New strategy for MS treatment with autoantigen-modified liposomes and their therapeutic effect

Shimizu, Kosuke; Agata, Kazuki; Takasugi, Shohei; Goto, Shungo; Asai, Tomohiro; Magata, Yasuhiro; Oku, Naoto

doi:10.1016/j.jconrel.2021.05.027

Cited by 18 publications

(5 citation statements)

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“…MS therapy may be classified into two groups: symptomatic treatments and disease-modifying therapies (DMT) that seek to change the disease's course, and the route of administration classifies DMT into self-injection, oral or intravenous preparations [42]. Improvements in MS therapy are unparalleled in any other field of neurology, and stem cell treatment and immunotherapy offered promise, but there has been no "magic bullet" capable of entirely curing the condition, which is currently deemed incurable [43][44][45][46][47][48]. The priority now is to limit the disease's effect throughout the disease course, enhance the quality of life, and promote a healthy philosophy for MS patients [34,49].…”

Section: Multiple Sclerosismentioning

confidence: 99%

Potential application of hydrogel to the diagnosis and treatment of multiple sclerosis

2022

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Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system. This disorder may cause progressive and permanent impairment, placing significant physical and psychological strain on sufferers. Each progress in MS therapy marks a significant advancement in neurological research. Hydrogels can serve as a scaffold with high water content, high expansibility, and biocompatibility to improve MS cell proliferation in vitro and therapeutic drug delivery to cells in vivo. Hydrogels may also be utilized as biosensors to detect MS-related proteins. Recent research has employed hydrogels as an adjuvant imaging agent in immunohistochemistry assays. Following an overview of the development and use of hydrogels in MS diagnostic and therapy, this review discussed hydrogel’s advantages and future opportunities in the diagnosis and treatment of MS. Graphical abstract

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Section: Multiple Sclerosismentioning

confidence: 99%

Potential application of hydrogel to the diagnosis and treatment of multiple sclerosis

2022

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“…Inspired by the “antigen-adjuvant” model of tumor vaccines, combining autoantigenic peptides with immunomodulators can tilt the immune response toward a more tolerant direction, thereby providing a non-inflammatory environment for DCs for further induction of Treg cells and improving the efficacy of RA treatment . For example, codelivery of MOG peptide with an immunomodulator (dexamethasone or rapamycin) remarkably decreased the quantity of CD4 + T cells to restore immune tolerance and relieved the symptoms of multiple sclerosis model mice compared to a single dose of MOG peptide or immunomodulator. , Therefore, we speculated that combining with autoantigenic peptides and immunomodulators may be a promising strategy for RA treatment by enhancing immune tolerance.…”

Section: Introductionmentioning

confidence: 99%

“…16 For example, codelivery of MOG peptide with an immunomodulator (dexamethasone or rapamycin) remarkably decreased the quantity of CD4 + T cells to restore immune tolerance and relieved the symptoms of multiple sclerosis model mice compared to a single dose of MOG peptide or immunomodulator. 17,18 Therefore, we speculated that combining with autoantigenic peptides and immunomodulators may be a promising strategy for RA treatment by enhancing immune tolerance. About 20−50% of RA patients have type II collagen (CII) antibody in their serum, suggesting that CII plays a key role in promoting the onset of RA, such as attacking and destroying cartilage tissue.…”

Section: Introductionmentioning

confidence: 99%

Autoantigenic Peptide and Immunomodulator Codelivery System for Rheumatoid Arthritis Treatment by Reestablishing Immune Tolerance

Mai,

Yu,

Gao

et al. 2024

ACS Appl. Mater. Interfaces

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Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by abnormal activation of CD4 + T cells and an imbalance of T helper 17 (Th17) and regulatory T (Treg) cells. Tolerogenic therapy via administration of self-antigens is a promising strategy for RA treatment, but delivery of autoantigens alone may exacerbate disease conditions. Current studies indicated that codelivery of autoantigens with immunomodulators can lead to a more tolerogenic immune response. Here, we constructed an autoantigen type II collagen peptide (CII 250−270 )-and immunomodulator leflunomide (LEF)coloaded phosphatidylserine liposome vaccine (CII 250−270 -LEF-PSL) for RA treatment via induction of tolerant dendritic cells (tolDC) for further activation of Treg cells. The in vivo results showed that CII 250−270 -LEF-PSL can effectively induce tolDC, regulate the balance of Th1/Th2 and Th17/Treg, and reduce the secretion of pro-inflammatory cytokines (IFN-γ, IL-1β, and IL-17A) and IgG antibodies to inhibit synovial inflammation and bone erosion. Furthermore, our study also suggested that LEF regulated Th1 cell differentiation by inhibiting the activation of the JAK1/STAT1 signaling pathway, further alleviating RA. Overall, this work proved that the combination of autoantigenic peptides and immunomodulators was a promising modality for RA treatment by reestablishing antigen-specific immune tolerance, which also inspired additional insights into the development of combination therapies for the tolerability of RA.

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“…Oral immunotherapy is a promising method for targeting the systemic immune system in autoimmune and inflammatory diseases, such as EAE [ 16 ]. A recent study showed reduced progression of encephalomyelitis symptoms in MS patients treated with MOG-modified liposomes encapsulating doxorubicin [ 17 ]. Moreover, the combined administration of MOG 35–55 associated with paricalcitol, a synthetic vitamin D receptor activator, controlled disease development and reduced clinical score in EAE [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

Haghmorad

Yousefi

Eslami

et al. 2022

CIMB

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Multiple Sclerosis (MS) is a demyelinating autoimmune disorder of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) has been widely used to determine the pathogenesis of the disease and evaluate new treatment strategies for MS. Therefore, we investigated the efficacy of oral administration of a Myelin Oligodendrocyte Glycoprotein (MOG) in the treatment of EAE. Female C57BL/6 mice were utilized in three groups (Control group, received PBS orally; prevention group, oral administration of MOG35–55 two weeks before EAE induction; treatment group, oral administration of MOG35–55 after EAE induction). MOG administration, both as prevention and treatment, significantly controlled clinical score, weight loss, CNS inflammation, and demyelination, mainly through the modulation of T cell proliferation, and reduction in pro-inflammatory cytokines and transcription factors, including TNF-α, IFN-γ, IL-17, T-bet, and ROR-γt. MOG administration, both as prevention and treatment, also induced anti-inflammatory cytokines and transcription factors, including IL-4, TGF-β, GATA-3, and Foxp3. The results showed that oral administration of MOG, both as prevention and treatment, could efficiently control EAE development. Immunomodulatory mechanisms include the induction of Th2 and Treg cells and the suppression of pro-inflammatory Th1 and Th17 cells.

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New strategy for MS treatment with autoantigen-modified liposomes and their therapeutic effect

Cited by 18 publications

References 50 publications

Potential application of hydrogel to the diagnosis and treatment of multiple sclerosis

Potential application of hydrogel to the diagnosis and treatment of multiple sclerosis

Autoantigenic Peptide and Immunomodulator Codelivery System for Rheumatoid Arthritis Treatment by Reestablishing Immune Tolerance

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses

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