Dr. Bradley is investigating the development of immune cells and developing ways to modulate immune cell responses during infection.
Dr. Bradley received her doctorate from the University of California, Berkeley.
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CD44 regulates survival and memory development in Th1 cells.
Baaten BJ, Li CR, Deiro MF, Lin MM, Linton PJ, Bradley LM
Immunity. 2010 Jan 29;32(1):104-15
Polyclonal adaptive regulatory CD4 cells that can reverse type I diabetes become oligoclonal long-term protective memory cells.
Godebu E, Summers-Torres D, Lin MM, Baaten BJ, Bradley LM
J Immunol. 2008 Aug 1;181(3):1798-805
Adaptive islet-specific regulatory CD4 T cells control autoimmune diabetes and mediate the disappearance of pathogenic Th1 cells in vivo.
Weber SE, Harbertson J, Godebu E, Mros GA, Padrick RC, Carson BD, Ziegler SF, Bradley LM
J Immunol. 2006 Apr 15;176(8):4730-9
Interleukin 7 regulates the survival and generation of memory CD4 cells.
Kondrack RM, Harbertson J, Tan JT, McBreen ME, Surh CD, Bradley LM
J Exp Med. 2003 Dec 15;198(12):1797-806
Migration and T-lymphocyte effector function.
Curr Opin Immunol. 2003 Jun;15(3):343-8
Costimulation via OX40L expressed by B cells is sufficient to determine the extent of primary CD4 cell expansion and Th2 cytokine secretion in vivo.
Linton PJ, Bautista B, Biederman E, Bradley ES, Harbertson J, Kondrack RM, Padrick RC, Bradley LM
J Exp Med. 2003 Apr 7;197(7):875-83
Availability of antigen-presenting cells can determine the extent of CD4 effector expansion and priming for secretion of Th2 cytokines in vivo.
Bradley LM, Harbertson J, Biederman E, Zhang Y, Bradley SM, Linton PJ
Eur J Immunol. 2002 Aug;32(8):2338-46
Withdrawal of stimulation may initiate the transition of effector to memory CD4 cells.
Harbertson J, Biederman E, Bennett KE, Kondrack RM, Bradley LM
J Immunol. 2002 Feb 1;168(3):1095-102
A critical role for B cells in the development of memory CD4 cells.
Linton PJ, Harbertson J, Bradley LM
J Immunol. 2000 Nov 15;165(10):5558-65
Linda Bradley's Research Focus
Type 1 Diabetes
The overall focus of the lab's research is to identify parameters that control the development of effector and memory CD4 T cells and how to best elicit their responses to augment immunity and downregulate their responses to control autoimmunity and inflammation. These cells are predominantly mobile populations that constantly receive signals from the environment as they migrate. Dr. Bradley hopes to identify molecular mechanisms engaged in this process that can be modulated and thereby enable specific targeting of effector and memory cell subsets. We use in vivo models and various gene knock out and transgenic mice to study CD4 cells in the immune responses to influenza viruses and in autoimmune diabetes.
About Linda Bradley
Dr. Bradley received her doctorate from the University of California, Berkeley, in 1981 in studies of CD4 T cell subsets that regulate humoral immune responses. Her work on the regulation of CD4 T cells continued during her postdoctoral training at the Oregon Primate Research center and at the University of California, San Diego where she was appointed Assistant Research Professor in 1991. It was at this time she developed NIH sponsored her research program on CD4 T cells and discovered the key associations between migration and function. She joined the Scripps Research institute as an Assistant Professor in 1996 where she expanded her work on CD4 T cells into the arena of autoimmunity and discovered the essential role of the cytokine, interleukin-7, in the regulation of CD4 cell homeostasis. She joined the Sidney Kimmel Cancer Center in 2001 as an Associate Professor, and was promoted to Professor in 2005. She joined Sanford-Burnham as a Professor in the Infectious and Inflammatory Diseases Center in 2009. Dr. Bradley is recognized as a key contributor in the field of CD4 T cell biology, is an invited speaker at many national and international meetings, and serves on several study sections for the NIH as well as the Welcome Trust, Medical Research Council, and the JDRF.