Yvette Latchman, PhD
Assistant Professor, Medicine, Division of Hematology
Adjunct Assistant Professor, Immunology

Puget Sound Blood Center
BRI, 3rd Floor Room 3015
921 Terry Avenue Seattle, WA 98104-1256
Tel: 206 398-5910
Fax: 206 587-6056
Email: latchman@u.washington.edu
and yvettel@psbc.org

Dr. Latchman received her PhD in Immunology from University College, University of London, UK in 1996. She received her postdoctoral training at the Royal Postgraduate Medical School (ICSM), University of London and at the Brigham and Women's Hospital and Harvard Medical School, Boston.
 
Dr Latchman’s laboratory investigates the role of costimulatory pathways in autoimmunity and tumor immunity. T cells require two signals from the antigen presenting cells (APC) to become fully functional. The first signal is the antigen provided by the APC and the second is through a group of molecules called costimulators. Costimulatory pathways contribute signals that are critical for both stimulating and inhibiting T cell activation. There are currently two areas of research in the laboratory.

Negative pathways and anti-tumor responses: We are analyzing the negative regulatory role of the PD-L:PD-1 pathway in controlling T and NKT cell responses using transgenic approaches and various tumor models. We have shown that negative pathways control the expansion and function of NKT cells and our results suggest that blockade of the interaction of PD-1 ligands and their receptor PD-1 may provide a means to enhance anti-tumor immunity.

SLAM family members and autoimmunity: We are investigating the function of the CD2:CD48 and CD244:CD48 costimulatory pathways in systemic lupus erythematosus. Utilizing mouse models, the role of CD48 in T, B and NK function is being delineated. Our recent studies have implied an obligatory role for CD48 in dendritic cell function and we are studying how dendritic cells participate in the development of autoimmune diseases.

Recent publications:

Peng Y., Latchman Y and Elkon KB. Ly6C low monocytes differentiate into dendritic cells and cross-tolerize T cells through PDL-1.  J Immunol 2009;182:2777-2785

Wang W., Carper, K., Malone, F., Latchman Y.E., Perkin J, Fu. Y., Reyes, J and Li, W. PD-L/PD-1 signal deficiency promotes allogeneic immune responses and accelerates heart allograft rejection. Transplantation 2008:86:836-844
 
Keir M.E., Liang S.C ., Guleria I., Latchman Y.E., Qipo A., Albacker L.A., Koulmanda M., Freeman G.J., Sayegh M and Sharpe A.H. Tissue expression of PD-L1 mediates peripheral T cell tolerance. JEM 2006;203:883-95.  

Keir M.E., Latchman Y.E., Freeman G.J and Sharpe A.H. PD-1:PD-L1 interactions inhibit TCR-mediated positive selection in thymocytes J Immunol 2005;175:7372-9.
  
Latchman Y.E., Liang S.C., Wu Y., Chernova T., Sobel R.A., Klemm M., Kuchroo V.K., Freeman G.J and Sharpe A.H. PD-L1-deficient mice show that PD-L1 on T cells, antigen-presenting cells, and host tissues negatively regulates T cells. PNAS 2004; 101: 10691-10696.
 
Liang S.C., Latchman Y.E., Buhlmann J.E., Tomczak M. F., Horwitz B.H., Freeman G.J and Sharpe A.H. Regulation and comparison of PD-1, PD-L1, and PD-L2 expression Eur J Immunol 2003; 33:2706-2716.

Latchman Y.E., Wood C.R., Chernova T., Chaudhary D., Borde M., Chernova I., Iwai Y., Long A.J., Brown J.A., Nunes J., Greenfield E.A., Bourque K., Boussiotis V.A., Carter L.L., Carreno B., Malenkovich N., Nishimura H., Okazaki T., Honjo T., Sharpe A. H. and Freeman G.J. PDL2 is a second ligand for PD1 and inhibits T cell activation. Nature Immunology 2001; 2: 261-268.

Updated 8/20/09