Yvette Latchman, PhD
Assistant Professor, Medicine/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 is interested in investigating 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. Three major families provide costimulation: the B7:CD28 superfamily, a TNF:TNFR subfamily that lack death domains, and the CD2 superfamily. There are currently two areas of research in the laboratory. Firstly, we are investigating the function of the CD2:CD48 and CD244:CD48 costimulatory pathways. 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 tolerance and therefore we are studying how this pathway participates in the development of autoimmune diseases such as systemic lupus erythematosus (SLE). Secondly, 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 tumor models. Our studies thus far suggest that blockade of the interaction of PD-1 ligands and their receptor PD-1 may provide a means to enhance anti-tumor immunity.

Recent publications:

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.

Greenwald R.J., Latchman Y.E. and Sharpe A.H. Negative co-receptors on lymphocytes. Current Opinion Immunology 2002; 14: 391-396.

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., 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.

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.

Lee K., Forman J., McNerney M., Stepp S., Kuppireddi S., Guzior D., Wei H., Latchman Y.E., Sayegh M.H., Yagita H., Wulfing C., Schatzle J., Mathew P.A., Sharpe A.H. and Kumar V. Homotypic NK cell interaction through 2B4/CD48 pair regulates the development of NK effector function. Blood 2006; 107:3181-3188.

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.

Updated August 2007