{"id":85,"date":"2014-08-21T14:39:16","date_gmt":"2014-08-21T18:39:16","guid":{"rendered":"http:\/\/geiselmed.dartmouth.edu\/huang\/?page_id=85"},"modified":"2024-06-19T17:24:55","modified_gmt":"2024-06-19T21:24:55","slug":"yina-h-huang-phd","status":"publish","type":"page","link":"https:\/\/geiselmed.dartmouth.edu\/huang\/lab-members\/yina-h-huang-phd\/","title":{"rendered":"Yina H. Huang, PhD"},"content":{"rendered":"

\"\"<\/a>Principal Investigator<\/em><\/p>\n

About Me<\/strong><\/p>\n

My interest in Immunology began while I was an undergraduate at UC Berkeley where in Dr. Nilabh Shastri\u2019s 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.<\/p>\n

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\u2019s 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\u2019s lab.<\/p>\n

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\u2019s 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.<\/p>\n

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<\/a>.<\/p>\n","protected":false},"excerpt":{"rendered":"

Principal Investigator About Me My interest in Immunology began while I was an undergraduate at UC Berkeley where in Dr. Nilabh Shastri\u2019s 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 [\u2026] <\/p>\n

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