unavailable for triggering of CD28. (wikipedia.org)
  • CTLA-4 can also affect signalling indirectly via competing with CD28 for CD80/86 binding. (wikipedia.org)
  • CD48 and CD2 molecular coupling together with other interaction pairs of CD28 and CD80, TCR and peptide-MHC and LFA-1 and ICAM-1 contribute to the formation of an immunological synapse between a T cell and an antigen presenting cell. (wikipedia.org)
  • Protein
  • In addition to that, it has been found, dendritic cell (DC) - Treg interaction causes sequestration of Fascin-1, an actin-bundling protein essential for immunological synapse formation, and skews Fascin-1-dependent actin polarization in antigen presenting DCs toward the T reg cell adhesion zone. (wikipedia.org)
  • Ligand
  • CD80 inmobilised into and ligand added. (cam.ac.uk)
  • Once bound to a cancer antigen, antibodies can induce antibody-dependent cell-mediated cytotoxicity, activate the complement system, or prevent a receptor from interacting with its ligand, all of which can lead to cell death. (wikipedia.org)
  • induce
  • The Ig induction was specific for BMDCs since viable thymocytes incubated with bacteria also failed to induce detectable antigen-specific Ig responses (Fig. 3), ruling out the possibility that carry-over of free bacteria was responsible for the observed Ig responses in vivo. (nih.gov)
  • presentation
  • In vitro, DC phenotype, alloreactivity, antigen processing and presentation, and interleukin (IL)-10 and IL-12 secretion were evaluated. (nih.gov)
  • activate
  • With the assistance of a phosphatase present on the intracellular section of CD45 (common leukocyte antigen), these molecules activate major Th cell intracellular pathways. (wikipedia.org)
  • thymocytes
  • We propose that these mechanisms represent two distinct clonal deletion strategies that are differentially implemented during development depending on whether immature thymocytes encounter antigen in the thymic cortex or thymic medulla. (nih.gov)