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Phil King

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Primary Appointment: Microbiology and Immunology
Primary PIBS Dept.: Microbiology and Immunology
PubMed Name: king pd
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  Upon encounter with antigen T cells may respond in a number of different ways. In productive immune responses, T cells proliferate and differentiate into mature Th1, Th2 or Th17 cells or killer cells. Alternatively, in responses associated with the maintenance of self tolerance, T cells undergo programmed cell death, enter into a state of prolonged hypo-responsiveness known as anergy, or develop into T regulatory cells. An important determinant that controls the type of T cell response is the nature of additional signals received by T cells at the time of antigenic challenge. These additional signals are derived from co-stimulatory, cytokine or inhibitory receptors which thus integrate (or not) with T cell antigen receptor signals to achieve different functional outcomes.

Research in our laboratory is aimed at a molecular understanding of mechanisms of signal integration in T cells. To this end we study the role of a variety of intracellular signaling molecules including protein and lipid kinases, phosphatases, adapter proteins and transcription factors as potential signal integrators. In our studies we employ a wide range of biochemical, cell and molecular-biological, and immunological techniques to answer important questions in this area. As well as attempting to elucidate mechanisms of signal integration at the molecular level, the laboratory uses Cre-loxP gene-targeting technology to explore the relevance of different signaling pathways to T cell function in whole animals. Studies are expected to reveal novel means by which T cell responses can be manipulated in different pathologic situations including cancer, autoimmunity and infectious disease.