B cells in chronically inflamed skin. (48.10)

Abstract

B cells infiltrate extralymphoid tissues in many chronic inflammatory diseases, including cutaneous manifestations of autoimmunity as well as infection. However, the phenotype and function of B cells in the skin remains poorly understood. In a granuloma model of cutaneous inflammation in sheep and mice, B cells increase during the chronic phase of inflammation in both percentage and absolute number in the skin and skin-draining afferent lymph. B cells in the skin and skin-draining lymph are a heterogeneous population that is phenotypically distinct from B cell populations in the spleen and lymph nodes. Many skin B cells exhibit an ‘innate-like’ phenotype co-expressing IgM and CD11b. Furthermore, skin B cells have increased MHCII and CD80/86 expression compared to lymph node or splenic B cells, suggesting that they are well-suited for T cell activation at the site of inflammation. Additionally, skin B cells are not responsive to ligands of chemokine receptors typically associated with skin homing. The data support a model in which innate-like B cells use alternative chemokine receptors to migrate to the skin where they support inflammatory or protective immune responses.