Anti-Cytokine Active Immunotherapy Based on Supramolecular Peptides for Alleviating IL-1β-Mediated Inflammation
IL-1β is a principal proinflammatory cytokine underlying multiple local and systemic chronic inflammatory conditions including psoriasis, rheumatoid arthritis, inflammatory bowel disease, and type 2 diabetes. Passive immunotherapies and biologic drugs targeting IL-1β, while offering significant clin...
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| Abstract | IL-1β is a principal proinflammatory cytokine underlying multiple local and systemic chronic inflammatory conditions including psoriasis, rheumatoid arthritis, inflammatory bowel disease, and type 2 diabetes. Passive immunotherapies and biologic drugs targeting IL-1β, while offering significant clinical benefit, nevertheless have limitations such as significant non-response rates, induction of anti-drug antibodies, and high costs. Here, an active immunotherapy raising antibody responses against IL-1β employing self-assembling peptide nanofibers is described. The nanofibers contain defined quantities of B-cell epitopes from IL-1β and exogenous T helper epitopes and employ the Q11 self-assembling peptide platform. Without adjuvant, the nanofibers raised durable anti-IL-1β antibody responses that inhibit IL-1β activity in vitro and in vivo. In a mouse model of imiquimod-induced psoriasis, prophylactic immunizations with the nanofibers diminished symptoms of epidermal thickening. This therapeutic effect is associated with biasing the immune response toward an anti-inflammatory IgG1/Th2 phenotype and a lowered expression of proinflammatory genes in the skin. Further, anti-IL-1β nanofibers induced therapeutic immunosuppressive CD62L+ Treg cells. This technology represents a potential alternative for passive immunotherapies and other biologics for treating chronic inflammatory conditions. |
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| AbstractList | IL-1β is a principal proinflammatory cytokine underlying multiple local and systemic chronic inflammatory conditions including psoriasis, rheumatoid arthritis, inflammatory bowel disease, and type 2 diabetes. Passive immunotherapies and biologic drugs targeting IL-1β, while offering significant clinical benefit, nevertheless have limitations such as significant non-response rates, induction of anti-drug antibodies, and high costs. Here, an active immunotherapy raising antibody responses against IL-1β employing self-assembling peptide nanofibers is described. The nanofibers contain defined quantities of B-cell epitopes from IL-1β and exogenous T helper epitopes and employ the Q11 self-assembling peptide platform. Without adjuvant, the nanofibers raised durable anti-IL-1β antibody responses that inhibit IL-1β activity in vitro and in vivo. In a mouse model of imiquimod-induced psoriasis, prophylactic immunizations with the nanofibers diminished symptoms of epidermal thickening. This therapeutic effect is associated with biasing the immune response toward an anti-inflammatory IgG1/Th2 phenotype and a lowered expression of proinflammatory genes in the skin. Further, anti-IL-1β nanofibers induced therapeutic immunosuppressive CD62L+ Treg cells. This technology represents a potential alternative for passive immunotherapies and other biologics for treating chronic inflammatory conditions.IL-1β is a principal proinflammatory cytokine underlying multiple local and systemic chronic inflammatory conditions including psoriasis, rheumatoid arthritis, inflammatory bowel disease, and type 2 diabetes. Passive immunotherapies and biologic drugs targeting IL-1β, while offering significant clinical benefit, nevertheless have limitations such as significant non-response rates, induction of anti-drug antibodies, and high costs. Here, an active immunotherapy raising antibody responses against IL-1β employing self-assembling peptide nanofibers is described. The nanofibers contain defined quantities of B-cell epitopes from IL-1β and exogenous T helper epitopes and employ the Q11 self-assembling peptide platform. Without adjuvant, the nanofibers raised durable anti-IL-1β antibody responses that inhibit IL-1β activity in vitro and in vivo. In a mouse model of imiquimod-induced psoriasis, prophylactic immunizations with the nanofibers diminished symptoms of epidermal thickening. This therapeutic effect is associated with biasing the immune response toward an anti-inflammatory IgG1/Th2 phenotype and a lowered expression of proinflammatory genes in the skin. Further, anti-IL-1β nanofibers induced