Shoichi Shimizu , Junko Shin , Takuma Ota , Hirofumi Kondo , Susumu Nakae , Katsuko Sudo , Eman M. Gaballah , Kentaro Morita , Yoshio Osada
{"title":"小鼠非致命性疟疾感染对胶原蛋白诱导的关节炎的缓解不需要IL-10。","authors":"Shoichi Shimizu , Junko Shin , Takuma Ota , Hirofumi Kondo , Susumu Nakae , Katsuko Sudo , Eman M. Gaballah , Kentaro Morita , Yoshio Osada","doi":"10.1016/j.parint.2024.102993","DOIUrl":null,"url":null,"abstract":"<div><div>We previously reported that <em>Plasmodium yoelii</em> 17XNL (Py), a non-lethal rodent malarial parasite, could suppress collagen-induced arthritis (CIA) and increase the production of T cell-derived interleukin (IL)-10. However, it remained unclear whether IL-10 is essential for the Py-induced suppression of CIA. Male IL-10 knockout (KO) DBA/1 J mice were immunized with bovine type II collagen (CII) and subsequently infected with Py at one week post-immunization. The development of arthritis was evaluated by an arthritis score up to 6 weeks post-immunization. At 3 weeks post-immunization, cytokine production from splenocytes and serum anti-CII IgG/IgG1/IgG2a levels were compared between non-infected control mice and Py-infected mice. Py infection inhibited the development of CIA in IL-10KO mice until 4 weeks post-immunization, after which the arthritis score reached levels comparable with the control mice. Both pro-arthritic (IL-17 and TNF-α) and anti-arthritic (IFN-γ and IL-4) cytokines were down-regulated during the periods of parasitemia, while no significant differences were observed in levels of anti-CII IgG antibodies. Our findings indicate that Py alleviates CIA via IL-10-independent mechanisms.</div></div>","PeriodicalId":19983,"journal":{"name":"Parasitology International","volume":"104 ","pages":"Article 102993"},"PeriodicalIF":1.5000,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"IL-10 is not required for the alleviation of collagen-induced arthritis by non-lethal malarial infection in mice\",\"authors\":\"Shoichi Shimizu , Junko Shin , Takuma Ota , Hirofumi Kondo , Susumu Nakae , Katsuko Sudo , Eman M. Gaballah , Kentaro Morita , Yoshio Osada\",\"doi\":\"10.1016/j.parint.2024.102993\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>We previously reported that <em>Plasmodium yoelii</em> 17XNL (Py), a non-lethal rodent malarial parasite, could suppress collagen-induced arthritis (CIA) and increase the production of T cell-derived interleukin (IL)-10. However, it remained unclear whether IL-10 is essential for the Py-induced suppression of CIA. Male IL-10 knockout (KO) DBA/1 J mice were immunized with bovine type II collagen (CII) and subsequently infected with Py at one week post-immunization. The development of arthritis was evaluated by an arthritis score up to 6 weeks post-immunization. At 3 weeks post-immunization, cytokine production from splenocytes and serum anti-CII IgG/IgG1/IgG2a levels were compared between non-infected control mice and Py-infected mice. Py infection inhibited the development of CIA in IL-10KO mice until 4 weeks post-immunization, after which the arthritis score reached levels comparable with the control mice. Both pro-arthritic (IL-17 and TNF-α) and anti-arthritic (IFN-γ and IL-4) cytokines were down-regulated during the periods of parasitemia, while no significant differences were observed in levels of anti-CII IgG antibodies. Our findings indicate that Py alleviates CIA via IL-10-independent mechanisms.</div></div>\",\"PeriodicalId\":19983,\"journal\":{\"name\":\"Parasitology International\",\"volume\":\"104 \",\"pages\":\"Article 102993\"},\"PeriodicalIF\":1.5000,\"publicationDate\":\"2024-11-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Parasitology International\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1383576924001442\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"PARASITOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Parasitology International","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1383576924001442","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PARASITOLOGY","Score":null,"Total":0}
IL-10 is not required for the alleviation of collagen-induced arthritis by non-lethal malarial infection in mice
We previously reported that Plasmodium yoelii 17XNL (Py), a non-lethal rodent malarial parasite, could suppress collagen-induced arthritis (CIA) and increase the production of T cell-derived interleukin (IL)-10. However, it remained unclear whether IL-10 is essential for the Py-induced suppression of CIA. Male IL-10 knockout (KO) DBA/1 J mice were immunized with bovine type II collagen (CII) and subsequently infected with Py at one week post-immunization. The development of arthritis was evaluated by an arthritis score up to 6 weeks post-immunization. At 3 weeks post-immunization, cytokine production from splenocytes and serum anti-CII IgG/IgG1/IgG2a levels were compared between non-infected control mice and Py-infected mice. Py infection inhibited the development of CIA in IL-10KO mice until 4 weeks post-immunization, after which the arthritis score reached levels comparable with the control mice. Both pro-arthritic (IL-17 and TNF-α) and anti-arthritic (IFN-γ and IL-4) cytokines were down-regulated during the periods of parasitemia, while no significant differences were observed in levels of anti-CII IgG antibodies. Our findings indicate that Py alleviates CIA via IL-10-independent mechanisms.
期刊介绍:
Parasitology International provides a medium for rapid, carefully reviewed publications in the field of human and animal parasitology. Original papers, rapid communications, and original case reports from all geographical areas and covering all parasitological disciplines, including structure, immunology, cell biology, biochemistry, molecular biology, and systematics, may be submitted. Reviews on recent developments are invited regularly, but suggestions in this respect are welcome. Letters to the Editor commenting on any aspect of the Journal are also welcome.