**About the Editor**

#### **Tomoaki Ishigami**

Tomoaki Ishigami was born in Tokyo, Japan. He obtained his medical degree and Ph.D. from Yokohama City University, Yokohama, Japan. Following this, he moved to the Eccles Institute of Human Genetics, Howard Hughes Medical Institute, University of Utah in the USA, where he worked as a post-doctoral fellow. His primary research interest is elucidating the molecular pathophysiology of salt-sensitive hypertension and atherosclerosis. Prof. Ishigami and colleagues developed a "high-sensitivity, high-throughput immunoglobulin auto-antibody screening system" using cell-free technology that can detect IgG-type antibodies against self-components with high sensitivity in atherosclerotic patients.(Ishigami T, et al. FASEB J, 2013) Prof. Ishigami and colleagues also conducted experiments using ApoE knockout mice, with the aim of clarifying the molecular biological mechanisms by which lifestyle habits induce atherosclerosis. As a result of the activation and conditioning of splenic B2 cells, they infiltrate PVAT, and an experiment was conducted to clarify the effect of B2 cell depletion on atherosclerosis. Using anti-CD23 antibody treatment, it was found to significantly suppress aortic plaque area and aortic annulus plaque area, as well as significantly suppress serum IgG/IgG3. (Chen L, Ishigami T, et al. eBioMedicine, 2016) Lubiprostone, a chloride channel activator, has the effect of improving the intestinal barrier function, and administration to ApoE knockout mice can also suppress atherosclerosis. (Arakawa K, Ishigami T, et al. Plos One, 2019).
