People
Back to Faculty Listing | Neuroscience Research Areas
Kelley, Keith W.
Professor, Immunophysiology, Department of Animal Sciences, College of ACES
B.A., SUNY at Stony Brook
M.A., Ph.D., University of Illinois
Research Areas
Cross talk between cytokine and hormone receptors
For the past 30 years, our laboratory has been involved in defining reciprocal systems of communication between the immune and central nervous systems. We are currently interested in defining receptor signaling pathways that occur following activation of receptors for both proinflammatory cytokines and growth factors in the brain and the periphery. We have also discovered the existence of intracellular crosstalk between receptors for proinflammatory cytokines ( TNFa , IL -1�) and hormones (IGF-I) in a variety of cells. This interaction .educes the ability of growth factor receptors to function in the presence of very low concentrations of proinflammatory cytokines. The result is that the biological response of cells to a growth factor, whether it be the proliferation of cancer cells or the differentiation of muscle progenitor cells, is .educed in the presence of proinflammatory cytokines. Collectively, these data show that the biological properties of a classical hormonal growth factor receptor are directly regulated by proinflammatory cytokines from the immune system. Other major research projects are aimed at determining the actions of proinflammatory cytokine receptors that are involved in sickness behavior, depressive-like behavior and memory. We have shown that IL-1� and TNFa serve as communication molecules between the immune and central nervous systems. In contrast, anti-inflammatory cytokines in the brain, such as IL-10 and IGF-I, .educe behavioral symptoms of sickness following infection. The major health impact of this research is directed at aging, affect and cognitive function and muscle wasting in AIDS and cancer.
Representative Publications
Shen WH, Yin Y, Broussard SR, McCusker RH, Freund GG, Dantzer R, and Kelley KW. 2004. Tumor necrosis factor a inhibits cyclin A expression and retinoblastoma hyperphosphorylation triggered by insulin-like growth factor-I induction of new E2F-1 synthesis. J. Biological Chemistry 279:7438-7446.
Broussard SR, McCusker RH, Novakofski JE, Strle KE, Shen WH, Johnson RW, Dantzer R and Kelley KW. 2004. IL-1b impairs insulin-like growth factor I-induced differentiation and downstream activation signals of the insulin-like I growth factor receptor in myoblasts. J. Immunology 172:7713-7720.
Kelley KW. 2004. Norman Cousins Lecture: From hormones to immunity: The physiology of immunology.Brain, Behavior, and Immunity 18:95-113.
Bluth RM, Frenois F, Kelley KW and Dantzer R. 2005. Pentoxifylline and insulin-like growth factor-I (IGF-I) abrogate kainic acid-induced cognitive impairment in mice. J. Neuroimmunology. 169:50-58.
Bluth RM, Kelley KW, and Dantzer R. 2006. Effects of insulin-like growth factor-I on cytokine-induced sickness behavior in mice. Brain, Behavior, and Immunity 20:57-63.
Strle, K., S.R. Broussard, R.H. McCusker, W.H. Shen, J.M. LeCleir, R.W. Johnson, G.G. Freund, R. Dantzer, and K.W. Kelley. (2006) C-jun N-terminal kinase mediates tumor necrosis factor-a suppression of differentiation in myoblasts. Endocrinology 147:4363-4373.
Additional Information
Collaborative Projects:
Professor Robert Dantzer - Neuroimmune control of biobehavioral processes
Contact information:
