Journal
NATURE BIOMEDICAL ENGINEERING
Volume 5, Issue 11, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41551-021-00738-5
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Funding
- Harvard Society of Fellows
- Swiss National Science Foundation [P400P2_183857]
- Dutch MS Research Foundation
- UiT The Arctic University of Norway
- NIH Director's Pioneer Award [1DP1AI150593-01]
- Swiss National Science Foundation (SNF) [P400P2_183857] Funding Source: Swiss National Science Foundation (SNF)
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Nanobodies recognizing MHCII molecules and conjugated to relevant self-antigens provide long-lasting protection in mouse models of autoimmune diseases. This approach may represent a novel means of treating autoimmune conditions.
Nanobodies recognizing class-II major-histocompatibility-complex molecules and conjugated to relevant self-antigens confer protection against autoimmune diseases in mice. The association of autoimmune diseases with particular allellic products of the class-II major histocompatibility complex (MHCII) region implicates the presentation of the offending self-antigens to T cells. Because antigen-presenting cells are tolerogenic when they encounter an antigen under non-inflammatory conditions, the manipulation of antigen presentation may induce antigen-specific tolerance. Here, we show that, in mouse models of experimental autoimmune encephalomyelitis, type 1 diabetes and rheumatoid arthritis, the systemic administration of a single dose of nanobodies that recognize MHCII molecules and conjugated to the relevant self-antigen under non-inflammatory conditions confers long-lasting protection against these diseases. Moreover, co-administration of a nanobody-antigen adduct and the glucocorticoid dexamethasone, conjugated to the nanobody via a cleavable linker, halted the progression of established experimental autoimmune encephalomyelitis in symptomatic mice and alleviated their symptoms. This approach may represent a means of treating autoimmune conditions.
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