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Xiao He, M.D., Ph.D.

Languages spoken: English

Academic Information

Departments: Pathology - Research Assistant Professor

Divisions: Microbiology and Immunology

Academic Office Information

(801) 585-3310

Emma Eccles Jones Medical Research Building
15 N Medical Dr E, Room: 1520
Salt Lake City, UT

Research Interests

  • Immunology
  • Gene Expression

Research Statement

zbtb7b (Zinc finger and BTB domain-containing protein 7B)/Th-POK (T-helper-inducing POZ/Kruppel factor): T lymphocytes, further divided into 2 major subpopulations: CD4 helper and CD8 cytotoxic T cells, play a crucial role in controlling microbial infections and cancer development. zbtb7b is a transcriptional factor, which we cloned from a CD4 helper deficiency (HD) mouse line several years ago. zbtb7b functions as a master regulator in determining the CD4 vs. CD8 T cell lineage choice. A point mutation in zbtb7b gene results in all mature T cells becoming D8 cells in HD mice, while over-expression of this factor leads totally lack of CD8 T cells in zbtb7b transgenic mice. We are looking for the up-stream regulator(s) and down-stream target(s) of zbtb7b. In addition, aberrant expression of zbtb7b causes T cell lymphoma. We are also investigating the potential implication of zbtb7b in CD4 helper cell-deficient and T-ALL patients.

GILT (?-IFN-inducible lysosomal thiol reductase): GILT is a unique thiol reductase, localized in lysosomes, with optimal activity at low pH, and is expressed in Ag presenting cells (APC). GILT is important in processing protein Ag by catalyzing disulfide bond reduction, thus facilitating the unfolding of native Ag containing disulfide bonds for further processing. GILT-/- mice are defective in processing exogenous protein Ag, which contains disulfide bonds, shown that GILT-/- APC is selectively impaired to process/present HEL to some, but not all, epitope specific T cell hybridomas. Moreover, GILT-/- mice are also defective in generation of Ab responses to some Ag. We are actively investigating the cellular and molecular mechanisms underling this deficiency.
CIIEM (MHC Class II Expression Modifier): APCs capture, process and present non-self Ag (from microorganisms or tumor cells) to T lymphocytes to initiate a specific immune response. MHC Class II proteins are expressed on cell surface of the professional APC (B cells, dendritic cells and macrophages). Human T cells also express HLA Class II products and present Ag. In many cases, human T cells can present self-Ag and are implicated in autoimmune diseases. Using bioinformatics, a putative novel gene, CIIEM, was identified and the full length of mouse CIIEM cDNA was cloned. We hypothesize that CIIEM can inhibit the expression of H-2 Class II genes in mouse T cells. Experiments to investigate the biological function of CIIEM are in progress.

Education History

Postdoctoral Fellowship Howard Hughs Medical Institute Research Laboratories
Postdoctoral Fellow
Postdoctoral Fellowship Medical College of Pennsylvania/Hahnemann University, Department of Microbiology & Immunology
Postdoctoral Fellow
Doctoral Training Wake Forest University Bowman Gray School of Medicine, Department of Microbiology & Immunology
Doctoral Training Medical College of Pennsylvania, Graduate School of Medical Sciences, Dept of Microbiology & Immunol
Graduate Training Shanghai Medical University School of Graduate Studies, Department of Pathophysiology
Professional Medical Chongqing Medical College School of Medicine

Global Impact