Immune Cells and Cell Death

Cell death is not only a fundamental biological process responsible for maintaining tissue homeostasis and eliminating abnormal cells, but also an important link connecting intracellular stress, innate immunity, adaptive immunity, and tumor immunity. Different types of cell death have distinct molecular mechanisms and immunological consequences. Some forms of cell death can promote inflammation and antigen presentation, thereby activating immune cells, whereas other forms of cell death may play important roles in immune cell development, functional maintenance, and immune homeostasis. Therefore, studying the interactions between cell death and immune cells helps to understand processes such as inflammatory responses, immune homeostasis, tumor immune escape, and immunotherapy.

Cell Death Topic

Apoptosis

Apoptosis is a classical form of programmed cell death that plays important roles in immune system development, selection, and homeostasis maintenance. During T-cell and B-cell development, apoptosis contributes to the elimination of immune cells that fail to generate effective antigen receptors or possess potential autoreactivity. After the completion of an immune response, large numbers of activated effector lymphocytes also need to be eliminated through apoptosis, allowing the immune system to return to a homeostatic state.

Pyroptosis

Pyroptosis is a form of programmed cell death with strong inflammatory characteristics and is closely associated with inflammasome activation. Typically, when cells are stimulated by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), inflammasomes such as NLRP3 can be activated, leading to Caspase-1 activation. Activated Caspase-1 can cleave Gasdermin D (GSDMD), forming membrane pores and disrupting cell membrane integrity, ultimately resulting in pyroptosis.

Meanwhile, Caspase-1 promotes the maturation of pro-IL-1β and pro-IL-18, leading to the release of IL-1β and IL-18 into the extracellular environment, thereby inducing and amplifying inflammatory responses.

Necroptosis

Necroptosis is a regulated cell death process with prominent inflammatory characteristics. Unlike apoptosis, necroptosis is typically accompanied by loss of cell membrane integrity and release of intracellular components, allowing damage signals to be transmitted to surrounding tissues and activating immune responses. The classical necroptosis pathway mainly involves RIPK1, RIPK3, and MLKL. Under specific stimulation conditions, RIPK1 and RIPK3 form signaling complexes and promote MLKL phosphorylation. Activated MLKL participates in cell membrane disruption, resulting in the release of cellular contents and DAMPs, thereby further activating innate immunity and inflammatory responses.

In cancer research, necroptosis has attracted increasing attention because induction of immunogenic cell death may not only directly reduce tumor cell numbers but also reshape the tumor microenvironment and promote anti-tumor immune responses.

Ferroptosis

Ferroptosis is a type of regulated cell death dependent on iron ions and lipid peroxidation. Its occurrence is closely associated with intracellular iron metabolism, lipid metabolism, and antioxidant systems. Among these, the SLC7A11–GSH–GPX4 axis represents an important defense system against ferroptosis. When cellular antioxidant capacity decreases and extensive lipid peroxidation occurs, ferroptotic cell death may ultimately occur.

Within the tumor microenvironment, ferroptosis and immune cells have complex bidirectional regulatory relationships. CD8⁺ T cells, macrophages, and other immune cells can influence tumor cell sensitivity to ferroptosis through cytokines, metabolites, and redox regulation. Conversely, lipid peroxidation products and other damage-associated signals produced by ferroptotic tumor cells may also affect the function of surrounding immune cells and the tumor microenvironment. Therefore, ferroptosis has become an important research direction connecting tumor metabolism, cell death, and anti-tumor immunity.

Autophagy

Autophagy is primarily an intracellular degradation and recycling mechanism rather than a classical form of cell death. Through autophagy, cells deliver damaged proteins, organelles, and other cellular components to lysosomes for degradation, thereby maintaining cellular homeostasis and metabolic balance.

In the immune system, autophagy participates in immune cell survival, differentiation, metabolic adaptation, and functional regulation. T cells, B cells, and myeloid cells are all regulated by autophagy pathways. For example, immune cells undergo significant metabolic reprogramming during activation, and autophagy helps immune cells adapt to these metabolic demands by maintaining organelle quality and energy supply. In addition, autophagy participates in antigen processing, inflammatory signaling, and immune cell functional regulation. Therefore, in studies of immune cells and cell death, autophagy serves as an important regulatory process connecting cellular metabolism, homeostasis, and immune function.

Immunogenic Cell Death (ICD)

Immunogenic Cell Death (ICD) is an important mechanism linking cell death with anti-tumor immunity. Unlike simple tumor cell death, ICD can generate or expose a series of danger signals during tumor cell death that can be recognized by the immune system, thereby promoting the activation of antigen-presenting cells and T cells.

Common experimental approaches and detection indicators for immune cells and cell death.

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