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S. Brydges, James Mueller, Matthew McGeough, C. Peña, A. Misaghi, Chhavi Gandhi, C. Putnam, D. Boyle, G. Firestein, A. Horner, P. Soroosh, W. Watford, J. O’Shea, D. Kastner, H. Hoffman (2009)
Inflammasome-mediated disease animal models reveal roles for innate but not adaptive immunity.Immunity, 30 6
C. Sutton, S. Lalor, C. Sweeney, Corinna Brereton, E. Lavelle, K. Mills (2009)
Interleukin-1 and IL-23 induce innate IL-17 production from gammadelta T cells, amplifying Th17 responses and autoimmunity.Immunity, 31 2
S. Masters, A. Simon, I. Aksentijevich, D. Kastner (2009)
Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*).Annual review of immunology, 27
R. Panush (2011)
An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonistYearbook of Medicine, 2011
M. Bianchi (2007)
DAMPs, PAMPs and alarmins: all we need to know about dangerJournal of Leukocyte Biology, 81
C. Sutton, Corinna Brereton, B. Keogh, K. Mills, E. Lavelle (2006)
A crucial role for interleukin (IL)-1 in the induction of IL-17–producing T cells that mediate autoimmune encephalomyelitisThe Journal of Experimental Medicine, 203
K. Mills (2008)
Induction, function and regulation of IL‐17‐producing T cellsEuropean Journal of Immunology, 38
Guangxun Meng, Fuping Zhang, I. Fuss, A. Kitani, W. Strober (2009)
A mutation in the Nlrp3 gene causing inflammasome hyperactivation potentiates Th17 cell-dominant immune responses.Immunity, 30 6
F. Martinon, K. Burns, J. Tschopp (2002)
The inflammasome: a molecular platform triggering activation of inflammatory caspases and processing of proIL-beta.Molecular cell, 10 2
C. Dinarello (2009)
Immunological and inflammatory functions of the interleukin-1 family.Annual review of immunology, 27
Sreelatha Reddy, S. Jia, R. Geoffrey, R. Lorier, M. Suchi, U. Broeckel, M. Hessner, J. Verbsky (2009)
An autoinflammatory disease due to homozygous deletion of the IL1RN locus.The New England journal of medicine, 360 23
Kaoru Geddes, J. Magalhaes, S. Girardin (2009)
Unleashing the therapeutic potential of NOD-like receptorsNature Reviews Drug Discovery, 8
There are many ways to modulate the immune response in a therapeutic setting. Drugs that target the proinflammatory mediator IL-1, for instance, can counteract disease in certain types of inflammatory conditions. But such drugs do not work well for other conditions, such as rheumatoid arthritis and other autoimmune diseases. New clinical studies, examined by Kingston Mills and Aisling Dunne, provide insight into this discrepancy. Another approach that has worked well in mice harnesses the ability of regulatory T cells to dampen the immune response. But one barrier in the way of successful application to people is the ability of such cells to change their character for the worse. Massimo Gadina and John O'Shea take a look at a basic research study that highlights this dilemma and examine what it means for the future of human trials.
Nature Medicine – Springer Journals
Published: Dec 1, 2009
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