Blockage of CXCL13 and LTβR inhibits de novo nasal follicle formation in an IL-17A high mouse model
Next, we investigated the role of CXCL13 and LTα1β2 on eLT formation in the IL-17A high mouse model induced by 100 μg curdlan. We found that blockage of CXCL13 or LTα1β2 completely prevented eLT formation, and partially diminished lymphocyte cluster development in nasal mucosa (Fig 7). Consistently, AID and CD21 mRNA expression in nasal mucosa were reduced in anti-CXCL13 and LTβR-Ig treated mice (Fig E9, A and D). The mRNA expression of CXCL13 and LTβ were decreased in anti-CXCL13 treatment mice (Fig 7, C), while only CXCL13 mRNA expression was significantly inhibited in mice treated with LTβR-Ig (Fig 7, F). The mRNA expression of CD31, but not Pdpn, was significantly inhibited by anti-CXCL13 and LTβR-Ig treatment (Fig E9, B and E). Nevertheless, there was no change of IL-17A or IL-17F mRNA levels in mice treated with anti-CXCL13 or LTβR-Ig (Fig E9, C and F). Together with the finding of abolished upregulation of CXCL13 and LTβ in il17a-/- mice, these data suggest that CXCL13 and LTα1β2 residue downstream of IL-17A in this model.