Figure 2.

Schematic representation of known and potential pathways by which eosinophils can contribute to the pathogenesis and maintenance of autoimmunity in bullous pemphigoid. (A) Eosinophils bind anti-BP180 IgG, aligning along the BMZ. (B) Dermal eosinophils express FcεRI which can bind to anti-BP180 IgE leading to DEJ separation. (C) Upon activation with IL-5 eosinophils can lead to DEJ separation and degranulation. (D) MMP9 is secreted from eosinophils and is capable of cleaving BP180. (E) Eotaxin and IL-8 are expressed in the epidermis, acting as eosinophil chemotactic chemokines, attracting further tissue eosinophilia. (F) Eotaxin and MCP-4 are released from eosinophil granules, further driving tissue eosinophilia and Th2 polarization. (G) IL-16 is released from eosinophils and is capable of stimulating T-cell response. (H) Eosinophils can directly degranulate on and (I) directly bind to neurons leading to increase branching and potentially pruritis. (J) Eosinophils secrete IL-31, a major pruritogen which can stimulate nerves. (K) Eosinophils are capable of acting as antigen presenting cells, potentially leading to T-cell responses by binding bound antigen via MHC-II to T-cell receptors. (L) Eosinophils express BAFF and APRIL, potentially stimulating local autoimmune B-cells.