دورية أكاديمية

Tn P Peptide Suppresses Experimental Autoimmune Encephalomyelitis (EAE) in a Preclinical Mouse Model.

التفاصيل البيبلوغرافية
العنوان: Tn P Peptide Suppresses Experimental Autoimmune Encephalomyelitis (EAE) in a Preclinical Mouse Model.
المؤلفون: Lima C; Immunoregulation Unit of the Laboratory of Applied Toxinology (CeTICs/FAPESP), Butantan Institute, São Paulo, Brazil., Maleski ALA; Immunoregulation Unit of the Laboratory of Applied Toxinology (CeTICs/FAPESP), Butantan Institute, São Paulo, Brazil., Bernardo JTG; Immunoregulation Unit of the Laboratory of Applied Toxinology (CeTICs/FAPESP), Butantan Institute, São Paulo, Brazil., Zelli VC; Immunoregulation Unit of the Laboratory of Applied Toxinology (CeTICs/FAPESP), Butantan Institute, São Paulo, Brazil., Komegae EN; Immunoregulation Unit of the Laboratory of Applied Toxinology (CeTICs/FAPESP), Butantan Institute, São Paulo, Brazil., Lopes-Ferreira M; Immunoregulation Unit of the Laboratory of Applied Toxinology (CeTICs/FAPESP), Butantan Institute, São Paulo, Brazil.
المصدر: Frontiers in immunology [Front Immunol] 2022 Mar 24; Vol. 13, pp. 857692. Date of Electronic Publication: 2022 Mar 24 (Print Publication: 2022).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مواضيع طبية MeSH: Encephalomyelitis, Autoimmune, Experimental* , Multiple Sclerosis*/drug therapy, Animals ; Fingolimod Hydrochloride/therapeutic use ; Glatiramer Acetate/therapeutic use ; Interferon beta-1b/adverse effects ; Mice ; Mice, Inbred C57BL ; Peptides/therapeutic use
مستخلص: Tn P is a family of patented synthetic peptides which is in a preclinical development stage with valuable potential therapeutic indication for multiple sclerosis (MS), an autoimmune demyelinating disease of the central nervous system (CNS). The use of a preclinical animal model, such as experimental autoimmune encephalomyelitis (EAE) has deepened our knowledge of the immunomodulatory functions of Tn P as a drug. We have shown that Tn P possesses a disease suppressive function in EAE, ameliorating disease severity by 40% and suppressing the accumulation of T helper (Th)1- and Th17-producing lymphocytes (by 55% and 60%, respectively) in CNS along with activated microglia/macrophages populations (by 33% and 50%, respectively), and also conferred a protective effect anticipating the remyelination process to day 66 compared to day 83 of untreated cuprizone-mice. Here we expanded our knowledge about its effects compared with current first-line disease-modifying therapies (DMT). We demonstrated that prophylactic treatment with Tn P generated similar protection to betaseron (30%) or was more effective than glatiramer (44% versus 6%) or fingolimod (50% versus 19%) against the development of clinical symptoms. Although Tn P controlled the leukocyte infiltration (87% versus 82%) into demyelinated areas of the spinal cord in the same way as betaseron and fingolimod, it was more effective (72% to 78% decrease) in the long-term control of neuronal degeneration compared to them. Also, when compared to glatiramer, Tn P was more efficient in reversing leukocytes infiltration into the spinal cord (55% versus 24%), as well as induced a higher percentage of regulatory cells in spleen (2.9-fold versus 2.3-fold increase over vehicle-treated EAE mice) an in the spinal cord (8-fold versus 6-fold increase over vehicle-treated EAE mice). This specialized Tn P profile for inducing immune tolerance and neuronal regeneration has significant therapeutic potential for the treatment of MS and other autoimmune diseases.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2022 Lima, Maleski, Bernardo, Zelli, Komegae and Lopes-Ferreira.)
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فهرسة مساهمة: Keywords: EAE; TnP; disease-modifying therapies; fish venom; pre-clinical; synthetic peptide
المشرفين على المادة: 0 (Peptides)
145155-23-3 (Interferon beta-1b)
5M691HL4BO (Glatiramer Acetate)
G926EC510T (Fingolimod Hydrochloride)
تواريخ الأحداث: Date Created: 20220411 Date Completed: 20220412 Latest Revision: 20220705
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8988151
DOI: 10.3389/fimmu.2022.857692
PMID: 35401524
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2022.857692