Cytokines (excluding IL-10) commonly reported to be involved in pathogenesis were compiled from (94) (95) (96) . IL-10 from effector T-cells was recently shown to limit inflammation during acute influenza (97) . HMGB1 up-regulates pro-inflammatory cytokine expression via its cellular receptors, the receptor for advanced glycation end products [RAGE; (41, 42, 98) ] and to a lesser extent, toll-like receptor (TLR) 2 and 4 (43, 99) . RAGE expression was recently shown to be associated with influenza A virus pneumonia, accompanied by increased levels of HMGB1 in bronchoalveolar lavage fluid (100).