Abstract: N e u ro i n f l a m m a t i o n i s a s s o c i a te d w i t h Parkinson’s disease: Reactive gliosis and neuroinflammation are hallmarks of Parkinson’s disease (PD), a multisystem neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons. Neuroinflammation has long been considered a mere consequence of neuronal loss, but whether it promotes PD or is a key player in disease progression remains to be determined. Human leukocyte antigen, also known as major histocompatibility complex class II (MHCII), is expressed on all antigenpresenting cells of the immune system including microglia and central nervous system resident macrophages, and interestingly, its expression is increased in post-mortem PD samples (McGeer, 1988; Imamura, 2003). The strongest evidence for a link between the immune system and PD comes from genome-wide association studies, which have identified several polymorphisms in human leukocyte antigen-DR that are associated with an increased risk of idiopathic PD (Harms, 2023). Neuroinflammation is a complex and dynamic process that requires a cross-talk between glial and peripheral immune cells. Understanding these interactions is crucial for developing immunomodulatory interventions that could delay disease progression.