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• W2041882486 abstract "•Sepsis is the leading cause of death in critically ill patients and novel therapies are necessary. •Immune suppression is frequently associated with sepsis-related deaths. •Therapies or immunomodulatory agents that enhance the immune response should be considered. •Cytokines and co-inhibitory receptors represent potential immunomodulatory agents. Sepsis is the leading cause of death among critically ill patients in intensive care units, and treatment options are limited. Therapies developed against the proinflammatory stage have failed clinically; therefore, new approaches that target the host immune response in sepsis are necessary. Increasing evidence suggests that a major pathophysiological event in sepsis is immune suppression, often resulting in secondary fungal, bacterial, or viral infections. Recent studies from animal sepsis models and patient samples suggest that cytokines such as interleukin-7 (IL-7), IL-15, granulocyte macrophage colony-stimulating factor (GM-CSF), as well as co-inhibitory molecule blockade, such as anti-programmed cell death receptor-1 (anti-PD-1) and anti-B and T lymphocyte attenuator (anti-BTLA), may have utility in alleviating the clinical morbidity associated with sustained sepsis. This review discusses some of these novel immunomodulatory agents and evaluates their potential use as therapeutics. Sepsis is the leading cause of death among critically ill patients in intensive care units, and treatment options are limited. Therapies developed against the proinflammatory stage have failed clinically; therefore, new approaches that target the host immune response in sepsis are necessary. Increasing evidence suggests that a major pathophysiological event in sepsis is immune suppression, often resulting in secondary fungal, bacterial, or viral infections. Recent studies from animal sepsis models and patient samples suggest that cytokines such as interleukin-7 (IL-7), IL-15, granulocyte macrophage colony-stimulating factor (GM-CSF), as well as co-inhibitory molecule blockade, such as anti-programmed cell death receptor-1 (anti-PD-1) and anti-B and T lymphocyte attenuator (anti-BTLA), may have utility in alleviating the clinical morbidity associated with sustained sepsis. This review discusses some of these novel immunomodulatory agents and evaluates their potential use as therapeutics. is expressed by T and B lymphocytes; it is an immunoglobin (Ig) domain superfamily member that contains a cytoplasmic tyrosine-based inhibitory motif. The ligand for BTLA is herpesvirus entry mediator (HVEM). The interactions between BTLA and HVEM involve bidirectional signaling and potentiate negative immune responses. Generally, T cell activation is negatively regulated upon HVEM engagement to BTLA. the CLP method is a clinical comparable rodent model of polymicrobial peritonitis used to investigate the pathological changes associated with sepsis/septic shock seen in patients. are cell surface molecules, such as PD-1, BTLA, and CTLA-4, that belong to the CD28/B7 gene family and have been shown to be upregulated on monocytes, macrophages, and lymphocyte populations in patient samples and animals exposed to experimental septic challenge. Traditionally, these molecules are thought to negatively regulate T cell receptor (TCR)-mediated activation as well as cytokine release from immune cells of the adaptive immune system and have been extensively investigated in the processes of viral infection and cancer. is usually succeeded by the proinflammatory phase during sepsis and is hallmarked by increased anti-inflammatory cytokines, such as IL-10, increased lymphocyte apoptosis, diminished human leukocyte antigen (HLA) receptors on monocytes, and decreased cytokine responses by monocytes as well as lymphocytes. IL-7 and IL-15 are closely related and have been shown to improve immune cell function (particularly CD8+ T, NK, and dendritic cells) and decrease lymphocyte apoptosis in sepsis animal models. GM-CSF, however, is a cytokine that improves neutrophil and macrophage functions, and increases HLA-DR expression on monocytes. These cytokines, if directed to the appropriate patient, may address the immune-suppressed state in critically ill patients. the excessive or uncontrolled release of proinflammatory cytokines in the context of acute tissue damage and/or infection, such as traumatic injury/shock/ischemia–reperfusion and/or sepsis. also known as CD152, is expressed on the surface of T lymphocytes, and a member of the Ig superfamily that competes with CD28 for binding to co-stimulatory molecules, CD80 and CD86, on antigen presenting cells. CTLA-4 binding prevents T cell proliferation, expansion, and activation. the inability of the host to mount an appropriate immune response to a defined antigenic stimuli and/or infectious challenge. ideal immunomodulatory therapy directed against sepsis would boost overall patient immunity, drive lymphocyte effector functions, decrease lymphoid apoptosis, and ultimately mitigate the development of immune suppression, which has been often associated with onset of secondary infections and death among critically ill patients. the co-inhibitory receptor molecule, PD-1, is expressed on T and B cells (lymphocytes), myeloid cells, NK cells, and NKT cells. Upon ligation by its ligand, programmed cell death ligand-1 (PD-L1) transduces an inhibitory signal to the leukocyte during the course of activation. the American College of Chest Physicians and the Society for Critical Care Medicine established criteria for SIRS. There are four categories, including body temperature, respiratory rate, white blood cell count, and heart rate. These criteria are not necessarily related to infection. T lymphocytes become functionally inactive or ‘anergic’ following an antigen encounter, typically in the absence of adequate co-stimulatory signaling, yet still remain viable in circulation and can regain responsiveness to select T cell stimuli under the appropriate conditions. this is a state of T cell dysfunction, which is typically defined by decreased lymphocyte effector functions and sustained expression of inhibitory receptors, the results of which the lymphocyte is nonresponsive to exogenous stimuli. T cell exhaustion prevents the clearance of bacterial and chronic viral infections." @default.
