Macrophages can be characterized as a very multifunctional cell type with a spectrum of phenotypes and functions being observed spatially and temporally in various disease states. Ample studies have now demonstrated a possible causal link between macrophage activation and the development of autoimmune disorders. How these cells may be contributing to the adaptive immune response and potentially perpetuating the progression of neurodegenerative diseases and neural injuries is not fully understood. Within this review, we hope to illustrate the role that macrophages and microglia play as initiators of adaptive immune response in various CNS diseases by offering evidence of: (1) the types of immune responses and the processes of antigen presentation in each disease, (2) receptors involved in macrophage/microglial phagocytosis of disease-related cell debris or molecules, and, finally, (3) the implications of macrophages/microglia on the pathogenesis of the diseases.
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http://dx.doi.org/10.3390/ijms24065925 | DOI Listing |
J Cent Nerv Syst Dis
January 2025
School of Pharmacy, National Defense Medical Center, Taipei, Taiwan.
Background: Parkinson's disease (PD) is one of the most common neurodegenerative disorders. Previous research has confirmed that isofraxidin can reduce macrophage expression and inhibit peripheral inflammation. However, its effects on the central nervous system remain underexplored.
View Article and Find Full Text PDFBiomaterials
January 2025
Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH, United States; Advanced Platform Technology Center, Louis Stokes Cleveland Department of Veterans Affairs Medical Center, Cleveland, OH, United States. Electronic address:
Intracortical microelectrodes (IMEs) are essential for neural signal acquisition in neuroscience and brain-machine interface (BMI) systems, aiding patients with neurological disorders, paralysis, and amputations. However, IMEs often fail to maintain robust signal quality over time, partly due to neuroinflammation caused by vascular damage during insertion. Platelet-inspired nanoparticles (PIN), which possess injury-targeting functions, mimic the adhesion and aggregation of active platelets through conjugated collagen-binding peptides (CBP), von Willebrand Factor-binding peptides (VBP), and fibrinogen-mimetic peptides (FMP).
View Article and Find Full Text PDFJ Cancer
January 2025
Department of Medical Imaging and Radiological Sciences, Chang Gung University, Taoyuan, 33302, Taiwan.
Previous studies revealed that tumor-associated macrophages/microglia (TAMs) promoted glioma invasiveness during tumor progression and after radiotherapy. However, the communication of TAMs with tumor cells remains unclear. This study aimed to examine the role of small extracellular vesicles (sEVs) derived from TAMs in TAMs-mediated brain tumor invasion.
View Article and Find Full Text PDFTheranostics
January 2025
Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Charlestown, Massachusetts, 02129, MA.
The mannose receptor (CD206, expressed by the gene ) is a surface marker overexpressed by anti-inflammatory and pro-tumoral macrophages. As such, CD206 macrophages play key roles in the immune response to different pathophysiological conditions and represent a promising diagnostic and therapeutic target. However, methods to specifically target these cells remain challenging.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
In multiple sclerosis (MS), microglia and macrophages within the central nervous system (CNS) play an important role in determining the balance among demyelination, neurodegeneration, and myelin repair. Phagocytic and regenerative functions of these CNS innate immune cells support remyelination, whereas chronic and maladaptive inflammatory activation promotes lesion expansion and disability, particularly in the progressive forms of MS. No currently approved drugs convincingly target microglia and macrophages within the CNS, contributing to the lack of therapies aimed at promoting remyelination and slowing disease progression for individuals with MS.
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