Unveiling Interleukins’s Role in Ischemic Stroke

Interleukins (ILs) represent a fascinating and diverse family of signaling molecules that play pivotal roles in regulating the immune system. These multifaceted proteins are involved in a wide array of physiological processes, influencing immune cell proliferation, differentiation, and communication. As we delve into the intricate world of interleukins, their significance becomes even more pronounced in the context of ischemic stroke-a condition marked by disrupted blood flow to the brain, leading to severe consequences. Understanding the complex interactions of interleukins in the immune response is key to unraveling their involvement in ischemic stroke.

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Introduction of ILs

IL, or interleukin, refers to the lymphocyte mediator involved in the interaction between white blood cells or immune cells. It belongs to the same category of cell factors as hematopoietic growth factors. Both IL and hematopoietic growth factors fall under the classification of cytokines, and they coordinate and interact with each other to collectively fulfill hematopoietic and immune regulatory functions. IL plays a crucial role in the transmission, activation, and regulation of immune cells, as well as in mediating the activation, proliferation, and differentiation of T cells and B cells, along with participating significantly in inflammatory responses.

The Role of Interleukins in Ischemic Stroke

IL plays a bidirectional role in ischemic stroke. Crosstalk between different ILs in different immune cells also affects the outcome of ischemic stroke. The role of different ILs in ischemic stroke is shown in the following table.

ILs	Function
IL-1	Aggravates cerebral infarction by polarizing microglia/macrophages, causing BBB dysfunction and apoptosis after ischemic stroke.
IL-2	Activates Tregs, increasing CD39/CD73 expression, contributing to anti-inflammatory responses in ischemic stroke.
IL-4	Promotes M2 macrophage polarization, decreasing pro-inflammatory cytokines, and supporting neuroprotection in ischemic stroke.
IL-5	Reduced in severe strokes, may predict edema and infarct volume; its role is linked to immune response in ischemic stroke.
IL-6	Activates JAK/STAT pathway, promoting pro-cytokine expression, exacerbating inflammation after ischemic stroke.
IL-8	Promotes neutrophil activation and infiltration into cerebral infarction, intensifying inflammatory response in ischemic stroke.
IL-9	Destructive effect on BBB, and its neutralization partially ameliorates ischemic stroke injury; role in immune response.
IL-10	Anti-inflammatory, reduces pro-inflammatory cytokines, maintains Th1 activity, exerting protective effects in ischemic stroke.
IL-12	Promotes chemokine expression, induces apoptosis, and exerts a pro-inflammatory effect in ischemic stroke.
IL-13	Increases M2 macrophage polarization, decreases pro-inflammatory cytokines, and reduces neuronal loss in ischemic stroke.
IL-15	Increases CD4+, CD8+, and NK cells, contributing to immune response in ischemic stroke.
IL-16	Activates CD4+ cells, increases TNF-α, IL-1, and IL-6 levels, intensifying inflammatory responses in ischemic stroke.
IL-17	Activates Th17 cells, increasing T cells, macrophages, and DC cells, contributing to inflammatory cascades in ischemic stroke.
IL-18	Promotes M1 microglia/macrophage polarization, enhances pro-inflammatory responses in ischemic stroke.
IL-19	Preserves immune cell numbers, reduces pro-inflammatory cytokines, exerting anti-inflammatory effects in ischemic stroke.
IL-21	Polymorphism increases susceptibility; IL-21R regulates collateral vascular anatomy, contributing to ischemic stroke outcomes.
IL-22	Exerts protective action through JAK2-STAT3 pathway, improving oxidative stress, inflammation, and neuronal apoptosis in ischemic stroke.
IL-23	Essential for Th17 activation, contributing to inflammatory cascades and exacerbating tissue injury in ischemic stroke.
IL-32	Silencing protects cells against ischemic injury, involving Nrf2/NF-κB pathway in ischemic stroke.
IL-33	Neuroprotective, inhibits inflammation via ST2/IL-33 signaling, regulates microglia, and improves outcomes in ischemic stroke.
IL-34	Elevated serum levels may serve as a diagnostic and prognostic biomarker in acute ischemic stroke.
IL-37	Controversial role; correlated with stroke recurrence but debated for its protective effects in ischemic stroke.
IL-38	Lower serum levels associated with poorer prognosis, a potential early predictor factor for ischemic stroke outcomes.

Reference

Zhu H.; et al. Interleukins and ischemic stroke. Frontiers in Immunology. 2022, 13: 828447.