Research Areas
- Allergy
- Asthma
- Autoimmunity/Rheumatology
- Basic Immunology
- Cellular and Molecular Biology
- Infectious Diseases
- Gender:
- Male
Education & Training
Education
- 1984
- Sun Yat-Sen University School of Medicine, Guangzhou, P. R. China, MD
- 1991
- University of Wisconsin-Madison, MS, Immunology
- 1993
- University of Wisconsin-Madison, PhD, Developmental Biology
Fellowship
- 1993-1995
- Leukemia Society Fellow, The Department of Molecular Biology, Princeton University, Stem Cell Biology
- 1995-1999
- Leukemia Society Fellow and Postdoctoral fellow, The Laboratory of Immunology, NIAID, NIH, Immunology
Special Interests
Research Interests
Our Lab Studies the Signaling and Transcriptional Regulation of Allergic Immune Responses and T Helper Cell Differentiation
CD4+ T helper cells (Th) are of critical importance in health and in disease. Many types of Th cell-mediated immune responses have been uncovered. Each type of Th responses is carried out by a specialized CD4+ Th subset and by a specialized innate effector cells. For example, type-2 immune responses is mounted by Th2 cells, as well as Th2 cytokine-producing innate effector cells, such as basophils, eosinophils and mast cells. Type-1 immune responses provide cellular defense against infection with intracellular pathogens, whereas Type-2 immune responses help antibody responses. Type-2 immune responses have also been shown to be dominant immune responses in allergic diseases and allergic asthma. Type-3 and 9 immune responses cells exert their biological effects on basophil and mast cell differentiation. Type-17 immune responses are critical in recruiting neutrophils, inducing chemokine production, and causing inflammation and fibrosis. Type-22 immune responses are involved in epidermal immunity and remodeling.
Our lab is interested in studying regulation of type-2 immune responses in general, specifically, we actively investigate three areas of research. Helper cell differentiation, innate type-2 effector cell differentiation, and interaction between CD4 Th cells and bone marrow allergic progenitor cells.
Teaching or Professional Positions
1999-2005: Assistant Professor (promoted to Associate Professor with tenure), the Department of Cell Biology, Loyola University Chicago, Stritch School of Medicine.
1997-1999: Intramural Research Fellow, the Laboratory of Immunology, NIAID, NIH.
1995-1997: Leukemia Society Fellow, the Laboratory of Immunology, NIAID, NIH.
1993-1995: Leukemia Society Fellow, the Department of Molecular Biology, Princeton University.
1989-1993: Research Assistant, the Department of Zoology, University of Wisconsin.
1988-1989: Visiting Scholar, Immunology, Radiation Effects Research Foundation (Hiroshima,
Japan).
1985-1986: Lecturer (on leave), Liu Zhou Nursing School (Liu Zhou, P. R. China).
1984-1988: Research Associate, the Laboratory of Industrial Hygiene, Ministry of Public Health (Beijing, P. R. China).
Affiliations with the University of Colorado Denver
2005-Present: Associate Professor, Integrated Immunology, University of Colorado Denver (Denver, Colorado).
Awards & Recognition
2006-Present: Ad hoc reviewer for Specialized Clinically-Oriented Ventures in Environmental Research (DISCOVER) Center, NIEHS, NIH
2005-Present: Ad hoc reviewer for Immunity and Host Defense Study Section, NIH
1999-Present: Member of American Association of Immunology.
2004: Travel Award by the Federation of Clinical Immunology Societies (FOCIS).
2001: The Lydia Schweppe Immunology Career Development Award. 2000: NIH K22 Research Career Award
1994: Leukemia Society of America Fellowship.
1998: Certification of Appreciation from the Radiation Effects Research Foundation (Japan)
1988: Visiting Scholarship awarded by the Radiation Effects Research Foundation (Japan)
Publications
Xiaopeng Qi, Jun Nishida, Lee Chaves, Keitaro Ohmori, and Hua Huang. C/EBPa is critical for interleukin-4 expression in response to FceR1a receptor cross-linking. JBC. 286:16063 (2011).
Keitaro Ohmori, Yuchun Luo, Yi Jia, Jun Nishida, Zhengqi Wang, Kevin D. Bunting, Demin Wang, and Hua Huang. IL-3 Induces Basophil Expansion In Vivo by Directing Granulocyte-Monocyte Progenitors to Differentiate into Basophil Lineage-Restricted Progenitors in the Bone Marrow and by Increasing the Number of Basophil/Mast Cell Progenitors in the Spleen. J Immunol 182: 2835-2841 (2009).
Huang Z, Xin JP, Coleman JM, and Huang H. IFN gamma suppresses STAT6 phosphorylation by inhibiting its recruitment to the IL-4 receptor. J Immunol 174(3):1332-1337 (2005).
Zhu YC, Chen L, Huang Z, Alkan S, Bunting KD, Wen RR, Wang D, and Huang H. IL-5 primes Th2 cytokine-producing capacity in eosinophils through a STAT5-dependent mechanism. Cutting Edge, J Immunol 173:2918-2922 (2004).
Zhang Y, Apilado R, Coleman J, Ben-Sasson SZ, Tsang S, Hu-Li J, Paul WE and Huang H. Inteferon gamma stabilizes the T helper cell type 1 phenotype. J Exp Med 194(2):165-172 (2001).
