MHC Class I Molecules in Aging and Brain homeostasis

Aging has been associated with an increase in the expression of MHC class I molecules (MHC-I, HLA-I in humans, and H-2 in mice) in the brain, a process linked to synaptic pruning and neurodegeneration. However, several studies have also suggested a role for MHC-I molecules in neuroregeneration. Chronic low-grade inflammation is a common feature of the aging brain and is related to cognitive decline. In Alzheimer's and Parkinson's diseases, increased expression of MHC-I molecules in the brain parenchyma (e.g., microglia, endothelial cells, neurons, etc.) has been associated with dysregulation of brain homeostasis and cognitive decline. Interestingly, certain HLA-I genes/alleles, such as HLA-A2, HLA-A23, HLA-A24, HLA-B7, and HLA-B8, are associated with neurodegeneration. In contrast, others, such as HLA-B40 and HLA-C03, confer protection, suggesting a common role for MHC-I molecules in fine-tuning the equilibrium between neurodegeneration and neuroregeneration.

In this special issue of Immune Discovery, we invite you to contribute original research articles, reviews, case reports, or expert perspectives and/or opinions on all aspects related to "MHC Class I Research in Aging and Brain Homeostasis (ABH)."

Relevant topics related to ABH might include:

• Molecular mechanisms regulating the expression of cell surface MHC-I heavy chains by brain parenchymal cells, both as B2m-associated and B2m-free.
• Novel insights into molecular associations (in cis or in trans) of cell surface MHC-I forms in mice and humans.
• Recent advances in experimental in vitro or in vivo models of ABH.
• ABH-related neurodegeneration vs. neuroregeneration.
• Genetic and epigenetic mechanisms regulating the balance between neurodegeneration and neuroregeneration in ABH.