Kiyoshi Ariizumi, Ph.D. Professor School Medical School Department Dermatology Graduate Programs Immunology Biography Immune responses are tightly regulated in nonlymphoid organs where the ability to defend against infections and cancers should be balanced. The key process is heavily dependent on proper switching the differentiation program of bone marrow-derived progenitors between the immuno-stimulators and the immunosuppressors. One-sided differentiation causes hyperactivation or immunosuppression, leading to autoimmune diseases or promoting cancer growth, respectively. We are studying molecular mechanisms through which myeloid cells (particularly, dendritic cells and macrophages) switch to the suppressors under the pathological conditions of inflammation and cancers, using mouse models (transgenic and gene-disrupted mice) and human clinical samples. We are also thinking about translational studies to make the results of basic research applicable to the development of new treatments for inflammatory and malignant diseases. Education Graduate School University of Tokyo (1985) Research Interest Cancer growth by myeloid-derived suppressor cells Immune checkpoint inhibitor for treatment of cancer patients Negative regulation of T cell-mediated immunity Regulation of metastasis by T cell immunity Publications Featured Publications Myeloid-derived Suppressor Cells in Psoriasis Are an Expanded Population Exhibiting Diverse T cell-Suppressor Mechanisms. Cao LY, Chung JS, Teshima T, Feigenbaum L, Cruz PD, Jacobe HT, Chong BF, Ariizumi K J. Invest. Dermatol. 2016 May DC-HIL-expressing Myelomonocytic Cells Are Critical Promoters of Melanoma Growth. Chung JS, Tamura K, Cruz PD, Ariizumi K J. Invest. Dermatol. 2014 Jun DC-HIL(+) CD14(+) HLA-DR(no/low) Cells Are a Potential Blood Marker and Therapeutic Target for Melanoma. Turrentine J, Chung JS, Nezafati K, Tamura K, Harker-Murray A, Huth J, Sharma RR, Harker DB, Ariizumi K, Cruz PD J. Invest. Dermatol. 2014 Jun DC-HIL is a negative regulator of T cell activation. Chung J-S, Sato K, Dougherty I, Cruz PD Jr, Ariizumi K. Blood Spring 2007 109 4320-4327 The DC-HIL/Syndecan-4 Pathway Regulates Autoimmune Responses through Myeloid-Derived Suppressor Cells. Chung JS, Tamura K, Akiyoshi H, Cruz PD, Ariizumi K J. Immunol. 2014 Feb Inhibition of T-cell activation by syndecan-4 is mediated by CD148 through protein tyrosine phosphatase activity. Chung JS, Cruz PD, Ariizumi K Eur. J. Immunol. 2011 Jun 41 6 1794-9 Sezary syndrome cells overexpress syndecan-4 bearing distinct heparan sulfate moieties that suppress T-cell activation by binding DC-HIL and trapping TGF-beta on the cell surface. Chung JS, Shiue LH, Duvic M, Pandya A, Cruz PD, Ariizumi K Blood 2011 Mar 117 12 3382-90 DC-HIL/glycoprotein Nmb promotes growth of melanoma in mice by inhibiting the activation of tumor-reactive T cells. Tomihari M, Chung JS, Akiyoshi H, Cruz PD, Ariizumi K Cancer Res. 2010 Jul 70 14 5778-87 Depleting syndecan-4+ T lymphocytes using toxin-bearing dendritic cell-associated heparan sulfate proteoglycan-dependent integrin ligand: a new opportunity for treating activated T cell-driven disease. Akiyoshi H, Chung JS, Tomihari M, Cruz PD, Ariizumi K J. Immunol. 2010 Apr 184 7 3554-61 Binding of DC-HIL to dermatophytic fungi induces tyrosine phosphorylation and potentiates antigen presenting cell function. Chung JS, Yudate T, Tomihari M, Akiyoshi H, Cruz PD, Ariizumi K J. Immunol. 2009 Oct 183 8 5190-8 Results 1-10 of 14 1 2 Next Last Honors & Awards Research career Development AwardAwarded by the Dermatology Foundation (1994) Henry Christian Memorial AwardAwarded by the American Federation for Clinical Research (1993) Professional Associations/Affiliations American Association for Cancer Research (2015) American Association of Immunologists (2000) Society of Investigative Dermatology (1994)
