The protective function of invariant natural killer T cells in the relapse of experimental autoimmune uveoretinitis
| Autor: | Natsumi Tajiri, Masaru Taniguchi, Nobuyoshi Kitaichi, Kazuya Iwabuchi, Misao Iizuka, Taiki Kato, Masashi Satoh |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Disease Enterotoxin medicine.disease_cause Lymphocyte Activation Autoimmunity Autoimmune Diseases Pathogenesis Uveitis 03 medical and health sciences Cellular and Molecular Neuroscience Mice 0302 clinical medicine Th2 Cells Recurrence medicine Animals Eye Proteins Cell Proliferation biology business.industry Retinitis Th1 Cells medicine.disease Flow Cytometry Sensory Systems Mice Inbred C57BL Retinol-Binding Proteins Ophthalmology Regimen Disease Models Animal 030104 developmental biology CD1D Immunology 030221 ophthalmology & optometry biology.protein Natural Killer T-Cells Th17 Cells Female business Function (biology) |
| Zdroj: | Experimental eye research. 203 |
| ISSN: | 1096-0007 |
| Popis: | Experimental autoimmune uveoretinitis (EAU) in mice provides a useful platform to study the pathogenesis and experimental therapeutics of human uveitis. One often used EAU model employs C57BL/6 (B6) mice sensitized with a peptide residue having 1 to 20 amino acids of human interphotoreceptor retinoid binding protein (hIRBP1-20). The model using the B6 background has permitted a liberal use of genetically engineered strains and has provided insights for understanding uveoretinitis. However, this is usually acute/monophasic and does not represent human uveoretinitis that is characterized as a chronic/recurrent disease. Several chronic/recurrent EAU models have been developed; of these, we employed administration of staphylococcal enterotoxin B (SEB) for relapse in the present study, and found that recurrence was induced at day 24 after primary immunization, which is thought to be the convalescent phase. We reported the activation of invariant natural killer T (iNKT)-cells upon primary immunization of the EAU model mice with the ligand RCAI-56, which was found to mitigate the disease in our previous study. Here, we first attempted to ameliorate EAU in the relapse model using a preventive regimen by activating iNKT cells at the same time relapse induction (day 24) or in a regimen after 3 days of relapse induction (day 27). The preventive as well as post-inductive regimens were successful in reducing histopathological scores by inhibiting the Ag-specific Th17-biased response. Collectively, activation of iNKT cells may be useful to mitigate the relapse response of EAU induced with SEB. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect