Acute allergic contact dermatitis (ACD) has been previously linked to secreted osteopontin (sOPN), a glycoprotein with cytokine and chemokine functions. OPN is known to attract myeloid dendritic cells (mDCs) to activate naïve T cells in draining lymph nodes in the skin and induce a TH1 phenotype.
Seier et al. (Am J Path 2010, 176:246-258) follow up on their work identifying osteopontin as a principal player in acute ACD with investigations into the pathophysiology that leads to the chronic condition, which is associated with severe eczema. They discover that OPN attracts memory T cells, monocytes, macrophages, and DCs to the skin in acute exposure. Cytokine function of OPN specifically induces IL-12 secretion and suppresses IL-10 production in macrophages. Then, OPN-related IL-12 production establishes Th1 conditions by skewing mDCs toward IL-12 production, which in turn, augments further OPN secretion. The authors also find that IFN-γ from antigen-specific T cells is critical for activation of OPN production in keratinocytes. The Th1 environment in the epidermis is maintained through cybernetic mechanisms involving OPN, IL-12, and antigen-specific T cells, which support persistent, chronic inflammatory conditions in the skin.
Seier et al. also report that anti-OPN antibody treatment can suppress response in established chronic ACD, suggesting possible prevention and intervention possibilities.
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