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Research Interests
My laboratory is currently interested in three different areas of research:
1. T Cell differentiation in mucosal tissues: Delivery
of immunogens to mucosal surfaces, such as the pulmonary airways, induces
different types of immune responses dependent on the type immunogen. We
are interested in how different T cell responses are initiated and how
they might be regulated. Specifically, we are focusing on: (a) the role
of antigen presenting cells (APC) and their capacity to prime na?ve T
cell into different subsets of effector T cells, and (b) the role of different
tissues within the pulmonary tract as sites of APC/T cell interaction.
2. Hookworm secretions in host immunomodulation: We have
recently identified a protein(s) secreted by hookworm parasites that binds
selectively to human natural killer (NK) cells and induces them to secrete
high levels of IFN-?. Studies are currently underway to further investigate
the interaction of this NK cell binding protein (NKBP) with other subsets
of leukocytes, as well as characterize and clone NKBP. In addition, we
are investigating the binding and effect of NKBP on leukocytes from patients
with active hookworm infections in Brazil to establish the physiologic
contribution of this protein(s) to the maintenance of a chronic infection.
This project is being conducted in collaboration with Drs. A. Loukas and
J. Bethony.
3. Cyclophilins in inflammation: Extracellular cyclophilins
have recently been shown to have potent chemotactic properties during
inflammatory responses. We are investigating the contribution of cyclophilins
to leukocyte recruitment during diseases associated with inflammation,
including rheumatoid arthritis and asthma. Studies are underway to assess
how blocking cyclophilin-mediated leukocyte migration might impact on
alleviating ongoing inflammatory responses. This project is being conducted
in collaboration with Dr. M. Bukrinsky.
Selected Publications Top
Constant, S., J. Brogdon, D. Piggott, C. Herrick, I. Visintin, N. Ruddle and K. Bottomly. 2002. Resident lung antigen presenting cells promote TH2 T cell differentiation in situ. J. Clin. Invest. 110:1441-1448.
Gorelick, L., S. Constant and R. Flavell. 2002. Mechanism of transforming growth factor ß-induced inhibition of t helper type 1 differentiation. J. Exp. Med. 195:1499-1505.
Colmenares, M., S. Constant, P. Kima, and D. McMahon-Pratt. 1001. Leishmania pifanoi pathogenesis: selective lack of a local cutaneous response in the absence of circulating antibody. Inf. Imm. 70:6597-6605.
Constant, S., K. Lee and K. Bottomly. 2000. Site of antigen delivery can influence T cell priming: pulmonary environment promotes preferential TH2-type differentiation. Eur. J. Immunol. 30:840-847.
Constant, S., C. Dong, D. Yang, M. Wysk, R Davis and R. Flavell. 2000. JNK1 is required for T cell-mediated immunity against Leishmania major infection. J. Immunol. 165:2671-2676.
Kima, P., S. Constant, L. Hannum, M. Colmenares, K.
Lee, A. Haberman, M. Shlomchik and D. McMahon-Pratt. 2000. Internalization
of Leishmania mexicana complex amastigotes via the Fc receptor
is required to sustain infection in murine cutaneous leishmaniasis. J.
Exp. Med. 191:1063-1067.
Contact Information Top
The George Washington University Medical Center
Ross Hall Room 738,
Washington DC 20037
Phone: (202) 994-1138
Email: mtmslc@gwumc.edu
see also: www.gwumc.edu/Faculty/Constant.htm
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