• W2041882486 created "2016-06-24" @default.
• W2041882486 creator A5001543982 @default.
• W2041882486 creator A5003446329 @default.
• W2041882486 creator A5025683989 @default.
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• W2041882486 date "2014-04-01" @default.
• W2041882486 modified "2023-09-30" @default.
• W2041882486 title "The new normal: immunomodulatory agents against sepsis immune suppression" @default.
• W2041882486 cites W1499659307 @default.
• W2041882486 cites W1509163238 @default.
• W2041882486 cites W1516476380 @default.
• W2041882486 cites W1549568102 @default.
• W2041882486 cites W1570331116 @default.
• W2041882486 cites W1601903230 @default.
• W2041882486 cites W1606631580 @default.
• W2041882486 cites W1661840774 @default.
• W2041882486 cites W1926790978 @default.
• W2041882486 cites W1969562496 @default.
• W2041882486 cites W1970990504 @default.
• W2041882486 cites W1971909938 @default.
• W2041882486 cites W1974971484 @default.
• W2041882486 cites W1976557086 @default.
• W2041882486 cites W1977905350 @default.
• W2041882486 cites W1978436252 @default.
• W2041882486 cites W1983691837 @default.
• W2041882486 cites W1990924485 @default.
• W2041882486 cites W1991180061 @default.
• W2041882486 cites W1993065921 @default.
• W2041882486 cites W1993197717 @default.
• W2041882486 cites W1994844769 @default.
• W2041882486 cites W1998427452 @default.
• W2041882486 cites W1999350238 @default.
• W2041882486 cites W2005857592 @default.
• W2041882486 cites W2005965937 @default.
• W2041882486 cites W2013860796 @default.
• W2041882486 cites W2017178436 @default.
• W2041882486 cites W2028646275 @default.
• W2041882486 cites W2037418955 @default.
• W2041882486 cites W2041461587 @default.
• W2041882486 cites W2048046456 @default.
• W2041882486 cites W2048164478 @default.
• W2041882486 cites W2049927822 @default.
• W2041882486 cites W2056411965 @default.
• W2041882486 cites W2057529688 @default.
• W2041882486 cites W2060122053 @default.
• W2041882486 cites W2060928633 @default.
• W2041882486 cites W2062549560 @default.
• W2041882486 cites W2063510122 @default.
• W2041882486 cites W2064783820 @default.
• W2041882486 cites W2065345742 @default.
• W2041882486 cites W2070743921 @default.
• W2041882486 cites W2071693928 @default.
• W2041882486 cites W2072439886 @default.
• W2041882486 cites W2077071726 @default.
• W2041882486 cites W2078704378 @default.
• W2041882486 cites W2081293223 @default.
• W2041882486 cites W2083513831 @default.
• W2041882486 cites W2086397613 @default.
• W2041882486 cites W2090751965 @default.
• W2041882486 cites W2096497265 @default.
• W2041882486 cites W2097250838 @default.
• W2041882486 cites W2097476575 @default.
• W2041882486 cites W2099572165 @default.
• W2041882486 cites W2101082552 @default.
• W2041882486 cites W2101653483 @default.
• W2041882486 cites W2105011122 @default.
• W2041882486 cites W2105400408 @default.
• W2041882486 cites W2108396254 @default.
• W2041882486 cites W2109642153 @default.
• W2041882486 cites W2111143066 @default.
• W2041882486 cites W2114408584 @default.
• W2041882486 cites W2114474071 @default.
• W2041882486 cites W2115476870 @default.
• W2041882486 cites W2118471749 @default.
• W2041882486 cites W2118705059 @default.
• W2041882486 cites W2118975078 @default.
• W2041882486 cites W2120599813 @default.
• W2041882486 cites W2127148037 @default.
• W2041882486 cites W2130473166 @default.
• W2041882486 cites W2130898753 @default.
• W2041882486 cites W2131577873 @default.
• W2041882486 cites W2132226366 @default.
• W2041882486 cites W2135171334 @default.
• W2041882486 cites W2136030067 @default.
• W2041882486 cites W2138550176 @default.
• W2041882486 cites W2141131774 @default.
• W2041882486 cites W2144716650 @default.
• W2041882486 cites W2145156671 @default.
• W2041882486 cites W2145577370 @default.
• W2041882486 cites W2146666488 @default.
• W2041882486 cites W2150539814 @default.
• W2041882486 cites W2150640296 @default.
• W2041882486 cites W2156230193 @default.
• W2041882486 cites W2157758657 @default.
• W2041882486 cites W2160578994 @default.
• W2041882486 cites W2160834915 @default.
• W2041882486 cites W2160893227 @default.

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