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Faculty Robert B. Clark
Associate Professor of Immunology
2007 Osborn Biomedical Science Graduate Teaching Award Recipient
rclark@nso2.uchc.edu
Areas of Interest:
Dr. Clark’s laboratory is interested in the cell biology of the T
lymphocyte as at relates to autoimmune diseases. The immune response in
autoimmune diseases such as Multiple Sclerosis and Rheumatoid Arthritis,
as well as animal models for these diseases are studied at the level of
the T cell. T cell gene usage, T cell function and activation, and T
cell migration and homing are studied using T cell cloning and molecular
biological approaches. The understanding of basic T cell function as it
relates to autoimmune mediated pathology is the overall goal of this
laboratory.
Lab Rotation Projects:
#1 -- New mouse models of the human autoimmune diseases, Multiple
Sclerosis and Lupus.
#2 – In vivo resistance to both regulatory T cells and TGF-
-mediated immunoregulation as a new model/mechanism in autoimmune
diseases.
#3 -- Studies at the molecular and protein level to
characterize the interaction of the T cell activation signaling pathway
and the TGF- signaling pathway.
Selected References:
1) Wohlfert E, Callahan M, Clark RB: Resistance to CD4+CD25+
Regulatory T Cells and TGF-b in Cbl-b-/- Mice. J Immunol. 173:
1059-1065, 2004.
2) Clark RB. The role of PPARs in inflammation and immunity. J
Leukocyte
Biology 71:388-400, 2002.
3) Clark RB, Bishop-Bailey D, Estrada-Hernandez T, Hla T, Puddington
L, Padula SJ: The nuclear receptor PPARg and immunoregulation. PPARg
mediates inhibition of helper T cell responses. J Immunol.
164:1364-1371, 2000.
4) Clark RB, Grunnet M, Lingenheld E: The generation of
encephalitogenic T cell lines from EAE-resistant strains of mice.
International Immunol. 9:1415-1422, 1997.
5) Barbarese E, Soares H, Yang S, Clark RB: Comparison of CNS homing
pattern among murine TH cell lines responsive to myelin basic protein. J
Neuroimmunol. 39:151?162, 1992.
6) Padula SJ, Lingenheld EG, Stabach PR, Chou CHJ, Kono DH, Clark RB:
Identification of encephalitogenic Vb-4? bearing T cells in SJL mice.
Further evidence for the V? region disease hypothesis? J Immunol.
146(3):879?883, 1991.
7) Ruddle NH, Bergman CM, McGrath MK, Lingenheld EG, Grunnet ML,
Padula SJ, Clark RB: An antibody to lymphotoxin and tumor necrosis
factor prevents transfer of experimental allergic encephalomyelitis. J
Exp Med. 11972:1193?1200, 1990.
8) Wong RL, Ruddle NH, Padula SJ, Lingenheld EG, Bergman CM, Rugen
RV, Epstein DI, Clark RB: Subtypes of helper cells: Noninflammatory Type
I helper T cells. J Immunol. 141:3329?3334, 1988.
9) Padula SJ, Sgroi D, Lingenheld EG, Clark RB: A T cell receptor
beta chain rearrangement shared by murine T cell lines derived from a
site of autoimmune inflammation. J Clin. Invest. 81:1810?1818, 1988.
10) Sgroi D, Cohen RN, Lingenheld EG, Strong M. K, Binder T,
Goldschneider I, Greiner D, Grunnet M, Clark RB: T cell lines derived
from the spinal cords of mice with experimental allergic
encephalomyelitis are self?reactive. J Immunol. 137:1850?1854, 1986.
11) Padula SJ, Pollard MK, Lingenheld EG, Clark RB: Maintenance of
antigen specificity by human IL?2 dependent T cell lines ? Use of
antigen presenting cells and OKT3 Antibody in the absence of antigen. J
Clin Invest. 75:788?797, 1985.
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