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Updated: Feb 7, 2026
Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
Published on: January 3, 2025
Association Between Programed Cell Death-1 and CD4+ T Cell Alterations in Different Phases of Ischemic Stroke
Yi Zhang1, Li Wei2, Yupeng Du3
1Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Insights
Ischemic stroke (IS) linked to immune depression? T cell dysfunction, particularly CD4+ T cells, occurs in IS phases. Programmed cell death-1 (PD-1) expression increases post-acute phase, potentially causing stroke-induced immune depression (SIID).
Area of Science:
- Immunology
- Neurology
- Pathophysiology
Background:
- Ischemic stroke (IS) can trigger stroke-induced immune depression (SIID).
- Understanding T cell subgroup dynamics is crucial for elucidating SIID mechanisms.
- Immune checkpoint receptors like PD-1 and Tim-3 play roles in T cell regulation.
Purpose of the Study:
- To analyze T cell subgroup alterations across different post-IS phases.
- To investigate the role of immune checkpoints (PD-1, Tim-3) in IS-related immune changes.
- To explore potential mechanisms of SIID.
Main Methods:
- Sixty-four IS patients were categorized into acute, sub-acute, and stable phases.
- Fourteen healthy individuals served as controls.
- Peripheral blood T cell phenotypes and immune checkpoint receptor expression (PD-1, Tim-3) were analyzed.
Main Results:
- CD4+ T cells and CD4+ T central memory (TCM) cells increased in the acute phase, then decreased in later phases.
- Programmed cell death-1 (PD-1) expression on CD4+ T cells rose significantly in the stable phase compared to the acute phase.
- PD-1 expression on CD4+ TCM and CD4+ T effector memory (TEM) cells decreased in the acute phase but increased in sub-acute and stable phases.
Conclusions:
- T cell dysfunction, specifically CD4+ T cell alterations, is evident throughout IS progression.
- Elevated PD-1 expression on CD4+ T cells post-acute phase is linked to T cell changes.
- PD-1's negative correlation with TCM cells may contribute to SIID.
Abstract:
Objective: We aimed to analyze alterations in T cell subgroups during different post-ischemic stroke (IS) phases to explore the possible mechanisms underlying stroke-induced immune depression (SIID). Methods: Sixty-four IS patients who met the entry criteria were divided into three groups: an acute phase group, a sub-acute phase group and a stable phase group. Fourteen healthy individuals were selected as normal controls. The phenotype distribution of T cells in patient peripheral blood was analyzed, and the immune checkpoint receptors programed cell death-1 (PD-1) and T cell immunoglobulin and mucin domain 3 (Tim-3) were detected in different T cell phenotypes. Results: Compared with the control group, the absolute number of CD4+ T cells and CD4+ T central memory (TCM) cells was significantly increased in the acute phase group but decreased in the sub-acute phase and stable phase groups compared with that in the acute phase group. PD-1 expression in CD4+ T cells in the stable phase group showed a significant increase compared with that in the acute phase group. The expression of PD-1 on CD4+ TCM cells and CD4+ T effector memory (TEM) cells showed significant decreases in the acute phase compared with control cells; however, in the sub-acute phase and the stable phase, PD-1 expression was significantly increased compared with that in the acute phase. Conclusions: T cell dysfunction, especially CD4+ T cell dysfunction, occurred during different IS phases. PD-1 was highly expressed in CD4+ T cells of different phenotypes after the acute phase and was associated with alterations in CD4+ T cells. Particularly, PD-1 was negatively correlated with the absolute number of TCM cells among different CD4+ T cell phenotypes, which may be one of the possible mechanisms of SIID.
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