The Bruestle Group - Inflammatory T Cell Responses

The Bruestle Group - Inflammatory T Cell Responses, is focusing on different T helper cell subsets and how they modulate immunity in diverse autoimmune mouse models. A special interest of this group is the CD4 subset of inflammatory Th17 cells. Using genetically modified mouse strains they analyse the differentiation and effector function of these cells in vitro as well as in in vivo models. Their research relates to human autoimmune diseases such as multiple sclerosis, psoriasis or inflammatory bowel disease, all of which have been associated with deregulated Th17 cell responses.

Enquiries are welcome from potential Honours or PhD students with an interest in autoimmunity and T cell biology. A variety of projects are available within all of the areas of research undertaken by this Group.

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Selected Publications:

Evita Bothur*, .., Anne Brüstle, et al. Antigen receptor-mediated depletion of FOXO3 in induced T-lymphocytes via PTPN2 and FOXO. Nat Comms. doi:10.1038/ncomms9576

Brüstle A*, Brenner D*, MALT1 is an intrinsic regulator of regulatory T cells. Cell Death Differ. doi: 10.1038/cdd.2015.104. [Epub ahead of print]

Harris IS, ..., Brüstle A, et al. Glutathione and thioredoxin antioxidant pathways synergize to drive cancer initiation and progression. . 2015 Feb 9;27(2):211-22. doi: 10.1016/j.ccell.2014.11.019.

Brüstle A. Is DUBA putting the brake on Th17 cells? Immunol Cell Biol. Feb:93(2):111-2 (2015)

Parish IA,..., Brüstle A, et al. Chronic viral infection promotes sustained Th1-derived immunoregulatory IL-10 via BLIMP-1. J Clin. Invest. 124(8): 3455-68 (2014)

Brenner D*, Brüstle A*, et al. Toso controls encephalitogenic immune responses by dendritic cells and regulatory T cells.. 111(3):1060-5 (2014)

Huber M*, Heink S*,..., Brüstle A, et al. J Clin Invest. 123(1):247-60 (2013)

Brüstle A*, Brenner D*, et al. The NF-kB regulator MALT1 determines the encephalitogenic potential of Th17 cells. J Clin Invest. 122(12):4698-709 (2012)

Sasaki M*, Knobbe CB*, ..., Brüstle Aet al. IDH1(R132H) mutation increases murine haematopoietic progenitors and alters epigenetics. Nature. 488(7413):656-9 (2012)

Bollig N, Brüstle A, et al. Transcription factor IRF4 determines germinal center formation through follicular T-helper cell differentiation. 109(22):8664-9 (2012)

Reardon C*, Lechmann M*, Brüstle A, et al. TSLP-induced expression of the endogenous inhibitory enzyme SLPI mediates recovery from colonic inflammation. . 35(2):223-35 (2011)

Huber M, Brüstle A, et al. IRF4 is essential for IL-21-mediated induction, amplification and stabilisation of the TH17 phenotype. . 105(52):20846-51(2008).

Brüstle A, Heink S, Huber M, Rosenplänter C, Stadelmann C, Yu P, Arpaia E, Mak TW, Kamradt T, Lohoff M, The development of inflammatory T(H)-17 cells requires IRF4. Nat Immunol. (9):958-66 (2007).