B cell traffic through skin increases during inflammation (161.13)

Abstract

B cells infiltrate skin in many chronic inflammatory diseases caused by autoimmunity or infection. Despite their potential to contribute to disease processes, skin-associated B cells remain poorly characterized. Here, we find in an ovine granuloma model of cutaneous inflammation, B cells increase during the chronic phase of inflammation in both relative and absolute number in the skin and skin-draining afferent lymph. Surprisingly, these B cells are a heterogeneous population that is phenotypically distinct from the B cell population in lymph nodes with more ‘innate-like’ B cells co-expressing high levels IgM and CD11b. Furthermore, skin B cells have increased MHCII and CD80/86 expression compared to lymph node B cells, suggesting that they are well-suited for T cell activation at the site of inflammation. Additionally, unlike co-isolated T cells, skin B cells are not responsive to ligands of chemokine receptors typically associated with skin homing, implying that they utilize alternative chemokine receptors to migrate to the skin. In summary, our data show that a population of B cells recirculates through uninflamed and inflamed skin, fulfilling a so far unappreciated role in skin immunity.