Kiyoshi Hirahara, Associate Professor, Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan

Dr. Hirahara graduated from Niigata University school of Medicine in 2001. He was engaged in clinical practice as a physician, specifically in respiratory medicine for more than three years and he started a Ph.D. course supervised by Prof. Toshinori Nakayama in the Department of Immunology at Chiba University in 2004. His project was to study the role of repressor of GATA3, which regulates the expression of Th2-related cytokines and he completed the Ph.D. program in 2008. From 2009 to 2013, he worked as a postdoctoral fellow with Dr. John J. O’Shea at the Molecular Immunology and Inflammation Branch of the US National Institute of Arthritis and Musculoskeletal and Skin Diseases. He identified new immunosuppressive mechanisms of a critical immunoregulatory cytokine, Interleukin (IL)-27. He also identified a crucial link between the role of a transcription factor, BACH2 and the immune balance of CD4 T cells.
In 2013, he joined the Department of Immunology at Chiba University as a faculty member and continued working on IL-27 and IL-6. He found that STAT1 contributes to transcriptomic diversity in response to cytokines and that the functional abnormality of STAT1 is involved in the pathogenicity of human primary immunodeficiency. Dr. Hirahara is now mainly carrying out research on the identification of the pathogenic roles of CD4+ T cells in intractable respiratory diseases, such as pulmonary fibrosis.
Dr. Hirahara acquired a grant from the JSPS Research Fellowship for Japanese Biomedical and Behavioral Researchers at NIH from January 2012 to March 2013. He also received the 10th Young Investigator Award from Japanese Society for Immunology in 2015.

Abstract from Young Investigator Award’s Session Presentation at Cytokine 2017 in Kanazawa:

Memory-type ST2+CD4+ T cells participate in the steroid-resistant pathology of eosinophilic pneumonia
Kiyoshi Hirahara1, Naoko Mato1, 2, Tomomi Ichikawa1, Jin Kumagai1, Masayuki Nakayama2, Hideaki Yamasawa2, Masashi Bando2, Koichi Hagiwara2, Yukihiko Sugiyama2, 3, Toshinori Nakayama1
1Department of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan, 2Division of Pulmonary Medicine, Department of Internal Medicine, Jichi Medical University, Tochigi, Japan, 3Department of Respiratory Medicine, Nerima-Hikarigaoka Hospital, Tokyo, Japan

The lung has an unique epithelial barrier system to protect host from continuous invasion of various harmful particles including viruses and bacteria. Interleukin (IL-)33, an epithelial cytokine, is released from epithelial cells in the lung and drives the type 2 immune response by activating ST2-expressed immune cells in a number of allergic diseases. However, the pathogenic roles of memory-type ST2+CD4+ T cells in such lung inflammation has been unclear. Here we showed that intratracheal administration of IL-33 induced the substantial increase of numbers of tissue-resident memory-type ST2+CD4+ T cells in the lung. Eosinophilic lung inflammation developed sequentially accompanied by enhanced production of IL-5 and IL-13. T cell-deficient Foxn1nu mice and NSG mice exhibited ameliorated eosinophilic inflammation induced by IL-33. Dexamethasone treatment showed small effects on both the cell number and function of memory-type ST2+CD4+ T cells. Taken together, our study provides novel insight into the pathogenesis of eosinophilic lung disease, showing that memory-type ST2+CD4+ T cells are involved in IL-33-induced eosinophilic inflammation and elicited steroid-resistance.