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Symbol CD69 contributors: mct - updated : 15-02-2016
HGNC name CD69 molecule
HGNC id 1694
  • an extracellular carbohydrate recognition domain homologous with C type lectin family member, group V, like Ly-49, C-type lectin-like domain (CTLD)
  • a glycosylation site with typical or atypical motif-representing the molecular basis for homo or heterodimerization
  • conjugated GlycoP , PhosphoP
    mono polymer homomer , dimer
    interspecies homolog to rattus Cd69
    homolog to murine Cd69
  • superfamily of type II transmembrane receptors as natural killer cell lectin like NKG2
  • CATEGORY antigen , receptor membrane
    SUBCELLULAR LOCALIZATION     plasma membrane
  • single-pass type II integral membrane glycoprotein
  • expressed at the cell surface as a type II homodimeric membrane protein
  • basic FUNCTION
  • acting as a T cell activation inducer molecule
  • playing a pivotal role in cellular signaling
  • involved in lymphocyte proliferation
  • functioning as a signal transmitting receptor in lymphocytes, natural killer (NK) cells, and platelets
  • may participate in such diverse functions as cell aggregation, cellular cytotoxicity, and release of cytokines and inflammatory mediators
  • inhibiting S1P1 chemotactic function and leading to downmodulation of S1P1
  • earliest lymphocyte activation antigen and a universal leukocyte triggering molecule expressed at sites of active immune response
  • plays a crucial role in the pathogenesis of allergen-induced eosinophilic airway inflammation and hyperresponsiveness
  • limits differentiation into proinflammatory helper T cells (Th17 cells)
  • early activation receptor acting as an intrinsic modulator of the T-cell differentiation program that conditions immune inflammatory processes
  • CD69 regulates S1P-induced skin dendritic cells migration by modulating S1P(1) function
  • is critical for the generation and maintenance of professional memory Th lymphocytes, which can efficiently help humoral immunity in the late phase
  • regulates the persistence of memory Th cells on survival niches organized by stromal cells
  • functions as a homing receptor on CD4 T cells and is required for relocation to, and persistence in, the bone marrow, and its function is essential for the generation of memory Th cells
  • is negative regulator of inflammatory responses in intestine as it decreases the expression of chemotactic receptors and ligands and reduces the accumulation of CD4 T cells in colonic lamina propria (cLP) during colitis
  • exerts a complex immunoregulatory role
  • CD69 is involved in immune cell homeostasis, regulating the T cell-mediated immune response through the control of Th17 cell differentiation
  • LGALS1 and CD69 are a novel regulatory receptor-ligand pair that modulates Th17 effector cell differentiation and function
  • CELLULAR PROCESS cell life, proliferation/growth
    PHYSIOLOGICAL PROCESS immunity/defense
    signaling signal transduction
    a component
  • disulfide-linked homodimer on the cell surface
  • homodimer composed of heavily glycosylated subunits
    small molecule metal binding, other,
  • Ca2+
  • carbohydrates
  • protein
  • CALR
  • integral membrane interaction between CD69 and S1PR1 (CD69 induces an S1PR1 conformation that shares some properties of the ligand-bound state, thereby facilitating S1PR1 internalization and degradation)
  • maintenance of immune tolerance by Foxp3+ regulatory T cells requires CD69 expression
  • expression of CD69, by interfering with S1PR1 function, is a critical determinant of prolonged T cell retention and local memory formation
  • cell & other
    induced by antigens, mitogens or activators of PKC on the surface of T and B lymphocytes. By interaction of IL-2 with the p75 IL-2R on the surface of NK cells
    corresponding disease(s)
    Variant & Polymorphism
    Candidate gene
    Therapy target
    target molecule for the therapy of immune-mediated diseases
    could be a possible therapeutic target for asthmatic patients
  • Cd69 -/- mice (Sancho, 2003)
  • CD69 knockout mice exhibit an enhanced or reduced susceptibility to different experimental models of inflammatory diseases, including those mediated by T helper 17 (Th17) lymphocytes