Mogamulizumab Suppresses Induction of Myelin-Reactive Antibodies After Experimental Spinal Cord Injury
5 affiliations
- 1Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Moscow 117997, Russia
- 2Moscow Center for Advanced Studies, Kulakova Str. 20, Moscow 123592, Russia
- 3Branch of Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Pushchino 142290, Russia
- 4Federal Budget Institution of Science «State Research Center for Applied Microbiology and Biotechnology» a part of the Federal Service for Supervision of Consumer Rights Protection and Human Welfare of the Russian Federation (FBIS SRCAMB), Obolensk 142279, Russia
- 5Department of Biological Chemistry, Russian University of Medicine, Ministry of Health of the Russian Federation, Moscow 127473, Russia
Abstract
Traumatic spinal cord injury (SCI) is believed to increase the risk of autoimmune diseases, including the autoimmune demyelinating disease multiple sclerosis (MS), in humans. The adaptive immune response against one of the key MS autoantigens, myelin basic protein (MBP), is elevated in mice and persists in patients with SCI even 10 years after the initial injury. Here, we show that β1i-enriched immunoproteasomes and PA28β subunits are elevated as early as 12 h post-SCI in DA rats, and all proteasome catalytic immunosubunits are highly abundant in the injured spinal cord of DA and SD rats 7–14 days post-SCI; these changes may therefore represent a primary event of the adaptive myelin-reactive immune response. Mogamulizumab bound a recombinant rat CCR4 N-terminal extracellular fragment, albeit less strongly than the corresponding human fragment, and treatment was associated with weaker CCR4-associated immunoreactivity in peripheral blood leukocyte lysates. Plasma samples from rats with SCI treated with mogamulizumab were characterized by lower levels of antibodies to MBP compared with those from the non-treated group, and by day 60 of the experiment, this discrepancy reached statistical significance. Compared with non-treated animals, rats treated with mogamulizumab showed a significantly decreased glial scar size and total area of cyst-like cavities. Thus, mogamulizumab therapy not only improves the morphological features of the glial scar but also suppresses the autoimmune response against myelin, and may offer a complementary immunological strategy for spinal cord protection following injury.
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BibTeX
@article{orlova2026mogamulizumab,
title = {{Mogamulizumab Suppresses Induction of Myelin-Reactive Antibodies After Experimental Spinal Cord Injury}},
author = {Darya A. Orlova and Aleksandr S. Chernov and Vitaly A. Kazakov and Georgii B. Telegin and Alexey A. Belogurov and Anna A. Kudriaeva},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15211999},
url = {https://www.mdpi.com/2073-4409/15/21/1999},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Mogamulizumab Suppresses Induction of Myelin-Reactive Antibodies After Experimental Spinal Cord Injury
AU - Darya A. Orlova
AU - Aleksandr S. Chernov
AU - Vitaly A. Kazakov
AU - Georgii B. Telegin
AU - Alexey A. Belogurov
AU - Anna A. Kudriaeva
PY - 2026
DA - 2026/10/31
JO - Cells
DO - 10.3390/cells15211999
UR - https://www.mdpi.com/2073-4409/15/21/1999
AB - Traumatic spinal cord injury (SCI) is believed to increase the risk of autoimmune diseases, including the autoimmune demyelinating disease multiple sclerosis (MS), in humans. The adaptive immune response against one of the key MS autoantigens, myelin basic protein (MBP), is elevated in mice and persists in patients with SCI even 10 years after the initial injury. Here, we show that β1i-enriched immunoproteasomes and PA28β subunits are elevated as early as 12 h post-SCI in DA rats, and all proteasome catalytic immunosubunits are highly abundant in the injured spinal cord of DA and SD rats 7–14 days post-SCI; these changes may therefore represent a primary event of the adaptive myelin-reactive immune response. Mogamulizumab bound a recombinant rat CCR4 N-terminal extracellular fragment, albeit less strongly than the corresponding human fragment, and treatment was associated with weaker CCR4-associated immunoreactivity in peripheral blood leukocyte lysates. Plasma samples from rats with SCI treated with mogamulizumab were characterized by lower levels of antibodies to MBP compared with those from the non-treated group, and by day 60 of the experiment, this discrepancy reached statistical significance. Compared with non-treated animals, rats treated with mogamulizumab showed a significantly decreased glial scar size and total area of cyst-like cavities. Thus, mogamulizumab therapy not only improves the morphological features of the glial scar but also suppresses the autoimmune response against myelin, and may offer a complementary immunological strategy for spinal cord protection following injury.
SN - 2073-4409
ER -