Parkinson's disease (PD) is a common progressive neurodegenerative disorder, mainly classified as a movement disorder which manifests among others nonmotor symptoms such as olfactory dysfunction. The etiopathogenesis of this disease has yet to be elucidated, though it seems to be interconnected with a complex set of genetic, environmental, and immunological interactions. This review unfolds the immune alterations observed in PD patients by describing the increase in the innate immune components including complement and cytokines within their substantia nigra and cerebrospinal fluid (CSF). These alterations extended to the adaptive immune response with the elevation of T cells and autoantibodies (anti-alpha-synuclein and anti-GM1-ganglioside) in the peripheral blood and CSF of PD patients. Interestingly, another etiopathogenic triad has recently emerged linking PD to autoimmunity through olfactory dysfunction. Smell deficit is one of the earliest signs of PD and a unique observation suggesting olfactory declines to be a consequence of autoimmune mechanisms. Therefore, we considered several undisputed autoimmune diseases known for their olfactory consequences as template examples that may shed more light on the relationship between autoimmunity and PD. We hope that understanding the nature of this disease may lay the ground for successes in the quest to halt the progressive neurodegenerative process.