Yina Huang

ORCID iD
https://orcid.org/0000-0002-0125-9351
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Yina Hsing Huang,

Sources:
Yina Huang (2015-04-02)

Yina Hsing

Sources:
Yina Huang (2015-04-02)

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Huang Lab Website

Sources:
Yina Huang (2015-04-02)

Biography

My interest in Immunology began while I was an undergraduate at UC Berkeley where in Dr. Nilabh Shastri’s lab I tried to identify the H-Y minor histocompatibility antigen. The H-Y antigen induces females to reject male cells and contributes to rejection of transplanted organs. Although I did not manage to expression clone the H-Y antigen, I became fascinated with how appropriate activation of the immune system can protect us against a myriad of different pathogens but unwanted activation can result in autoimmunity or transplant rejection. My love for identifying molecular mechanisms that activate lymphocytes to respond to pathogenic challenge developed during my graduate studies with Dr. Gail Bishop at the University of Iowa. In Gail’s lab, I studied the co-stimulatory molecule CD40, whose mutation results in a combined immunodeficiency disease due to defects in B and T cell responses. My interest in how extracellular cues activate intracellular signals to specify different effector responses was born in Gail’s lab. To better understand how cell fate decisions were made, I pursued postdoctoral studies with Dr. Ellen Robey at UC Berkeley, where I examined the fundamental question of how T cells establish their identity as they develop in the thymus. To uncover new pathways impacting T cell fate decisions, I joined Dr. Karsten Sauer’s lab, first at the Genomics Institute of the Novartis Research Foundation and then at the Scripps Research Institute. There, I pursued mechanistic studies with several lines of immunodeficient mice that we identified in a forward genetics screen. Analysis of one of these models, mice deficient in IP3-kinase (ItpkB), led us to identify IP4 as a physiologically important second messenger required for B cell, NK cell and T cell development and activation. Importantly, we found that IP4 differentially regulates PI3 kinase effectors such as Akt and Itk kinases, which promote cell survival/proliferation and differentiation/effector responses, respectively. My lab at Dartmouth is focused on understanding how T cells interpret activation and migration cues to mediate appropriate immune responses. Misinterpretation of these cues by generating hypo-responses can increase disease susceptibility while hyper-responses can cause autoimmunity. For more details, please see our research page at: http://geiselmed.dartmouth.edu/huang/
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