IL-20 controls resolution of experimental colitis by regulating epithelial IFN/STAT2 signalling.

Objective: We sought to investigate the role of interleukin (IL)-20 in IBD and experimental colitis.

Design: Experimental colitis was induced in mice deficient in components of the IL-20 and signal transducer and activator of transcription (STAT)2 signalling pathways. In vivo imaging, high-resolution mini-endoscopy and histology were used to assess intestinal inflammation.

Interferon Lambda Promotes Paneth Cell Death Via STAT1 Signaling in Mice and Is Increased in Inflamed Ileal Tissues of Patients With Crohn's Disease.

Background & Aims: Interferon lambda (IFNL) is expressed at high levels by intestinal epithelial cells (IECs) and mucosal immune cells in response to infection and inflammation. We investigated whether IFNL might contribute to pathogenesis of Crohn's disease (CD).

Methods: We obtained serum samples and terminal ileum biopsies from 47 patients with CD and 16 healthy individuals (controls).

Blister-inducing antibodies target multiple epitopes on collagen VII in mice.

Epidermolysis bullosa acquisita (EBA) is an autoimmune subepidermal blistering disease of mucous membranes and the skin caused by autoantibodies against collagen VII. In silico and wet laboratory epitope mapping studies revealed numerous distinct epitopes recognized by EBA patients' autoantibodies within the non-collagenous (NC)1 and NC2 domains of collagen VII. However, the distribution of pathogenic epitopes on collagen VII has not yet been described.

IL-9 and its receptor are predominantly involved in the pathogenesis of UC.

Objective: Several pathogenic roles attributed over the past two decades to either T helper (Th)1 or Th2 cells are increasingly becoming associated with interleukin (IL)-17 and most recently IL-9 signalling. However, the implication of IL-9 in IBD has not been addressed so far.

Design: We investigated the expression of IL-9 and IL-9R by using peripheral blood, biopsies and surgical samples.

IgG antibodies against immunodominant C-terminal epitopes of BP230 do not induce skin blistering in mice.

Bullous pemphigoid, the most common autoimmune blistering disease in Western Europe and the USA is characterized by the presence of circulating and tissue-bound autoantibodies against the hemidesmosomal proteins BP230 and BP180/collagen XVII. After binding to their target antigens at the basement membrane of the dermal-epidermal junction these autoantibodies are thought to trigger an inflammatory cascade comprising complement- and granulocyte-dependent reactions that result in tissue damage. Whereas the role of anti-BP180 antibodies has been extensively characterized, few and conflicting data is available on the contribution of anti-BP230 antibodies to bullous pemphigoid pathogenesis.

Passive transfer of collagen XVII-specific antibodies induces sustained blistering disease in adult mice.

Background: Bullous pemphigoid is a subepidermal blistering disorder associated with tissue-bound and circulating autoantibodies directed mainly to the hemidesmosomal component collagen XVII. While recapitulating the main immunopathological features of the human disease, frank skin blistering does not develop in the absence of skin rubbing in experimental pemphigoid models that have been established in neonatal mice. Moreover, due to their experimental design they only allow for short-term disease observation.

Induction of granulocyte-dependent dermal-epidermal separation by autoantibodies ex vivo.

Disease models represent powerful tools used by biomedical researchers to address various questions related to the pathogenesis and the possible therapeutic targets in different diseases. To get a complete picture of the process one needs complementary animal and ex vivo disease models. While subsequent chapters dwell upon animal models, this chapter describes an ex vivo model for granulocyte-dependent dermal-epidermal separation induced by autoantibodies to the basal membrane.