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Immunomodulatory biomaterials for implant-associated infections: from conventional to advanced therapeutic strategies

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Compromised intestinal epithelial barrier due to intestinal epithelial-specific loss of JAM-A induces adaptive immune compensation that protects from colitis The findings in mice manipulated for MLCK or occludin expression differed from those obtained in mice lacking the JAM-A (encoded by F11r)

These inflammatory responses comprise immune mediators including TNF, IL-6 and IL-17 that are also likely to contribute to the systemic spread of these newly modified proteins in the joints and stimulate immune-mediated tissue damage (Fig

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