therapeutic immunosuppressive CD62L+ Treg cells. This technology represents a potential alternative for passive immunotherapies and other biologics for treating chronic inflammatory conditions. IL-1β is a principal proinflammatory cytokine underlying multiple local and systemic chronic inflammatory conditions including psoriasis, rheumatoid arthritis, inflammatory bowel disease, and type 2 diabetes. Passive immunotherapies and biologic drugs targeting IL-1β, while offering significant clinical benefit, nevertheless have limitations such as significant non-response rates, induction of anti-drug antibodies, and high costs. Here, an active immunotherapy raising antibody responses against IL-1β employing self-assembling peptide nanofibers is described. The nanofibers contain defined quantities of B-cell epitopes from IL-1β and exogenous T helper epitopes and employ the Q11 self-assembling peptide platform. Without adjuvant, the nanofibers raised durable anti-IL-1β antibody responses that inhibit IL-1β activity in vitro and in vivo. In a mouse model of imiquimod-induced psoriasis, prophylactic immunizations with the nanofibers diminished symptoms of epidermal thickening. This therapeutic effect is associated with biasing the immune response toward an anti-inflammatory IgG1/Th2 phenotype and a lowered expression of proinflammatory genes in the skin. Further, anti-IL-1β nanofibers induced therapeutic immunosuppressive CD62L+ Treg cells. This technology represents a potential alternative for passive immunotherapies and other biologics for treating chronic inflammatory conditions. Abstract IL‐1β is a principal proinflammatory cytokine underlying multiple local and systemic chronic inflammatory conditions including psoriasis, rheumatoid arthritis, inflammatory bowel disease, and type 2 diabetes. Passive immunotherapies and biologic drugs targeting IL‐1β, while offering significant clinical benefit, nevertheless have limitations such as significant non‐response rates, induction of anti‐drug antibodies, and high costs. Here, an active immunotherapy raising antibody responses against IL‐1β employing self‐assembling peptide nanofibers is described. The nanofibers contain defined quantities of B‐cell epitopes from IL‐1β and exogenous T helper epitopes and employ the Q11 self‐assembling peptide platform. Without adjuvant, the nanofibers raised durable anti‐IL‐1β antibody responses that inhibit IL‐1β activity in vitro and in vivo. In a mouse model of imiquimod‐induced psoriasis, prophylactic immunizations with the nanofibers diminished symptoms of epidermal thickening. This therapeutic effect is associated with biasing the immune response toward an anti‐inflammatory IgG1/Th2 phenotype and a lowered expression of proinflammatory genes in the skin. Further, anti‐IL‐1β nanofibers induced therapeutic immunosuppressive CD62L+ Treg cells. This technology represents a potential alternative for passive immunotherapies and other biologics for treating chronic inflammatory conditions. |
| Author | Liu, Yining Shetty, Shamitha Lloyd, Christopher Z Mehta, Nalini Wu, Yaoying Woodruff, Mia E Segura, Tatiana Collier, Joel H |
| Author_xml | – sequence: 1 givenname: Shamitha orcidid: 0000-0001-8771-5225 surname: Shetty fullname: Shetty, Shamitha organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 2 givenname: Yaoying surname: Wu fullname: Wu, Yaoying organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 3 givenname: Christopher Z surname: Lloyd fullname: Lloyd, Christopher Z organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 4 givenname: Nalini surname: Mehta fullname: Mehta, Nalini organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 5 givenname: Yining surname: Liu fullname: Liu, Yining organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 6 givenname: Mia E surname: Woodruff fullname: Woodruff, Mia E organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 7 givenname: Tatiana surname: Segura fullname: Segura, Tatiana organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA – sequence: 8 givenname: Joel H orcidid: 0000-0003-3536-4827 surname: Collier fullname: Collier, Joel H organization: Department of Biomedical Engineering, Duke University, Durham, NC, 27705, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39113323$$D View this record in MEDLINE/PubMed |
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| Title | Anti-Cytokine Active Immunotherapy Based on Supramolecular Peptides for Alleviating IL-1β-Mediated Inflammation |
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