Kiyoshi Ariizumi, PhD

Associate Professor
Dermatology
Graduate Program: Immunology

Contact Information

UT Southwestern Medical Center
5323 Harry Hines Boulevard
Dallas, Texas 75390

Office Phone: 214-633-1835
Office Fax: 214-648-5554

kiyoshi.ariizumi@utsouthwestern.edu

Biography

Immune responses need to be tightly regulated, particularly in the skin where the ability to defend against infections and cancers should be balanced.  This key process is heavily dependent on proper switching the differentiation program of myeloid cells between the immuno-stimulators and the immunosuppressors.  One-sided differentiation causes hyperactivation or immunosuppression, leading to autoimmune diseases (e.g., psoriasis on the skin) or promoting skin 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 psoriatic inflammation and melanoma, 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 these skin diseases.  

Education

Graduate SchoolUniversity of Tokyo - Japan (1985)

Research Interests

Immune evasion by melanoma
Inflammation-associated carcinogenesis
Negative regulation of T cell-mediated immunity

Publications

Featured
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

Featured
Cloning of a second dendritic Cell-associated C-type lectin (Dectin-2) and its alternatively spliced isoforms.

Ariizumi K, Shen G-L, Shikano S, Ritter RIII, Zukas P, Edelbaum D, Morita A, Takashima A. , J Biol Chem , 2000; (275):11957-11963

Inhibition of T-cell activation by syndecan-4 is mediated by CD148 through protein tyrosine phosphatase activity.

Chung JS, Cruz PD, Ariizumi K, European journal of immunology, 2011 Jun; 41 (6):1794-9

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 research, 2010 Jul; 70 (14):5778-87

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, Journal of immunology (Baltimore, Md. : 1950), 2009 Oct; 183 (8):5190-8

The DC-HIL/syndecan-4 pathway inhibits human allogeneic T-cell responses.

Chung JS, Bonkobara M, Tomihari M, Cruz PD, Ariizumi K, European journal of immunology, 2009 Apr; 39 (4):965-74

Immunization with a lentivector that targets tumor antigen expression to dendritic cells induces potent CD8+ and CD4+ T-cell responses.

Lopes L, Dewannieux M, Gileadi U, Bailey R, Ikeda Y, Whittaker C, Collin MP, Cerundolo V, Tomihari M, Ariizumi K, Collins MK, Journal of virology, 2008 Jan; 82 (1):86-95

Syndecan-4 mediates the co-inhibitory function of DC-HIL on T cell activation.

Chung J-S, Dougherty I, Cruz PD Jr, Ariizumi K. , J. Immunol , 2007; (179):5778-5784

Honors/Awards

Research career Development Award

Awarded by the Dermatology Foundation (1994)

Henry Christian Memorial Award

Awarded by the American Federation for Clinical Research (1993)

Professional Associations/Affiliations

American Association of Immunologists

Society for Investigative Dermatology