Effects of <scp>CXCL</scp>13 inhibition on lymphoid follicles in models of autoimmune disease

Abstract The chemokine CXCL 13 has a key role in secondary lymphoid tissue orchestration and lymphoid neogenesis. Transgenic mice deficient in CXCL 13 or its receptor CXCR 5 have severely impaired lymph node development, lack peritoneal B‐lymphocytes and are deficient in circulating antibodies to common bacterial antigens. However, total circulating numbers of B‐lymphocytes are slightly elevated and humoral responses to T‐dependent or blood‐borne antigens are relatively normal. Lymphoid neogenesis is an aberrant process that occurs in chronically inflamed tissue and provides a microenvironment supportive of pathogenic B‐cell survival and activation. Here, we describe the impact of therapeutic dosing of a CXCL 13 antibody in a mouse model of arthritis, and detail the contribution CXCL 13 makes to lymphoid follicle microenvironment, without affecting humoral immune responses.