{"title":"Matrix reboot: IL-17 signals CAFs to create a second tumor T cell checkpoint","authors":"M. McGeachy","doi":"10.1084/jem.20220444","DOIUrl":"https://doi.org/10.1084/jem.20220444","url":null,"abstract":"IL-17 promotes collagen deposition by cancer-associated fibroblasts and enhances immune exclusion of tumors.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73731252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R. Hasebe, K. Murakami, Masaya Harada, N. Halaka, H. Nakagawa, F. Kawano, Y. Ohira, T. Kawamoto, F. Yull, T. Blackwell, J. Nio-Kobayashi, Toshihiko Iwanaga, Masahiko Watanabe, N. Watanabe, H. Hotta, T. Yamashita, D. Kamimura, Yuki Tanaka, M. Murakami
{"title":"ATP spreads inflammation to other limbs through crosstalk between sensory neurons and interneurons","authors":"R. Hasebe, K. Murakami, Masaya Harada, N. Halaka, H. Nakagawa, F. Kawano, Y. Ohira, T. Kawamoto, F. Yull, T. Blackwell, J. Nio-Kobayashi, Toshihiko Iwanaga, Masahiko Watanabe, N. Watanabe, H. Hotta, T. Yamashita, D. Kamimura, Yuki Tanaka, M. Murakami","doi":"10.1084/jem.20212019","DOIUrl":"https://doi.org/10.1084/jem.20212019","url":null,"abstract":"Local inflammation spreads to remote positions via sensory neuron–interneuron crosstalk using ATP. This neural pathway, or remote inflammation gateway reflex, may be a therapeutic target for inflammatory diseases with remote inflammation, such as rheumatoid arthritis.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86780798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yikun Yao, Ping Du Jiang, B. Chao, D. Çağdaş, S. Kubo, Arasu Balasubramaniyam, Yu Zhang, B. Shadur, A. NaserEddin, L. Folio, Benjamin Schwarz, Eric Bohrnsen, Lixin Zheng, Matthew Lynberg, Simone Gottlieb, Michael A. Leney-Greene, Ann Y. Park, I. Tezcan, A. Akdoğan, R. Gocmen, S. Onder, A. Rosenberg, E. Soilleux, Errin Johnson, P. Jackson, J. Demeter, Samuel D. Chauvin, F. Paul, M. Selbach, H. Bulut, M. Clatworthy, Z. Tuong, Hanlin Zhang, B. Stewart, C. Bosio, P. Stepensky, S. Clare, S. Ganesan, J. Pascall, O. Daumke, G. Butcher, A. McMichael, A. Simon, M. Lenardo
{"title":"GIMAP6 regulates autophagy, immune competence, and inflammation in mice and humans","authors":"Yikun Yao, Ping Du Jiang, B. Chao, D. Çağdaş, S. Kubo, Arasu Balasubramaniyam, Yu Zhang, B. Shadur, A. NaserEddin, L. Folio, Benjamin Schwarz, Eric Bohrnsen, Lixin Zheng, Matthew Lynberg, Simone Gottlieb, Michael A. Leney-Greene, Ann Y. Park, I. Tezcan, A. Akdoğan, R. Gocmen, S. Onder, A. Rosenberg, E. Soilleux, Errin Johnson, P. Jackson, J. Demeter, Samuel D. Chauvin, F. Paul, M. Selbach, H. Bulut, M. Clatworthy, Z. Tuong, Hanlin Zhang, B. Stewart, C. Bosio, P. Stepensky, S. Clare, S. Ganesan, J. Pascall, O. Daumke, G. Butcher, A. McMichael, A. Simon, M. Lenardo","doi":"10.1084/jem.20201405","DOIUrl":"https://doi.org/10.1084/jem.20201405","url":null,"abstract":"Yao et al. describe GIMAP6 deficiency in humans and mice showing immune dysfunction and susceptibility to bacterial infections. They find impaired autophagy in GIMAP6-deficient immune cells and define a functional complex composed of GIMAP6, GIMAP7, and GABARAPL2.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89330039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Role of adipose tissue macrophages in obesity-related disorders","authors":"S. Chakarov, Camille Blériot, F. Ginhoux","doi":"10.1084/jem.20211948","DOIUrl":"https://doi.org/10.1084/jem.20211948","url":null,"abstract":"As the first immune cells to colonize tissues and long-lived resident cells, macrophages play important roles in tissue functions during early development, homeostasis, and disease. Here, Chakarov et al. discuss macrophage origin and functions in adipose tissue and how these features are modulated in obesity.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76313113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Sex biases in infectious diseases research","authors":"S. Dhakal, Sabal Chaulagain, S. Klein","doi":"10.1084/jem.20211486","DOIUrl":"https://doi.org/10.1084/jem.20211486","url":null,"abstract":"Reporting the distribution and inclusion of both males and females in immunology and infectious diseases research is improving, but rigorous analyses of differential outcomes between males and females, including mechanistic inquiries into the causes of sex differences, still lags behind.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84309407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Trophoblast antigens, fetal blood cell antigens, and the paradox of fetomaternal tolerance.","authors":"Gabrielle Rizzuto, Adrian Erlebacher","doi":"10.1084/jem.20211515","DOIUrl":"10.1084/jem.20211515","url":null,"abstract":"<p><p>The paradox of fetomaternal tolerance has puzzled immunologists and reproductive biologists alike for almost 70 yr. Even the idea that the conceptus evokes a uniformly tolerogenic immune response in the mother is contradicted by the long-appreciated ability of pregnant women to mount robust antibody responses to paternal HLA molecules and RBC alloantigens such as Rh(D). Synthesizing these older observations with more recent work in mice, we discuss how the decision between tolerance or immunity to a given fetoplacental antigen appears to be a function of whether the antigen is trophoblast derived-and thus decorated with immunosuppressive glycans-or fetal blood cell derived.</p>","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9011327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75536869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joseph Kelich, Tomas Aramburu, Joanne J van der Vis, Louise Showe, Andrew Kossenkov, Jasper van der Smagt, Maarten Massink, Angela Schoemaker, Eric Hennekam, Marcel Veltkamp, Coline H M van Moorsel, Emmanuel Skordalakes
