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      <image:title>Technology - Immune dysfunction in sepsis survivors.</image:title>
      <image:caption>Legend: Immune dysfunction in sepsis survivors. Early in sepsis, both inflammation and immunosuppression occur concurrently. If inflammation is uncontrolled, this leads to organ failure and death. Those that avoid early death will either return to immune homeostasis, or progress to prolonged immunosuppression that continues after discharge. Prolonged immunosuppression predisposes survivors to infections, rehospitalizations, and ultimately late death. This phenomenon is marked by impaired cytokine secretion, dysfunctional T-cells, and cellular reprogramming. It is still unknown why prolonged immunosuppression occurs; however, epigenetic processes may be involved to “lock in” certain immunophenotypes. Expansion of regulatory T-cells and myeloid derived suppressor cell (MDSC) populations also occur early in sepsis and persist after sepsis, suggesting their role in maintaining this immunosuppressive phenotype. TNFα: tumor necrosis factor alpha, IL-6: interleukin-6, DAMPs: damage-associated molecular patterns, Treg: regulatory T-cell, MDSC: myeloid derived suppressor cell.</image:caption>
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