論文

国際誌
2021年5月

Prolonged residence of an albumin-IL-4 fusion protein in secondary lymphoid organs ameliorates experimental autoimmune encephalomyelitis.

Nature biomedical engineering
  • Ako Ishihara
  • Jun Ishihara
  • Elyse A Watkins
  • Andrew C Tremain
  • Mindy Nguyen
  • Ani Solanki
  • Kiyomitsu Katsumata
  • Aslan Mansurov
  • Erica Budina
  • Aaron T Alpar
  • Peyman Hosseinchi
  • Lea Maillat
  • Joseph W Reda
  • Takahiro Kageyama
  • Melody A Swartz
  • Eiji Yuba
  • Jeffrey A Hubbell
  • 全て表示

5
5
開始ページ
387
終了ページ
398
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1038/s41551-020-00627-3

Interleukin-4 (IL-4) suppresses the development of multiple sclerosis in a murine model of experimental autoimmune encephalomyelitis (EAE). Here, we show that, in mice with EAE, the accumulation and persistence in the lymph nodes and spleen of a systemically administered serum albumin (SA)-IL-4 fusion protein leads to higher efficacy in preventing disease development than the administration of wild-type IL-4 or of the clinically approved drug fingolimod. We also show that the SA-IL-4 fusion protein prevents immune-cell infiltration in the spinal cord, decreases integrin expression in antigen-specific CD4+ T cells, increases the number of granulocyte-like myeloid-derived suppressor cells (and their expression of programmed-death-ligand-1) in spinal cord-draining lymph nodes and decreases the number of T helper 17 cells, a pathogenic cell population in EAE. In mice with chronic EAE, SA-IL-4 inhibits immune-cell infiltration into the spinal cord and completely abrogates immune responses to myelin antigen in the spleen. The SA-IL-4 fusion protein may be prophylactically and therapeutically advantageous in the treatment of multiple sclerosis.

リンク情報
DOI
https://doi.org/10.1038/s41551-020-00627-3
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/33046864
ID情報
  • DOI : 10.1038/s41551-020-00627-3
  • PubMed ID : 33046864

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