{"title":"Telomere dysfunction implicates POT1 in patients with idiopathic pulmonary fibrosis.","authors":"Joseph Kelich, Tomas Aramburu, Joanne J van der Vis, Louise Showe, Andrew Kossenkov, Jasper van der Smagt, Maarten Massink, Angela Schoemaker, Eric Hennekam, Marcel Veltkamp, Coline H M van Moorsel, Emmanuel Skordalakes","doi":"10.1084/jem.20211681","DOIUrl":"10.1084/jem.20211681","url":null,"abstract":"<p><p>Exonic sequencing identified a family with idiopathic pulmonary fibrosis (IPF) containing a previously unreported heterozygous mutation in POT1 p.(L259S). The family displays short telomeres and genetic anticipation. We found that POT1(L259S) is defective in binding the telomeric overhang, nuclear accumulation, negative regulation of telomerase, and lagging strand maintenance. Patient cells containing the mutation display telomere loss, lagging strand defects, telomere-induced DNA damage, and premature senescence with G1 arrest. Our data suggest POT1(L259S) is a pathogenic driver of IPF and provide insights into gene therapy options.</p>","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9014792/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75423007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Madeline J Churchill, Haley du Bois, Taylor A Heim, Tenny Mudianto, Maria M Steele, Jeffrey C Nolz, Amanda W Lund
{"title":"Infection-induced lymphatic zippering restricts fluid transport and viral dissemination from skin.","authors":"Madeline J Churchill, Haley du Bois, Taylor A Heim, Tenny Mudianto, Maria M Steele, Jeffrey C Nolz, Amanda W Lund","doi":"10.1084/jem.20211830","DOIUrl":"10.1084/jem.20211830","url":null,"abstract":"<p><p>Lymphatic vessels are often considered passive conduits that flush antigenic material, pathogens, and cells to draining lymph nodes. Recent evidence, however, suggests that lymphatic vessels actively regulate diverse processes from antigen transport to leukocyte trafficking and dietary lipid absorption. Here we tested the hypothesis that infection-induced changes in lymphatic transport actively contribute to innate host defense. We demonstrate that cutaneous vaccinia virus infection by scarification activates dermal lymphatic capillary junction tightening (zippering) and lymph node lymphangiogenesis, which are associated with reduced fluid transport and cutaneous viral sequestration. Lymphatic-specific deletion of VEGFR2 prevented infection-induced lymphatic capillary zippering, increased fluid flux out of tissue, and allowed lymphatic dissemination of virus. Further, a reduction in dendritic cell migration to lymph nodes in the absence of lymphatic VEGFR2 associated with reduced antiviral CD8+ T cell expansion. These data indicate that VEGFR2-driven lymphatic remodeling is a context-dependent, active mechanism of innate host defense that limits viral dissemination and facilitates protective, antiviral CD8+ T cell responses.</p>","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8972184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78855850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Masahiko Nishitani-Isa, Kojiro Mukai, Y. Honda, H. Nihira, Takayuki Tanaka, H. Shibata, K. Kodama, E. Hiejima, K. Izawa, Yuri Kawasaki, M. Osawa, Yu Katata, Sachiko Onodera, Tatsuya Watanabe, T. Uchida, S. Kure, J. Takita, O. Ohara, M. Saito, R. Nishikomori, T. Taguchi, Y. Sasahara, T. Yasumi
{"title":"Trapping of CDC42 C-terminal variants in the Golgi drives pyrin inflammasome hyperactivation","authors":"Masahiko Nishitani-Isa, Kojiro Mukai, Y. Honda, H. Nihira, Takayuki Tanaka, H. Shibata, K. Kodama, E. Hiejima, K. Izawa, Yuri Kawasaki, M. Osawa, Yu Katata, Sachiko Onodera, Tatsuya Watanabe, T. Uchida, S. Kure, J. Takita, O. Ohara, M. Saito, R. Nishikomori, T. Taguchi, Y. Sasahara, T. Yasumi","doi":"10.1084/jem.20211889","DOIUrl":"https://doi.org/10.1084/jem.20211889","url":null,"abstract":"Using induced pluripotent stem cells carrying CDC42R186C, trapping of CDC42 C-terminal variants within the Golgi apparatus is shown to trigger autoinflammation by promoting pyrin inflammasome assembly through a mechanism independent of their GTPase activity.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73056184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CD36, a signaling receptor and fatty acid transporter that regulates immune cell metabolism and fate","authors":"Yiliang Chen, Jue Zhang, W. Cui, R. Silverstein","doi":"10.1084/jem.20211314","DOIUrl":"https://doi.org/10.1084/jem.20211314","url":null,"abstract":"CD36 functions as both a signaling receptor and fatty acid transporter in various immune and non-immune cells. This review summarizes how its dual functions determine immune cell functions and fates, which contribute to common diseases including atherosclerosis and tumor progression.","PeriodicalId":23015,"journal":{"name":"The Tokushima journal of experimental medicine","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75170283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}