Assistant Professor, Department of Pathobiology
317 Hill Pavilion
380 South University Avenue
Philadelphia, PA 19104-4539
Temporary email address:
Effector and memory lymphocytes, unlike naïve lymphocytes, can efficiently
enter non-lymphoid tissues as well as sites of inflammation and infection.
Subsequently, lymphocytes enter the afferent lymph to reach draining lymph
nodes. After a short time period of residency, lymphocytes exit the lymph
node via the efferent lymph, which brings them back into the blood. This
dynamic process of lymphocyte recirculation, which is tightly regulated at
each step, is essential for immune surveillance and efficient defense against
pathogens, but it can also contribute to the development of inflammatory
My laboratory seeks to understand the regulation of lymphocyte recirculation
as well as the microenvironmental localization of effector and memory lymphocytes
within non-lymphoid tissues. Currently, we are interested in defining the
molecules involved in lymphocyte exit from peripheral tissues and its significance
to protective as well pathologic immune responses in the tissue. We employ
modern approaches of multi-color flow cytometry, molecular biology, gene
expression profiling, histology, and in vivo models. We complement
genetic and adoptive transfer mouse models with a classic model of lymph
cannulation in the sheep that allows us to analyze cell compartments that
are inaccessible in rodents because of their small size.
Understanding the mechanisms involved in cellular localization and recirculation
will provide tools to therapeutically manipulate protective as well as inflammatory
- Mechanisms of lymphocyte exit from tissues in the resting state and during
inflammation and infection. Significance to pathogen clearance and inflammation.
control of lymphocyte retention in non-lymphoid tissues. Long-term protection
against influenza virus infection.
- Recirculation strategies of specialized
lymphocyte subset (such as specialized effector CD4 and CD8 T cell subsets,
gamma-delta T cells and memory B cells).
Sigmundsdottir, H., J. Pan, G.F. Debes, C. Alt, A. Habtezion,
D. Soler, and E.C. Butcher. 2007. Dendritic cells metabolize sunlight-induced
Vitamin D3 to program T cell attraction to the epidermal chemokine CCL27. Nature
Debes, G.F., M.E. Dahl,
A.J. Mahiny, K. Bonhagen, D.J. Campbell, K. Siegmund, K.J. Erb, D.B. Lewis,
T. Kamradt, and A. Hamann. 2006. Chemotactic responses of IL-4-, IL-10- and
IFN-g-producing CD4+ T cells depend on tissue origin and microbial stimulus. The
Journal of Immunology. 176:557-566.
Debes, G.F., C.N. Arnold, A.J. Young, S. Krautwald, M.
Lipp, J.B. Hay, and E.C. Butcher. 2005. Chemokine receptor CCR7 required
for T lymphocyte exit from peripheral tissues. Nature Immunology.
Debes, G.F., K. Bonhagen, T. Wolff, U. Kretschmer, S. Krautwald,
T. Kamradt and A. Hamann. 2004. CC-chemokine receptor 7 expression
by effector/memory CD4+ T cells depends on antigen-specificity and tissue
localization during influenza A virus infection. Journal of Virology. 78:7528-7535.
Campbell, D.J., G.F. Debes, B. Johnston, E. Wilson, and
E.C. Butcher. 2003. Targeting T cell responses by selective chemokine receptor
expression. Seminars in Immunology. 15:227-286.
Debes, G.F., U.E. Höpken, and A. Hamann. 2002. In
vivo differentiated cytokine-producing CD4+ T cells express functional
CCR7. The Journal of Immunology.168:5441-5447