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Interaction of epithelial cells with meningococcal type IV pili and other minor adhesins triggers the polymerization of cortical actin and the clustering of ICAM1, CD44, EGFR, and ezrin underneath the microcolony, ultimately forming a cortical plaque (Merz et al., 1999)

A compensatory anti-inflammatory mechanism then typically follows (59), causing an imbalance in immune responses (58, 59) combined with hypothesised autoimmunity (52, 85, 182)

doi: 10.1097/BCR.0b013e318240540a

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Free radicals can hurt cells and cause aging or illness