Numerous recent findings indicate the possible involvement of an immune mechanism in the pathogenesis of neurodegeneration. The immune reaction could either act as a primary event, generating changes leading to cell death, or could be a secondary response to neuronal injury. In various neurodegenerative disorders such as Alzheimer's, Huntington's or Pick's disease, Down's syndrome, multiple sclerosis and the AIDS-dementia complex, the inflammatory pathomechanism is strongly supported by experimental and clinical studies. Such inflammatory mechanisms have also been postulated in Parkinson's disease (PD). This review summarizes some generalities about inflammation and immune reactions in the context of the brain, and provides clinical, epidemiological and experimental data showing that inflammation and immunity, or even auto-immunity, could be implicated in PD, either in its initial step or in its progression. Different experimental models useful for studying the role(s) of inflammation and (auto)immunity in the neurodegenerative process of the dopaminergic neurons in PD are examined. The major similarities and differences between PD and other neurodegenerative disorders are discussed.