Associations of T helper 1, 2, 17 and regulatory T lymphocytes with mortality in severe sepsis

Wu, Huang-Pin; Chung, Kian Fan; Lin, Chun-Yao; Jiang, Bor-Yiing; Chuang, Duen-Yau; Liu, Yu-Chih

doi:10.1007/s00011-013-0630-3

Cited by 58 publications

(52 citation statements)

References 34 publications

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“…Lymphocyte apoptosis is increased in CD 4+ and CD 8+ T cells in sepsis as compared with non-sepsis patients. The CD 4+ cells might facilitate the early clearance of bacteria by regulating neutrophil function (Wu et al, 2013). It has also been proved that a reduction in lymphocyte apoptosis was associated with improvement in survival rate in the CLP mouse model (Molostvov et al, 2008).…”

Section: Discussionmentioning

confidence: 98%

Calcium-sensing receptor in the T lymphocyte enhanced the apoptosis and cytokine secretion in sepsis

et al. 2015

Molecular Immunology

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Section: Discussionmentioning

confidence: 98%

Calcium-sensing receptor in the T lymphocyte enhanced the apoptosis and cytokine secretion in sepsis

et al. 2015

Molecular Immunology

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“…However, the sepsis‐induced immune impact is not only relegated to Th1 and Th2 CD4 + T cells but also to Th17 subsets and the other Th subsets as well. Th17 cytokine production is reduced in sepsis and probably negatively impacts long‐term mortality . Given the fundamental role of Th17 in eradication of pathologic fungal infections, reduced Th17 cytokine production in sepsis is probably responsible for the increased susceptibility to fungal infections frequently observed in critically ill populations .…”

Section: Adaptive Immunitymentioning

confidence: 99%

“…Th17 cytokine production is reduced in sepsis and probably negatively impacts long-term mortality. 189 Given the fundamental role of Th17 in eradication of pathologic fungal infections, reduced Th17 cytokine production in sepsis is probably responsible for the increased susceptibility to fungal infections frequently observed in critically ill populations. 190 Circulating CD4 + and CD8 + cells from patients with candidemia display an immune phenotype consistent with immune suppression, T-cell exhaustion, and downregulation of positive co-stimulatory molecules.…”

Section: T H Cell Subpopulationsmentioning

confidence: 99%

The immune system's role in sepsis progression, resolution, and long‐term outcome

Delano

Ward

2016

Immunological Reviews

592

488

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SUMMARY Sepsis occurs when an infection exceeds local tissue containment and induces a series of dysregulated physiologic responses that result in organ dysfunction. A subset of patients with sepsis progress to septic shock, defined by profound circulatory, cellular, and metabolic abnormalities, and associated with a greater mortality. Historically, sepsis-induced organ dysfunction and lethality were attributed to the complex interplay between the initial inflammatory and later anti-inflammatory responses. With advances in intensive care medicine and goal-directed interventions, early 30-day sepsis mortality has diminished, only to steadily escalate long after “recovery” from acute events. Since so many sepsis survivors succumb later to persistent, recurrent, nosocomial and secondary infections, many investigators have turned their attention to the long-term sepsis-induced alterations in cellular immune function. Sepsis clearly alters the innate and adaptive immune responses for sustained periods of time after clinical recovery, with immune suppression, chronic inflammation, and persistence of bacterial representing such alterations. Understanding that sepsis-associated immune cell defects correlate with long-term mortality, more investigations have centered on the potential for immune modulatory therapy to improve long term patient outcomes. These efforts are focused on more clearly defining and effectively reversing the persistent immune cell dysfunction associated with long-term sepsis mortality.

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“…However, the sepsis-induced immune impact is not only relegated to Th1 and Th2 CD4 + T cells, but also to Th17 cell subsets and probably other Th cell subsets as well. The Th17 cytokine response is diminished in sepsis and may negatively impact mortality (87). Given the fundamental role of Th17 in the eradication of fungal infections, reduced Th17 cytokine production in sepsis may be responsible for the increased susceptibility to fungal infections frequently encountered in critically ill patient populations (88).…”

Section: Introductionmentioning

confidence: 99%

Sepsis-induced immune dysfunction: can immune therapies reduce mortality?

Delano¹,

Ward²

2016

Journal of Clinical Investigation

502

472

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Sepsis affects the immune system by directly altering the lifespan, production, and function of the effector cells responsible for Sepsis is a systemic inflammatory response induced by an infection, leading to organ dysfunction and mortality. Historically, sepsis-induced organ dysfunction and lethality were attributed to the interplay between inflammatory and antiinflammatory responses. With advances in intensive care management and goal-directed interventions, early sepsis mortality has diminished, only to surge later after "recovery" from acute events, prompting a search for sepsis-induced alterations in immune function. Sepsis is well known to alter innate and adaptive immune responses for sustained periods after clinical "recovery," with immunosuppression being a prominent example of such alterations. Recent studies have centered on immune-modulatory therapy. These efforts are focused on defining and reversing the persistent immune cell dysfunction that is associated with mortality long after the acute events of sepsis have resolved.

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Associations of T helper 1, 2, 17 and regulatory T lymphocytes with mortality in severe sepsis

Cited by 58 publications

References 34 publications

Calcium-sensing receptor in the T lymphocyte enhanced the apoptosis and cytokine secretion in sepsis

Calcium-sensing receptor in the T lymphocyte enhanced the apoptosis and cytokine secretion in sepsis

The immune system's role in sepsis progression, resolution, and long‐term outcome

Sepsis-induced immune dysfunction: can immune therapies reduce mortality?

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