MD TP2: Pharmacological manipulation of HF-IP as pre-clinical model for IP-dependent autoimmunity disease: Role of VIP
The autoimmune hair loss disorder, alopecia areata (AA), largely results from the collapse of a – normally carefully maintained – protective system by which hair follicles (HF) guard themselves against damaging attacks by the immune system. AA treatment has remained inefficient because clinically applicable strategies for restoring this protective system - the so-called HF immune privilege (IP) – remain to be developed. In the current project, we shall culture healthy human scalp HFs, and shall imitate the collapse of their IP by experimental manipulation, adding INFgamma, a key cytokine of AA pathogenesis. Vasoactive intestinal peptide (VIP), an important neuropeptide with immunomodulatory activities which play a role in the eye IP, will then be tested for its efficiency in preventing HF-IP collapse, and/or in effectively restoring it. This will quickly probably identify promising new candidate for more effective AA therapy.
The work has been concluded and is currently summarized in my thesis.
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- MD TP1 - Ig Glycolysation
- MD TP2 - Immunoprivilege
- MD TP3 - ANA antibodies
- MD TP4 - Autoantibody prevalence
- MD TP5 - Treatment of EBA
- MD TP6 - Autoantibody-induced tissue injury
- MD TP7 - Neutrophil signalling
- MD TP7b - IgG-IC-induced signalling
- MD TP8 - The role of IL-33 and its receptor ST2
- MD TP9 - Detection of antigen-specific B cells
- MD TP9b - Detection of antigen-specific B cells in BP
- MD TP10 - Old drugs to block T cells
- MD TP10b - Combination of T cell inhibitory compounds
- MD TP10c - T cell inhibitory compounds (in vivo)
- MD TP11 - Identification of "genetic biomarkers"
- MD TP12 - Combinations of B cell modulatory compounds
- MD TP13 - TREM1 in cutaneous inflammation
- MD TP14 - Signaling in PV
- MD TP15 - Autoantibodies in relatives
- MD TP16 - Drug-induced pemphigoid
- MD TP17 - Keratinocyte lipid mediators
- MD TP18 - Neutrophils + IL-17A-Inhibition
- MD TP19 - C5aR-Inhibition
- MD TP20 - IgG-Subclasses
- MD TP21 - NF-kB in EBA
- MD TP22 - Biochip Mosaics in AIBD
- MD TP23 - Diagnostic Techniques on AIBD
- MD TP24 - Anti-stimulatory effects on Neutrophil-signaling
- MD TP25 - Phage library on systemic scleroderma
- MD TP26 - New EBA-scoring sytem
- MD TP27 - Neutrophil signaling-pathway inhibition
- MD TP28 - Inhibition of Keratinocytes
- MD TP29 - Monoclonal antibodies in EBA
- MD TP30 - Enhancing vaccinations under Immunosuppression
- MD TP31 - Non-desmoglein autoantibodies in PV
- MD TP32 - Neutrophil adhesion
- MD TP33 - MicroRNA-21 in BP
- MD TP34 - PI3K-subunits in EBA
- MD TP35 - Signaling cascade inhibition in EBA
- MD TP36 - Signaling cascades in keratinocytes
- MD TP37 - AT1R-antibodies
- MD TP38 - Cell migration regulation
- MD TP39 - mACh-Receptors in systemic sclerosis
- MD TP40 - Hair and EBA
- MD TP41 - CMV-specific T cells
- MD TP42 - Necroptosis in GPA
- MD TP43 - Neutrophils and NETs
- MD TP44 - Mitochondrial genome in AIBD
- MD TP45 - Target antigens in pemphgoid diseases
- MD TP46 - Alpha-adrenoceptors in Raynaud´s phenomenon
- MD TP47 - T cell-receptor-sequences in autoimmune skin diseases
- MD TP48 - Epitope specificity and glycolization
- MD TP49 - Inhibition of keratinocyte-dissociation
- MD TP50 - Transcriptome profile of endothelial cells induced by autoantibodies targeting AT1R/ETAR in systemic sclerosis
- MD TP52 - Expression of B4GALT1 and ST6GAL1 ....
- MD TP54 - Reactivity of serum antibodies ....
- MD TP55 - Identification of potential therapeutics .....
- MD TP56 - Validation of the inhibition of different signalling pathways ...
- MD TP57 - Inhibition of IFN-γ as therapy for epidermolysis bullosa acquisita
- MD TP58 - Characterization of immunoglobulin G subclass distribution ...
- MD TP59 - Development of an experimental pemphigus vulgaris model in adult mice
- MD TP60 - Interactions between GPCR and anti-GPCR IgG autoantibodies...
- MD TP61 - Glycosyltransferases B4GALT1 and ST6GAL1 in...
- MD TP62 - Sensitivity of diagnostic test systems in dermatitis herpetiformis Duhring
- Concluded Ass. MD TP