دورية أكاديمية
أعرض في EDS

Engineered erythrocytes covalently linked to antigenic peptides can protect against autoimmune disease.

التفاصيل البيبلوغرافية
العنوان: Engineered erythrocytes covalently linked to antigenic peptides can protect against autoimmune disease.
المؤلفون: Pishesha N; Whitehead Institute for Biomedical Research, Cambridge, MA 02142.; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115., Bilate AM; Whitehead Institute for Biomedical Research, Cambridge, MA 02142., Wibowo MC; Whitehead Institute for Biomedical Research, Cambridge, MA 02142.; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142., Huang NJ; Whitehead Institute for Biomedical Research, Cambridge, MA 02142., Li Z; Whitehead Institute for Biomedical Research, Cambridge, MA 02142.; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115., Deshycka R; Whitehead Institute for Biomedical Research, Cambridge, MA 02142.; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142., Bousbaine D; Whitehead Institute for Biomedical Research, Cambridge, MA 02142.; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115.; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142., Li H; Whitehead Institute for Biomedical Research, Cambridge, MA 02142., Patterson HC; Whitehead Institute for Biomedical Research, Cambridge, MA 02142., Dougan SK; Whitehead Institute for Biomedical Research, Cambridge, MA 02142., Maruyama T; Whitehead Institute for Biomedical Research, Cambridge, MA 02142., Lodish HF; Whitehead Institute for Biomedical Research, Cambridge, MA 02142; lodish@wi.mit.edu hidde.ploegh@childrens.harvard.edu.; Department of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02142.; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142., Ploegh HL; Whitehead Institute for Biomedical Research, Cambridge, MA 02142; lodish@wi.mit.edu hidde.ploegh@childrens.harvard.edu.; Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA 02115.; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142.
المصدر: Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2017 Mar 21; Vol. 114 (12), pp. 3157-3162. Date of Electronic Publication: 2017 Mar 07.
نوع المنشور: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: National Academy of Sciences Country of Publication: United States NLM ID: 7505876 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1091-6490 (Electronic) Linking ISSN: 00278424 NLM ISO Abbreviation: Proc Natl Acad Sci U S A Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Washington, DC : National Academy of Sciences
مستخلص: Current therapies for autoimmune diseases rely on traditional immunosuppressive medications that expose patients to an increased risk of opportunistic infections and other complications. Immunoregulatory interventions that act prophylactically or therapeutically to induce antigen-specific tolerance might overcome these obstacles. Here we use the transpeptidase sortase to covalently attach disease-associated autoantigens to genetically engineered and to unmodified red blood cells as a means of inducing antigen-specific tolerance. This approach blunts the contribution to immunity of major subsets of immune effector cells (B cells, CD4 + and CD8 + T cells) in an antigen-specific manner. Transfusion of red blood cells expressing self-antigen epitopes can alleviate and even prevent signs of disease in experimental autoimmune encephalomyelitis, as well as maintain normoglycemia in a mouse model of type 1 diabetes.
التعليقات: Comment in: Sci Transl Med. 2017 Mar 22;9(382):. (PMID: 28330859)
Erratum in: Proc Natl Acad Sci U S A. 2017 Apr 25;114(17 ):E3583. Dhesycka, Rhogerry [corrected to Deshycka, Rhogerry]. (PMID: 28396403)
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معلومات مُعتمدة: K08 GM102718 United States GM NIGMS NIH HHS; P01 HL032262 United States HL NHLBI NIH HHS; R01 AI087879 United States AI NIAID NIH HHS; United States HHMI Howard Hughes Medical Institute
فهرسة مساهمة: Keywords: antigen-specific tolerance; autoimmune diseases; engineered red blood cells; sortase
تواريخ الأحداث: Date Created: 20170309 Date Completed: 20180423 Latest Revision: 20220718
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5373388
DOI: 10.1073/pnas.1701746114
PMID: 28270614
قاعدة البيانات: MEDLINE
الوصف
تدمد:1091-6490
DOI:10.1073/pnas.1701746114