Human granulocytic anaplasmosis, caused by the tick-transmitted <i>Anaplasma phagocytophilum</i>, is not controlled by innate immunity, and induces a proinflammatory disease state with innate immune cell activation.In <i>A. phagocytophilum</i> murine infection models, hepatic injury occurs with production of IFNγ thought to be derived from NK, NKT cells, and CD8 T lymphocytes.Specific <i>A. phagocytophilum</i> ligands that drive inflammation and disease are not known, but suggest a clinical and pathophysiologic basis strikingly like macrophage activation syndrome (MAS) and hemophagocytic syndrome (HPS).
Compared with control tissues, we found elevated macrophage inflammatory protein-1alpha (MIP-1alpha) and interferon-gamma (IFN-gamma) expression, but not macrophage-derived chemotactic factor (MDC) or TNF-alpha, in tissues of patients with HPS irrespective of the cause or setting.