Research TopicsSpecies | Deborah FowellSummaryAffiliation: University of Rochester Country: USA Publications
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Publications
Signals for the execution of Th2 effector functionDeborah J Fowell
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, 601 Elmwood Avenue, Box 609, Rochester, NY 14642, USA
Cytokine 46:1-6. 2009..We also discuss how provision of these execution signals may be spatially segregated in vivo occurring at tissue sites of inflammation and subject to modulation by the pathogen itself...
Interaction between GATA-3 and the transcriptional coregulator Pias1 is important for the regulation of Th2 immune responsesXinyan Zhao
David H Smith Center for Vaccine Biology and Immunology, Aab Institute for Biomedical Sciences, Department of Microbiology, University of Rochester School of Medicine and Dentistry, NY 14642, USA
J Immunol 179:8297-304. 2007..In contrast, IL-5 promoter was modestly enhanced by Pias1 and no effect was observed on IL-4 promoter. Thus, both promoter activation and additional mechanisms are responsible for regulation by Pias1...
Pathogen-imposed skewing of mouse chemokine and cytokine expression at the infected tissue siteShoshana D Katzman
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, Rochester, New York 14642, USA
J Clin Invest 118:801-11. 2008..Thus, pathogens may edit the LN cytokine repertoire through differential recruitment of cytokine-producing cells...
T regulatory and primed uncommitted CD4 T cells express CD73, which suppresses effector CD4 T cells by converting 5'-adenosine monophosphate to adenosineJames J Kobie
David H Smith Center for Vaccine Biology and Immunology and Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA
J Immunol 177:6780-6. 2006..Infiltration of either Treg or Thpp cells at inflammatory sites could potentially convert 5'-AMP generated by neutrophils or dying cells into the anti-inflammatory mediator adenosine, thus dampening excessive immune reactions...
CTLA-4 is required by CD4+CD25+ Treg to control CD4+ T-cell lymphopenia-induced proliferationDorothy K Sojka
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, Rochester, NY 14642, USA
Eur J Immunol 39:1544-51. 2009..Thus, while Treg developing in the absence of CTLA-4 appear to acquire some compensatory suppressive mechanisms in vitro, we identify a non-redundant role for CTLA-4 in Treg function in vivo...
Critical requirement for the Wiskott-Aldrich syndrome protein in Th2 effector functionVanessa Morales-Tirado
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, NY, USA
Blood 115:3498-507. 2010..Moreover, dominant-negative WASp expression in WT effector T cells blocked IL-4 production, but had no effect on IFNgamma. Thus WASp plays a selective, posttranscriptional role in Th2 effector function...
Cutting edge: selective requirement for the Wiskott-Aldrich syndrome protein in cytokine, but not chemokine, secretion by CD4+ T cellsVanessa Morales-Tirado
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, and Department of Microbiology and Immunology, University of Rochester, Rochester, NY 14642, USA
J Immunol 173:726-30. 2004..We propose that the use of different secretory pathways for cytokines and chemokines enables CD4(+) T cell activity to be further fine-tuned to serve specialized effector functions...
Cutting edge: Itk-dependent signals required for CD4+ T cells to exert, but not gain, Th2 effector functionByron B Au-Yeung
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, NY 14642, USA
J Immunol 176:3895-9. 2006..We suggest that the liberation of effector function is tightly controlled through qualitative changes in TCR signals, facilitating postdifferentiation regulation of cytokine responses...
Uncoupling of proliferation and cytokines from suppression within the CD4+CD25+Foxp3+ T-cell compartment in the 1st year of human type 1 diabetesAngela Hughson
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, Rochester, New York, USA
Diabetes 60:2125-33. 2011..In humans, the CD4+CD25+Foxp3+ T-cell compartment contains both effector and regulatory T cells, and it is not known how their relative proportions vary in disease states...
Mechanisms of regulatory T-cell suppression - a diverse arsenal for a moving targetDorothy K Sojka
David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, Department of Microbiology and Immunology, University of Rochester, Rochester, NY 14624, USA
Immunology 124:13-22. 2008..Understanding when and where each suppressive tool is most effective will help to fine tune therapeutic strategies to promote or constrain specific arms of Treg suppression...
A key role for Itk in both IFN gamma and IL-4 production by NKT cellsByron B Au-Yeung
Department of Microbiology and Immunology, David H Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA
J Immunol 179:111-9. 2007..The severe defect in NKT cell function may underlie a number of the Th1 and Th2 immune defects in Itk-deficient mice...
Distinct molecular program imposed on CD4+ T cell targets by CD4+CD25+ regulatory T cellsTeresa L Sukiennicki
Department of Microbiology and Immunology, David H. Smith Center for Vaccine Biology and Immunology, Aab Institute of Biomedical Sciences, University of Rochester, Rochester, NY 14642, USA
J Immunol 177:6952-61. 2006..We suggest that Tregs function by the induction of a distinct set of negative regulatory factors that initiate or maintain target T cells in a nonproliferative state...
Research Grants
- Target T Cell Modulation by CD4+CD25+ Regulatory T CellsDeborah J Fowell; Fiscal Year: 2010....
- Target T Cell Modulation by CD4+CD25+ Regulatory T CellsDeborah Fowell; Fiscal Year: 2007....
- The Role of Itk in Th DifferentiationDeborah Fowell; Fiscal Year: 2005..Our central hypothesis is that Itk conveys information on the quality of TCR/MHC interaction from the cell surface to the nucleus to modulate Th differentiation and survival ..
- Visualization of Th2 development in vivoDeborah Fowell; Fiscal Year: 2003..We wish to further develop the imaging methods to track the developing immune response on infectious challenge. ..
- Remodeling of lymph node-derived cytokine responses at the infected tissue siteDeborah J Fowell; Fiscal Year: 2010..Developing ways of harnessing a diverse lymph node repertoire to retune immune responses at the infection site, by manipulating the type of effectors recruited to the site, has great therapeutic potential for many disease states. ..
