In
antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), the
diagnostic value of assays for ANCAs is now widely accepted. ANCAs are known to
bind two key antigens found in neutrophil granules and monocyte lysosomes:
proteinase-3 (PR3) and myeloperoxidase (MPO). ANCAs can activatecytokine-primed neutrophils, causing an oxidative burst, degranulation, therelease of inflammatory cytokines, and damage to endothelial cells in vitro,and an intravenous injection of mouse antibodies specific for mouse MPO induced
pauci-immune necrotizing and crescentic glomerulonephritis in a mouse model
that closely mimics the human disease. The pathogenicity of anti-MPO antibodies
has been demonstrated in vitro and in vivo , but the mechanisms of MPO-ANCA
production have not been clarified. Moreover, the MPO-ANCA titer is not always
associated with disease activity.
The
interaction between CD40 and its ligand (CD40L) is critical to the control of
thymus-dependent humoral immunity and cell-mediated immune responses. CD40L on
the T cells stimulates the B-cell secretion of immunoglobulin isotypes in the
presence of cytokines. The interaction of CD40L with CD40 not only induces a
proliferation of B lymphocytes and their isotype switching; it also mediates a
broad variety of other immune and inflammatory responses. CD40 signaling has
been linked with pathogenic processes of chronic inflammatory diseases such as
autoimmune diseases, neurodegenerative disorders and graft-versus-host disease.
Soluble forms of CD40L, produced by proteolytic cleavage, lack the
transmembrane region and a portion of the extracellular domain, but they
contain the entire tumor necrosis. Read more............
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