HLA-DQ is also known as MHC class II DQ monomorphic antigen. The major histocompatibility complex is composed of two heterodimeric glycoproteins (α and β chains) with apparent molecular weights of 27 and 32 kD. In contrast to other MHC class II molecules, both polypeptide chains of HLA-DQ are polymorphic, with the α chain showing an extremely high degree of polymorphism. HLA-DQ is expressed on B cells in the peripheral blood, and weakly expressed on activated T cells and some monocytes. HLA-DQ is absent on hematopoietic progenitors, resting T cells, erythrocytes, and platelets. HLA-DQ is expressed after HLA-DR and HLA-DP in hematopoietic development. HLA-DQ presents peptide fragments mainly from degraded intravesicular and extracellular proteins to CD4+ T lymphocytes. Specific alleles of HLA-DQ have been linked to the pathogenesis of several autoimmune diseases (including diabetes), both as a susceptibility and resistance factor depending on the particular polymorphism.
HLA-DR is a heterodimeric cell surface glycoprotein comprised of a 36 kD α (heavy) chain and a 27 kD β (light) chain. It is expressed on B cells, activated T cells, monocytes/macrophages, dendritic cells, and other non-professional APCs. In conjunction with the CD3/TCR complex and CD4 molecules, HLA-DR is critical for efficient peptide presentation to CD4+ T cells.
Interferon-γ is a potent multifunctional cytokine which is secreted primarily by activated NK cells and T cells. Originally characterized based on anti-viral activities, IFN-γ also exerts anti-proliferative, immunoregulatory, and proinflammatory activities. IFN-γ can upregulate MHC class I and II antigen expression by antigen-presenting cells. The B27 antibody reacts with the human interferon-γ. The B27 antibody can neutralize the bioactivity of natural or recombinant IFN-γ.
IgD, a member of the immunoglobulin (Ig) family, is expressed in naïve B cells. It has 3 Ig-like domains and exists in a transmembrane and a soluble form. In general, IgD is not secreted and usually its expression is lost after the Ig isotype switch. After antigen binding, IgD signals through the CD79a/CD79b (Igα/Igβ) heterodimer, resulting in the activation of the B cell.
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