Skin inflammation: Psoriasis in vitro model
Psoriasis is a chronic, non-contagious autoimmune disease that affects skin and joints with a prevalence of 2-3 % in Western populations. It causes red, scaly patches (psoriatic plaques) on skin which are areas of inflammation and excessive skin production. The cause of psoriasis is not known but should involve both a genetic predisposition and an environmental response.
Recently, it was proposed that autoimmunity in psoriasis could be driven by a complex consisting in the LL-37 antimicrobial peptide and DNA. Such an autoantigen has been shown to sense plasmacytoid dendritic cells to induce the psoriatic Th17-type response, leading to an inflammatory loop between keratinocytes and infiltrating cells. This results in the production of large amounts of antimicrobial peptides, chemokines and in an abnormally differentiated hyperplasic epidermis.
BIOalternatives offers an array of in vitro assays for psoriasis-targeting compounds (screening, profiling, mechanism of action...) that focus on:
Psoriasis initiation
Keratinocyte & blood cell models
- LL-37 production by keratinocytes, macrophages & neutrophils (mRNA & protein)
Psoriasis progression
T cell models (including T cells from psoriatic lesions)
- Th17 cytokine production/release (IL-17, IL-22..., mRNA & protein)
Granulocyte & monocyte/macrophage models
- Pro-inflammatory cytokine production/release (IL-1a/b, OSM, TNFa..., mRNA & protein)
- Functional assays (chimiotactism...)
Psoriasis physiopathology
Keratinocytes & 3 D skin models: induction by validated cytokine cocktails or conditionned media from psoriasic T cells
- Modifications of epidermal differentiation and disease markers (mRNA & protein)
- Antimicrobial peptide production/release (mRNA & protein)
- Chemokine production/release (mRNA & protein)
- Cytokine signaling; STAT-3/STAT-1, MAPK, NFkB & other involved pathways
