About the Project
A PhD position is available in the group of PD Dr. Friederike Berberich-Siebelt at the Institute for Pathology, University of Würzburg. The successful candidate will be part of a research consortium ‘Functional clustering of T cell and other immune cell sub-phenotypes across plasticity and individualities of immune-mediated diseases’ supported by Else-Kröner / Fresenius. Furthermore, enrollment in the Graduate School of Life Sciences (GSLS) would ensure structured doctoral research training in a highly interdisciplinary research environment.
The subsets of Tregs and ILCs do not only vary, but may transdifferentiate due to inflammation, direct and indirect interactions, and the signal transduction events, which are circumstantially induced. We hypothesize that more advanced screenings will discover unappreciated subtypes and that accordingly designed animal models will evaluate their functional role.
Therefore, in this position you will:
• Isolate and characterize Tregs and ILCs from human freshly resected gut of IBD and CAC patients by flow cytometric and CyTOF® analyses.
• Compare the results obtained from human samples with murine-derived GALT under different conditions (steady state, immunization, transfer colitis and GvHD).
• Establish health vs disease parameters for Foxp3+ T cells and ILCs by analyses of mice mutated in presumable key molecules evaluated by the listed screens to be distinct for health vs disease.
• Adoptive transfer experiments with defined Treg and / or ILC subsets to define the unique regulatory feature and the inter-dependence of both.
• Once more, analyze human samples led by the insights gained by the manipulated mouse models.
We are looking for a highly motivated and enthusiastic student with training in immunology and at best with an experience in pre-clinical mouse models.
Applications must contain a CV including records, a short motivation letter and the names of two references to [Email Address Removed]
References
Vaeth M, Bauerlein CA, Pusch T, Findeis J, Chopra M, Mottok A, Rosenwald A, Beilhack A, Berberich-Siebelt F. Selective NFAT targeting in T cells ameliorates GvHD while maintaining antitumor activity. Proc Natl Acad Sci U S A, 2015;112:1125-30.
Dietz L, Frommer F, Vogel AL, Vaeth M, Serfling E, Waisman A, Buttmann M, Berberich-Siebelt F. NFAT1 deficit and NFAT2 deficit attenuate EAE via different mechanisms. Eur J Immunol, 2015;45:1377-89.
Vaeth M, Muller G, Stauss D, Dietz L, Klein-Hessling S, Serfling E, Lipp M, Berberich I, Berberich-Siebelt F. Follicular regulatory T cells control humoral autoimmunity via NFAT2-regulated CXCR5 expression. J Exp Med, 2014;211:545-61.
Vaeth M, Schliesser U, Muller G, Reissig S, Satoh K, Tuettenberg A, Jonuleit H, Waisman A, Muller MR, Serfling E, Sawitzki BS, Berberich-Siebelt F. Dependence on nuclear factor of activated T-cells (NFAT) levels discriminates conventional T cells from Foxp3+ regulatory T cells. Proc Natl Acad Sci U S A, 2012;109:16258-63.
Benkert TF, Dietz L, Hartmann EM, Leich E, Rosenwald A, Serfling E, Buttmann M, Berberich-Siebelt F. Natalizumab exerts direct signaling capacity and supports a pro-inflammatory phenotype in some patients with multiple sclerosis. PLoS One, 2012;7:e52208.