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We conclude that T-cell involvement in skin blistering diseases such as epidermolysis bullosa acquisita relates not only to T-cell help for B cells that produce pathogenic autoantibodies but also to autoreactive T helper type 1 effector cells that migrate into injured skin sites, exacerbate inflammation through production of inflammatory cytokines such as IFNγ, and prevent wound healing. In psoriasis, non-lesional skin shows alterations at the dermal-epidermal junction (DEJ) compared to healthy skin. Cartilage oligomeric matrix protein (C
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