Immune Mechanisms in Acute Kidney Injury
Summary
Acute kidney injury (AKI) arises from a variety of insults—ischemia, toxins, sepsis or immune‐mediated injury—that trigger a complex interplay between renal parenchymal cells and the host immune system. The immediate response is dominated by innate immune activation: tubular epithelial cells release danger signals that engage Toll‐like receptors and inflammasome complexes, driving the secretion of proinflammatory cytokines and chemokines. Neutrophils and classical macrophages rapidly infiltrate the injured tissue, exacerbating tubular cell death through oxidative stress and protease release. Subsequently, a reparative phase ensues in which alternatively activated macrophages and specialised lymphocyte subsets, notably regulatory T cells, modulate inflammation and promote epithelial proliferation and extracellular matrix remodelling. Failure to resolve this biphasic response can lead to persistent inflammation, maladaptive repair and progression to chronic kidney disease. Current research emphasises the importance of immune metabolism, single‐cell profiling and targeted immunomodulation as avenues to translate mechanistic insight into effective therapies for AKI of diverse aetiologies.
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Immune Mechanisms in Acute Kidney Injury publication trend
The graph below shows the total number of articles in immune mechanisms in acute kidney injury across all publications each year (not limited to Nature Index journals).
Technical terms
Adaptive immunity: The antigen-specific arm of the immune system involving lymphocytes that provides long-term memory and targeted responses.
Chemokine: A small signalling protein that recruits immune cells to sites of injury or infection.
Cytokine: A broad category of secreted proteins that regulate inflammation, cell growth and immune interactions.
Inflammasome: A multiprotein complex that activates inflammatory caspases and promotes secretion of interleukin-1β and interleukin-18.
Metabolic reprogramming: The alteration of cellular energy pathways that supports immune cell activation, proliferation and function.
Regulatory T cell (Treg): A specialised T lymphocyte subset that suppresses excessive immune responses and facilitates tissue repair.
References
- T cell metabolic reprogramming in acute kidney injury and protection by glutamine blockade. JCI Insight (2023).
- Innate Immune Response in Kidney Ischemia/Reperfusion Injury: Potential Target for Therapy. Journal of Immunology Research (2017).
- Immune cell landscaping reveals a protective role for regulatory T cells during kidney injury and fibrosis. JCI Insight (2020).
- Role of leukocytes in the pathogenesis of acute kidney injury. Critical Care (2012).
- B Lymphocyte–Derived CCL7 Augments Neutrophil and Monocyte Recruitment, Exacerbating Acute Kidney Injury. The Journal of Immunology (2020).
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