Experimental Models to Study Immune Dysfunction in the Pathogenesis of Parkinson’s Disease

Parkinson’s disease (PD) is a chronic, age-related, progressive multisystem disease associated with neuroinflammation and immune dysfunction. This review discusses the methodological approaches used to study the changes in central and peripheral immunity in PD, the advantages and limitations of the techniques, and their applicability to humans. Although a single animal model cannot replicate all pathological features of the human disease, neuroinflammation is present in most animal models of PD and plays a critical role in understanding the involvement of the immune system (IS) in the pathogenesis of PD. The IS and its interactions with different cell types in the central nervous system (CNS) play an important role in the pathogenesis of PD. Even though culture models do not fully reflect the complexity of disease progression, they are limited in their ability to mimic long-term effects and need validation through in vivo studies. They are an indispensable tool for understanding the interplay between the IS and the pathogenesis of this disease. Understanding the immune-mediated mechanisms may lead to potential therapeutic targets for the treatment of PD. We believe that the development of methodological guidelines for experiments with animal models and PD patients is crucial to ensure the validity and consistency of the results

Additional file 1 of Increased regulatory activity of intestinal innate lymphoid cells type 3 (ILC3) prevents experimental autoimmune encephalomyelitis severity

Additional file 1: Figure S1. Th1 and Th17 gating in SCIC. Figure S2. CD45RA (B cell) and MHC class II gating in SCIC. Figure S3. Treg gating in LPIC. Figure S4. ILC gating in LPIC. Figure S5. Composition of SCIC in the moderate and severe groups. DA rats immunized with SCH were sacrificed on days 24–28 p.i. SCIC were isolated and percentage (A–C) and cell number (D–F) of cell populations were determined by flow cytometry. Data are expressed as mean ± SD (n = 5). *p < 0.05, ns—not significant. Figure S6. Antigen response of PLNC in moderate and severe groups. DA rats immunized with SCH were sacrificed at days 24–28 p.i. PLNC were isolated and counted (A). PLNC were exposed to MBP (B) or myelin (C–G) for 48 h. IFN-γ levels in cell culture supernatants were determined by ELISA (B, C). CD4+CD25+ T cells (D, E) and Treg (F, G) were detected by flow cytometry. Data are presented as mean ± SD (n = 4–5). ns—not significant. Figure S7. Immunoblots. Full, uncropped immunoblot images for zonulin, occludin, and actin. Samples m5, s5, m6, and s6 are presented in Fig. 6D. Blot membranes were cut in three pieces, making cuts above markers 95 kDa and 55 kDa. Protein ladder Thermo Scientific #26,619 was used. m—moderate, s—severe, h—healthy