031 Type XVII collagen-specific CD4+ T cell clones induce bullous pemphigoid in mice by producing IL-5

Pemphigoid in Mice Type XVII Collagen and Leads to Bullous Repetitive Immunization Breaks Tolerance to

Bullous Pemphigoid: IGA Autoantibodies Target Epitopes on of Bullous Pemphigoid Antigen 180 Using Recombinant Ectodomains of Collagen XVII

Type XVII collagen (BP180), promotes adhesion of basal keratinocytes to epidermal basement membrane, and is the target of disease in patients with certain inherited or acquired blistering diseases. Therefore, the aim of the present study was to investigate IgA autoantibodies using recombinant BP 180 proteins against bullous pemphigoid in the sera of patients. Thirty consecutive BP sera were ana...

Noncollagenous 16A domain of type XVII collagen-reactive CD4+ T cells play a pivotal role in the development of active disease in experimental bullous pemphigoid model.

Bullous pemphigoid (BP), the most common autoimmune blistering disease, is caused by autoantibodies against type XVII collagen (COL17). We recently demonstrated that CD4+ T cells were crucial for the production of anti-COL17 IgG and for the development of the BP phenotype by using a novel active BP mouse model by adoptively transferring immunized splenocytes into immunodeficient COL17-humanized...

Clinically resolved psoriatic lesions contain psoriasis-specific IL-17-producing αβ T cell clones.

In psoriasis, an IL-17-mediated inflammatory skin disease, skin lesions resolve with therapy, but often recur in the same locations when therapy is discontinued. We propose that residual T cell populations in resolved psoriatic lesions represent the pathogenic T cells of origin in this disease. Utilizing high-throughput screening (HTS) of the T cell receptor (TCR) and immunostaining, we found t...

Human Langerhans cells induce distinct IL-22-producing CD4+ T cells lacking IL-17 production.

IL-22 is a cytokine that acts mainly on epithelial cells. In the skin, it mediates keratinocyte proliferation and epidermal hyperplasia and is thought to play a central role in inflammatory diseases with marked epidermal acanthosis, such as psoriasis. Although IL-22 was initially considered a Th17 cytokine, increasing evidence suggests that T helper cells can produce IL-22 even without IL-17 ex...