Table 1.
Relationship | Research object | Evidence | References |
---|---|---|---|
Genetic regulation of autoimmunity in PD | PINK1, Parkin | Absence of PINK1/Parkin leads to the mitochondrial aberrations by triggering immune system disorders (reduced immuno-surveillance or activated autoimmunity). | (34, 43–47) |
DJ-1 | Absence of DJ-1 leads to abnormal proliferation of nTregs and iTregs, and result in autoimmunity. | (48–50) | |
Pathogenic protein function in autoimmunity- associated PD | α-syn | Post-translational modifications and mutation of α-syn can be recognized as the autoantigen by the central immune system. | (56–58, 62, 64, 65) |
Immune cells and autoimmunity in PD | DC | NM is an autoantigen released from dead DNs that stimulates the functional activation of DCs, triggering an autoimmune response and leading to microglial activation. | (28, 72–75) |
Microglia | Auto-aggressive loop initiated by DCs along with NM would be enhanced and amplified by microglial activation. | (78–80) | |
Clinical features and autoimmunity in PD | Tremor/dyskinesia/depression | Various autoantibodies have a strong positive correlation with these motor/non-motor symptoms. | (29, 83, 84) |
Constipation | Constipation is related to the gut dysbiosis and/or SIBO, which incurring the activation of enteric glial cells and contributing to the initiation of α-syn misfolding. | (90–93) | |
Other autoimmune diseases combined with PD | Hypothyroidism/hyperthyroidism/BP/SLE/ARD | Other autoimmune diseases may share genetic pathways with PD and are correlated closely with some clinical manifestations of PD. | (97–102) |
PD, Parkinson's disease; α-syn, α-synuclein; DC, dendritic cell; NM, neuromelanin; SIBO, small intestinal bacterial overgrowth; BP, bullous pemphigoid; SLE, systemic lupus erythematous; ARD, autoimmune rheumatic disease.