Faculty Profile, National Health Research Institutes, Taiwan

Faculty Profiles

Rong-Tai Wei, Ph.D.

Assistant Investigator
Institute of Population Health Sciences


- Ph.D. Department of Biological Sciences, Rutgers University, USA, 1998
- B.S., Department of Zoology, National Taiwan University, Taiwan, 1986


- Assistant Investigator, Division of Mental Health and Substance Abuse Research, National Health Research Institutes, Taiwan
- Research Associate, Division of Molecular and Genomic Medicine, National Health Research Institutes, Taiwan
- Visiting Fellow, Integrative Neural Immune Program, National Institute of Mental Health, NIH, USA
- Teaching Assistant, Department of Biological Sciences, Rutgers University, USA
- Research Assistant, Institute of Biochemistry, College of Medicine, National Taiwan University, Taiwan


Dr. Wei is devoting himself to the investigation of neuroendocrine-immune interactions. After joining the Division of Mental Health and Substance Abuse Research, NHRI, Dr. Wei would like to apply his expertise of neuroimmunology and neuroendocrine to focus on the investigation of the pathophysiological relevance of microglia-mediated inflammation to neurological and psychiatric disorders.


The long-term goal of Dr. Wei is to understand how neuroendocrine-immune interactions modulate microglial phenotypes, thereby influencing subsequent inflammation and neural activities. To pursue this goal, Dr. Wei intends to decipher microglial plasticity by determining how pro- and anti-inflammatory cytokines are regulated in microglia under the influence of neuroendocrine-immune interactions, and how microglial cytokine expression modulates diverse microglial functions. The central hypothesis for his current research is that microglial cytokine production is dynamically modulated within the microenvironment in response to neuroendocrine-immune interactions. His laboratory recently observed the reciprocal mRNA expression patterns between pro- and anti-inflammatory cytokines in activated microglia. Identifying the mechanisms underlying this phenomenon certainly paves the way for the understanding of cytokine plasticity of microglia. His laboratory is exploring the mechanisms by which microglia are instructed to express either pro- or anti-inflammatory cytokines, which may lead to the identification of molecular targets for interference of cytokine imbalance. At the same time, fundamental new knowledge about the relationships between microglial activation and their commitment to phenotypes with respect to cytokine production will be also obtained.


- 1998 Recipient of the Keshav C. Sondhi Memorial Award from Rutgers University, Honored "for promise as an investigator in the biological science."


  1. Wei, R. and Sternberg, E.M. IL-1b-mediated neuropeptide and immediate early gene mRNA induction is defective in Lewis hypothalamic cell cultures. J. Neuroimmunol. 146:114-125, 2004.
  2. Wei, R., Listwak, S.J., Sternberg, E.M. Lewis hypothalamic cells constitutively and upon stimulation express higher levels of mRNA for pro-inflammatory cytokines and related molecules: comparison with inflammatory resistant Fischer rat hypothalamic cells. J. Neuroimmunol. 135: 10-28, 2003.
  3. Wei, R., Phillips, T.M., Sternberg, E.M. Specific upregulation of CRH or AVP secretion by acetylcholine or lipopolysaccharide in inflammatory susceptible Lewis rat fetal hypothalamic cells. J. Neuroimmunol. 131: 31-40, 2002.
  4. Wei, R. and Jonakait, G.M. Neurotrophins and the anti-inflammatory agents interleukin-4 (IL-4), IL-10, IL-11 and transforming growth factor-b1 (TGF-b1) down-regulate T cell costimulatory molecules B7 and CD40 on cultured rat microglia. J. Neuroimmunol. 95: 8-18, 1999.
  5. Jonakait, G.M., Luskin, M.B., Wei, R., Tian, X., Ni, L. Conditioned medium from activated microglia promotes cholinergic differentiation in the basal forebrain in vitro. Dev. Biol. 177: 85-95, 1996.
  6. Jonakait, G.M., Wei, R., Sheng, Z., Hart, R.P., Ni, L. Interferon-g promotes cholinergic differentiation of embryonic septal nuclei and adjacent basal forebrain. Neuron 12: 1149-1159, 1994.