title: Critical Illness-Induced Immune Suppression: Current State of the Science.
abstract: Critical illness comprises a heterogeneous group of serious medical conditions that typically involve an initial proinflammatory process. A compensatory anti-inflammatory response may occur that, if severe and persistent, places the patient at high risk for adverse outcomes including secondary infection and death. Monitoring strategies can identify these patients through measurement of innate and adaptive immune function. Reductions in monocyte HLA-DR expression, reduced cytokine production capacity, increased inhibitory cell surface molecule expression, and lymphopenia have all been associated with this immune-suppressed state. Intriguing data suggest that critical illness-induced immune suppression may be reversible with agents such as interferon-γ, granulocyte macrophage colony-stimulating factor, interleukin 7, or anti-programmed death-1 therapy. Future approaches for characterization of patient-specific immune derangements and individualized treatment could revolutionize how we recognize and prevent complications in critically ill patients.
authors.affiliation: Kristin C. Greathouse is a doctoral student in nursing at The Ohio State University and an advanced practice nurse in the Cardiothoracic Intensive Care Unit at Nationwide Children's Hospital, Columbus, OH. Mark W. Hall is the chief of the Division of Critical Care Medicine at Nationwide Children's Hospital and an immunobiology researcher in the Center for Clinical and Translational Research at The Research Institute at Nationwide Children's Hospital, Columbus, OH.
authors.forename: Kristin C
authors.initials: KC
authors.lastname: Greathouse
authors.affiliation: Kristin C. Greathouse is a doctoral student in nursing at The Ohio State University and an advanced practice nurse in the Cardiothoracic Intensive Care Unit at Nationwide Children's Hospital, Columbus, OH. Mark W. Hall is the chief of the Division of Critical Care Medicine at Nationwide Children's Hospital and an immunobiology researcher in the Center for Clinical and Translational Research at The Research Institute at Nationwide Children's Hospital, Columbus, OH. mark.hall@nationwidechildrens.org.
authors.forename: Mark W
authors.initials: MW
authors.lastname: Hall
mesh_terms: D056704:Adaptive Immunity; D060908:CTLA-4 Antigen / Q000037:antagonists & inhibitors; D016638:Critical Illness; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000627:therapeutic use; D006801:Humans; D007113:Immunity, Innate; D007153:Immunologic Deficiency Syndromes / Q000175:diagnosis* / Q000188:drug therapy* / Q000276:immunology; D007371:Interferon-gamma / Q000627:therapeutic use; D015851:Interleukin-7 / Q000627:therapeutic use; D061026:Programmed Cell Death 1 Receptor / Q000037:antagonists & inhibitors; D012307:Risk Factors
chemical_list: D060908:CTLA-4 Antigen; D015851:Interleukin-7; C105992:PDCD1 protein, human; D061026:Programmed Cell Death 1 Receptor; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor