LTB4R and arthritic joint disease: Adoptive transfer of wild-type neutrophils to BLT1-deficient mice was able to restore arthritis development in the K/BxN serum-transfer model, and it also triggered recruitment of BLT1-deficient recipient neutrophils.47 Besides LTB4, IC activation of neutrophils also triggered the release of neutrophil-acting chemokines (e.g. CXCL2) that are also present at the site of autoantibody-induced in vivo inflammation.115 Therefore, neutrophils appear to release neutrophil-attracting inflammatory mediators other than LTB4.