Interactions between synaptic homeostatic mechanisms: an attempt to reconcile BCM theory, synaptic scaling, and changing excitation/inhibition balance
Transplantation, Bioengineering, and Regeneration of the Endocrine Pancreas
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Mice that are deficient in or have inhibited type I NKT cells show reduced liver injury.73 Cytokines and chemokines, including osteopontin and CXCL2, were significantly reduced in type I NKT cell-deficient mice with ethanol feeding, further highlighting their central role in liver inflammation.73 Moreover, NKT cells interact with other immune cells, such as KCs and neutrophils, to exacerbate liver injury in ALD, emphasising the complex immune crosstalk involved in alcohol-related liver damage.74 MAIT cells are a specialised population of T cells that recognise microbial metabolites presented by MHC-related protein, MR1 molecules.75 These cells are abundant in the liver and play a vital role in controlling gut microbiota, responding to bacterial infections, and regulating inflammatory diseases.76 77 In ALD, exposure to bacterial products can result in the depletion and dysfunction of MAIT cells, further exacerbating the disease.78 This highlights the intricate interplay between immune cell populations in the pathogenesis of ALD, where the disruption of one immune component can intensify liver inflammation and injury
