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Tim Sparwasser

Researcher at University of Mainz

Publications -  236
Citations -  21756

Tim Sparwasser is an academic researcher from University of Mainz. The author has contributed to research in topics: FOXP3 & Immune system. The author has an hindex of 70, co-authored 229 publications receiving 19018 citations. Previous affiliations of Tim Sparwasser include Hannover Medical School & Technische Universität München.

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Selective depletion of Foxp3+ regulatory T cells induces a scurfy-like disease.

TL;DR: Experimental evidence that the absence of Foxp3+ T reg cells is indeed sufficient to induce a scurfy-like phenotype is provided, and the generation of DEREG mice will allow a more precise definition of the function of Fox p3+T reg cells in immune reactions in vivo.
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Bacterial DNA and immunostimulatory CpG oligonucleotides trigger maturation and activation of murine dendritic cells

TL;DR: It is demonstrated that bacterial DNA or i.s. CpG‐ODN cause maturation and activation of DC to bring about conversion of immature DC into professional APC, which is associated with the acquisition of professional antigen‐presenting cell (APC) function.
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Card9 controls a non-TLR signalling pathway for innate anti-fungal immunity

TL;DR: A novel innate immune pathway is defined and it is indicated that evolutionarily distinct ITAM receptors in innate and adaptive immune cells use diverse adaptor proteins to engage selectively the conserved Bcl10–Malt1 module.
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Intestinal tolerance requires gut homing and expansion of FoxP3+ regulatory T cells in the lamina propria

TL;DR: A model of stepwise oral tolerance induction induction comprising the generation of Treg cells in the gut-draining lymph nodes, followed by migration into the gut and subsequent expansion of T Reg cells driven by intestinal macrophages is proposed.
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CpG-DNA-specific activation of antigen-presenting cells requires stress kinase activity and is preceded by non-specific endocytosis and endosomal maturation.

TL;DR: It is demonstrated that CpG‐DNA induces phosphorylation of Jun N‐terminal kinase kinase 1 (JNKK1/SEK/MKK4) and subsequent activation of the stress kinases JNK1/2 and p38 in murine macrophages and dendritic cells, and that cellular uptake via endocytosis and subsequent endosomal maturation is essential for signalling.