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Kissler lab publications

Zheng P, Kissler S. PTPN22 silencing in the NOD model indicates the type 1 diabetes associated allele is not a loss of function variant. Diabetes 62: 896-904 (2013)

Joseph J, Bittner S, Kaiser FMP, Wiendl H, Kissler S. IL-17 silencing does not protect NOD mice from autoimmune diabetes. J Immunol 188: 216-221 (2012)

Kissler S. From genome wide association studies to etiology: probing autoimmunity genes by RNAi. Trends Mol Med 17: 634-640 (2011)

Gerold KD, Zheng P, Rainbow DB, Zernecke A, Wicker LS, Kissler S. The soluble CTLA-4 splice variant protects from type 1 diabetes and potentiates regulatory T cell function. Diabetes 60: 1955-1963 (2011)

Acharya M, Mukhopadhyay S, Paidassi H, Jamil T, Chow C, Kissler S, Stuart LM, Hynes RO, Lacy-Hulbert A. αv Integrin expression by DCs is required for Th17 cell differentiation and development of experimental autoimmune encephalomyelitis in mice. J Clin Invest 120: 4445-4452 (2010)

Beyersdorf N, Braun A, Vögtle T, Varga-Szabo D, Rivera Galdos R, Kissler S, Kerkau T, and Nieswandt B. STIM1-independent T cell development and effector function in vivo. J Immunol 182: 3390-3397 (2009)

Kissler S 'Studying autoimmunity by in vivo RNAi' in Reidhaar J.F. and Rondinone C.M. (Eds.) 'Therapeutic applications of RNAi' Methods in Molecular Biology, Vol. 555: 109-118 (2009)

Thum T, Gross C, Fiedler J, Fischer T, Kissler S, Bussen M, Galuppo P, Just S, Rottbauer W, Frantz S, Castoldi M, Soutscheck J, Koteliansky V, Rosenwalad A, Basson MA, Licht JD, Pena JTR, Rouhanifard SH, Muckenthaler MU, Tuschl T, Martin GR, Bauersachs J, and Engelhardt S. MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts. Nature 456: 980-984 (2008)

Kissler S*, Stern P, Takahashi K, Hunter K, Peterson L, Wicker LS. In vivo RNAi demonstrates a role for Nramp1 in modifying susceptibility to type 1 diabetes. Nature Genetics 38(4):479-483 (2006) (*corresponding author)

Dillon CP, Sandy P, Nencioni A, Kissler S, Rubinson DA, van Parijs L. RNAi as an Experimental and Therapeutic Tool to Study and Regulate Physiological and Disease Processes. Ann Rev Physiol 67: 147-173 (2005)

Kissler S and van Parijs L. Exploring the genetic basis of disease using RNAi. Expert Reviews of Molecular Diagnostics 4(5): 89-95 (2004)

Kissler S, Lu L, Cantor H. Thymic selection can compensate for mutations affecting T cell activation and generate a normal T cell repertoire in mutant mice. Proc Natl Acad Sci USA 101: 210-214 (2004)

Ye Q, Press B, Kissler S , Yang XF, Lu L, Bassing CH, Sleckman BP, Jansson M, Panoutsakopoulou V, Trimble LA, Alt FW, Cantor H. T cell costimulation through CD28 depends on induction of Bcl-xg isoform: analysis of Bcl-xg-deficient mice. J Exp Med 196: 87-95 (2002)

Kissler S, Anderton SM, Wraith DC. Cross-reactivity and TCR antagonism of MBP-reactive T cells is modulated by the activation state of the antigen presenting cell. J Autoimmunity 17: 183-193 (2002)

Kissler S, Anderton SM, Wraith DC. Antigen presenting cell activation: a link between infection and autoimmunity? J Autoimmunity 16: 303-308 (2001)

Anderton SM, Kissler S , Lamont AG, Wraith DC. Therapeutic potential of TCR antagonists is determined by their ability to modulate a diverse repertoire of autoreactive T cells. Eur J Immunol. 29(6): 1850-1857 (1999)

Kissler S, Susal C, Opelz G. Anti-MIP 1a and anti-Rantes antibodies: New allies of HIV-1? Clin Immunol Immunopath 84(3): 338-341 (1997)

 


 

Page last updated: October 25, 2014