David Richards, PhD

Mentor: Daniel Mueller, MD

Current Position:  Post-doctoral Fellow in Immunology & Microbiology, UCLA

T32 Support: 1999 - 2004

Education:

1992 – 1996, B.A., Carleton College, Northfield, MN
1998 – 2004, Ph.D., University of Minnesota

Project:  David completed five years on the T32 as a predoc and earned his Ph.D.  With Dr. Daniel Mueller, he developed a model to track a minor antigen-specific CD4 and an MHC-specific CD8 transgenic T cell through the course of OB. They were also able to show that both types of T cells are involved in the development of OB. They were also able to phenotype these cells after they entered the graft tissue and proceeded to influence their activities through antigen-specific and nonspecific tolerance/therapy.

Publications:

Richards DM, Hertz MI, Mueller DL.  Directly allo-MHC reactive TCR-transgenic CD8+ T cells accumulate in heterotopic tracheal allografts in an activated, differentiated and highly divided state.  American Journal of Transplantation 2002; 3(2)S:228.

Richards DM, Dalheimer SL, Ehst BD, Hertz MI, Mueller DL.  Demonstration of indirect minor antigen presentation by host/antigen presenting cells using TCR-transgenic CD4+ T cells and heterotopic tracheal allotransplantation.  American Journal of Transplantation.  2002; 3(2)S:217.

Richards DM, Dalheimer SL, Hertz MI, Mueller DL.  Activation, retention and enrichment of direct alloreactive CD8+T cells within transplanted tissue undergoing chronic rejection.  Journal of Immunology.  2003: 171(12):6919-28.

Richards DM, Dalheimer SL, Ehst BD, Hertz MI, Mueller DL.  Indirect recognition of minor histocompatibility antigens presented by recipient APC within draining lymph nodes promotes obliterative airway disease following tracheal allotransplantation.  American Journal of Transplantation 2003; 5(3)S:403.

Dalheimer SL, Richards DM, Hertz MI, Mueller DL.  Immunohistochemical and flow cytometric analysis of graft-reactive TCR-transgenic T cells that infiltrate tracheal allografts during the development of obliterative airway disease.  American Journal of Transplantation 2003; 5(3)S:403.

Richards DM, Dalheimer SL, Hertz MI, Mueller DL.  Trachea allograft class I molecules directly activate and retain CD8+ T cells that cause obliterative airways disease. Journal of Immunology 2003; 171(12):6919-28.

Richards DM, Dalheimer SL, Ehst BD, Vanasek TL, Jenkins MK, Hertz MI, Mueller DL.  Indirect recognition of minor histocompatibility antigens presented by recipient antigen-presenting cells within draining lymph nodes causes obliterative airways disease following tracheal allotransplantation.  Journal of Immunology.  2004; 172(6):3469-79.

Dalheimer SL. Richards DM. Mueller DL. Sharing of class I MHC molecules between donor and host promotes the infiltration of allografts by mHAg-reactive CD8 T cells. American Journal of Transplantation.  2005; 5(4 Pt 1):832-8.

Last updated 3-27-2008