Type I interferon induces CXCL13 to support ectopic germinal center formation

• DOI: 10.1084/jem.20181216
• Publication Date: 2019-02-05T20:14:24Z
• Authors: Alice E. Denton; Silvia Innocentin; Edward J. Carr; Barry M. Bradford; Fanny Lafouresse; Neil A. Mabbott; Urs Mörbe; Burkhard Ludewig; Joanna R. Groom; Kim L. Good-Jacobson; Michelle A. Linte...
• Keywords: CXCL13; Ectopic expression

Ectopic lymphoid structures form in a wide range of inflammatory conditions, including infection, autoimmune disease, and cancer. In the context this response can be beneficial for host: influenza A virus infection–induced pulmonary ectopic germinal centers give rise to more broadly cross-reactive antibody responses, thereby generating cross-strain protection. However, despite ubiquity their role both health little is known about mechanisms by which inflammation able convert peripheral tissue into one that resembles secondary organ. Here, we show type I IFN produced after viral infection induce CXCL13 expression phenotypically distinct population lung fibroblasts, driving CXCR5-dependent recruitment B cells initiating center formation. This identifies as novel inducer CXCL13, which, combination with other stimuli, promote remodeling, converting nonlymphoid permissive functional tertiary structure