Fig. 3.

Late-phase multisystem inflammation and vascular damage. The response by bone marrow as infection progresses may determine the clinical phenotype. Persons suffering bone marrow suppression with severe disease will not release new MDSC into the circulation. These persons will show reduced numbers of circulating monocytes and neutrophils and will tend to progress towards macrophage activation syndrome as MDSC suppression wanes. Those without bone marrow suppression maintain higher numbers of circulating cells. These include early phase MDSC, which can be stimulated through CD33 and Siglec-5. These cells are immunosuppressive but also proinflammatory, particularly promoting Th17 responses. In both groups, a separate prothrombotic pathway will be driven by SGP stimulation of Siglec-5⁺ cells within atherosclerotic plaques.