Interleukin-6–Associated Pyroptosis, Apoptosis, and Necroptosis via JAKs/STAT3-RIPK1 Axis: A Potential Mechanism for CD4+ T-Cell Depletion in Bacterial Sepsis
Authors' conclusion
PANoptosis has been observed to be a form of CD4 + T-cell death in sepsis patients.
Study context
- Population
- Adults with sepsis or septic shock without documented immune comorbidity, adult ICUs at a university hospitalplus 30 sepsis, 10 controls (mechanistic)
- Participants
- 93 / 58 / 20
- Exposure
- Sepsis and septic shock vs controls
- Sepsisn = 93
- Septic shockn = 58
- Controlsn = 20reference
Methodological detailsmechanistic in vitro experiments, RNA sequencing, single-centre, Additional 30 sepsis patients and 10 controls recruited for mechanistic studies
- Mechanistic in vitro experiments
- RNA sequencing
- Single-centre
- Additional 30 sepsis patients and 10 controls recruited for mechanistic studies
Main finding
As reported in the abstract
- Significant CD4+ T-cell loss in both sepsis and septic shock, strongly correlating with elevated IL-6 levels
- Sepsis PBMC RNA sequencing (RNA-seq): activated IL-6/JAKs/STAT3 signaling and upregulated apoptosis/pyroptosis/necroptosis genes
- In vitro, IL-6 induced pyroptosis, apoptosis, and necroptosis (PANoptosis) in CD4+ T cells via IL-6/JAKs/STAT3-dependent RIPK1-PANoptosome assembly
- Inhibiting JAKs/STAT3 or RIPK1 significantly reduced PANoptosis and partially restored CD4+ T-cell viability and function
Observational data: associations, not effects.
Original publication
Interleukin-6–Associated Pyroptosis, Apoptosis, and Necroptosis via JAKs/STAT3-RIPK1 Axis: A Potential Mechanism for CD4+ T-Cell Depletion in Bacterial Sepsis. Crit Care Med. Published 5 March 2026. doi:10.
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