Immune Checkpoint Ligand Bioengineered Schwann Cells as Antigen‐Specific Therapy for Experimental Autoimmune Encephalomyelitis

Failure to establish immune tolerance leads to the development of autoimmune disease. The ability to regulate autoreactive T cells without inducing systemic immunosuppression represents a major challenge in the development of new strategies to treat autoimmune disease. Here, a translational method f...

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Bibliographic Details
Published in:Advanced materials (Weinheim) 2022-02, Vol.34 (5), p.e2107392-n/a
Main Authors: Au, Kin Man, Tisch, Roland, Wang, Andrew Z.
Format: Article
Language:English
Subjects:
Animals
Antigens
Autoimmune diseases
Bioengineering
bioorthogonal click chemistry
Central nervous system
Differentiation
Encephalomyelitis
Encephalomyelitis, Autoimmune, Experimental - pathology
Encephalomyelitis, Autoimmune, Experimental - therapy
experimental autoimmune encephalomyelitis
immune checkpoint
Immunosuppression
Ligands
Lymphocytes
Materials science
metabolic glycoengineering
Mice
Mice, Inbred C57BL
Multiple sclerosis
Multiple Sclerosis - therapy
Myelin
Schwann cells
Schwann Cells - pathology
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Summary:Failure to establish immune tolerance leads to the development of autoimmune disease. The ability to regulate autoreactive T cells without inducing systemic immunosuppression represents a major challenge in the development of new strategies to treat autoimmune disease. Here, a translational method for bioengineering programmed death‐ligand 1 (PD‐L1)‐ and cluster of differentiation 86 (CD86)‐functionalized mouse Schwann cells (SCs) to prevent and ameliorate multiple sclerosis (MS) in established mouse models of chronic and relapsing‐remitting experimental autoimmune encephalomyelitis (EAE) is described. It is shown that the intravenous (i.v.) administration of immune checkpoint ligand functionalized mouse SCs modifies the course of disease and ameliorates EAE. Further, it is found that such bioengineered mouse SCs inhibit the differentiation of myelin‐specific helper T cells into pathogenic T helper type‐1 (Th1) and type‐17 (Th17) cells, promote the development of tolerogenic myelin‐specific regulatory T (Treg) cells, and resolve inflammatory central nervous system microenvironments without inducing systemic immunosuppression. A translational method for bioengineering programmed death‐ligand 1 and cluster of differentiation 86‐functionalized Schwann cells to prevent and ameliorate multiple sclerosis is developed.
ISSN:0935-9648
1521-4095
1521-4095
DOI:10.1002/adma.202107392