Internal Seminar: Tripp Unit and Ishikawa Unit

Join us for March's second Internal Seminar Series on Mar. 20, from 17:00 to 18:00 in C209. This month's second seminars feature the Human Developmental Neurobiology Unit (Eileen Gail Tripp) and the Immune Signal Unit (Hiroki Ishikawa).

Human Developmental Neurobiology Unit (Eileen Gail Tripp)

Speaker : Dr Emi Furukawa

Title : Reward Sensitivity and Striatal BOLD Responses in ADHD

Abstract : Attention Deficit and Hyperactivity Disorder (ADHD) is a commonly diagnosed psychiatric disorder. However, the etiology remains unclear. We hypothesize that the transfer of dopamine release from reward to reward-predicting cues, as normally observed in animal studies, may be deficient in ADHD. Functional magnetic resonance imaging (fMRI) was used to investigate striatal responses to reward-predicting cues and reward delivery in a classical conditioning paradigm. The results indicated increased striatal blood-oxygen-level dependent (BOLD) responses to reward cues in healthy adults, while increased responses to reward delivery in those with ADHD. The BOLD response patterns are consistent with impaired predictive dopamine signaling in ADHD, which may explain altered reward-contingent behaviors and symptoms of ADHD.

Immune Signal Unit (Hiroki Ishikawa)

Speaker : Hayato Yamada

Title : Analysis of the molecular mechanism of the Th17 late differentiation responsible for autoimmune diseases

Abstract : Upon antigen recognition, T cells differentiate into various T helper (Th) subsets such as Th1, Th2 and Th17, and play a central role in our immune systems. Each Th subset leads to distinct immune responses, which are specialized to eliminate different kinds of nonself-antigens in our bodies. However, Th17 cells, which are critical for host defense against extracellular pathogens, are also involved in autoimmune diseases. In the presence of TGFβ and IL-6, antigen-activated CD4 T cells differentiate into Th17 cells in association with induction of Th17 signature genes including IL-23 receptor. It has been shown that the IL-23 stimulation in Th17 cells is essential for the Th17 late differentiation. At this late stage, Th17 cell property is dramatically changed in a context dependent manner. This Th17 functional plasticity gives rise to highly heterogeneous populations, which is likely important for autoimmune responses. However, it is not clear how these Th17 late differentiation events are regulated. To provide new insights into the mechanism of Th17-dependent autoimmunity, we are focusing on two new possible regulators of the Th17 late differentiation. We have identified an uncharacterized homeobox transcription factor, as a gene whose expression is augmented by IL-23. We also found that an ES cell-specific epigenetic factor is specifically induced in in vivo Th17 cells in an inflammation-dependent manner. In this presentation, I will talk about the data regarding these two genes in Th17 cells, including the preliminary in vivo data of the knockout mouse of the homeobox gene.