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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Related Experiment Video

Updated: Jan 5, 2026

Author Spotlight: THP-1 Macrophage Response to LPS/ATP &#8212; Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
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[Progress in programmed death-1 signaling pathway in sepsis].

Chang Xu1, Li Li2, Jing Yan2

  • 1Second Clinical Medical College, Zhejiang Chinese Medicine University, Hangzhou 310053, Zhejiang, China.

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
|October 29, 2019
PubMed
Summary

Programmed death-1 (PD-1) plays a key role in sepsis-induced immunosuppression. Targeting PD-1 may offer new therapeutic strategies for improving patient outcomes in sepsis.

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Area of Science:

  • Immunology
  • Critical Care Medicine
  • Molecular Biology

Background:

  • Sepsis involves complex inflammatory and anti-inflammatory responses.
  • Previous treatments targeting early inflammation in sepsis have shown limited efficacy.
  • Patient prognosis in sepsis is linked to immunosuppression and co-inhibitory molecule expression.

Purpose of the Study:

  • To review the role of the programmed death-1 (PD-1) signaling pathway in sepsis-induced immunosuppression.
  • To explore the impact of PD-1 on patient prognosis and risk stratification in sepsis.
  • To identify PD-1 as a potential therapeutic target for immune regulation in sepsis.

Main Methods:

  • Literature review of studies on PD-1 signaling in sepsis.
  • Analysis of the correlation between PD-1 expression, immunosuppression, and patient outcomes.
  • Evaluation of PD-1's role in both innate and adaptive immunity during sepsis.

Main Results:

  • Programmed death-1 (PD-1) is a critical co-inhibitory molecule involved in immune regulation.
  • PD-1 signaling pathway significantly influences sepsis-induced immunosuppression.
  • Overexpression of PD-1 correlates with poorer prognosis and increased mortality in sepsis patients.

Conclusions:

  • PD-1 is a valuable biomarker for risk stratification and prognosis prediction in sepsis.
  • Targeting the PD-1 pathway presents a promising new direction for sepsis treatment.
  • Immune modulation via PD-1 offers potential for improving sepsis management.