BACKGROUND: Keloid is a fibrotic skin disease for which immune cell infiltration is a primary pathological hallmark. Meanwhile, in autoimmune diseases, triggering of the inflammation response can lead to tissue injury and subsequent organ fibrosis. When the skin is involved in autoimmune disease, skin fibrosis such as that seen in scleroderma can occur. In this study, we propose that keloid possesses features of autoimmune disease. METHODS: To verify whether keloid possesses features of autoimmune disease, immune cell infiltration and immune complex deposits were detected with immunohistochemical staining and immunofluorescence, respectively, in keloid and normal skin tissues. A routine antinuclear antibody profile was tested in sera from 28 keloid patients and 28 healthy controls. Lastly, the anti-hnRNPA2B1 autoantibody in sera was evaluated by enzyme-linked immunosorbent assay. RESULTS: The numbers of CD1α(+) Langerhans cells, CD3(+) T lymphocytes, CD68(+) macrophages, and CD20(+) B lymphocytes increased in keloid tissues compared to normal skin. IgA, IgM, C3, and C1q deposits were found in keloid tissues but not in normal skin, while anti-hnRNPA2B1 levels in sera from keloid patients were elevated. CONCLUSION: The above findings suggest that keloids have some characteristics that are similar to autoimmune disease and might be mediated by autoimmune responses. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
BACKGROUND: Keloid is a fibrotic skin disease for which immune cell infiltration is a primary pathological hallmark. Meanwhile, in autoimmune diseases, triggering of the inflammation response can lead to tissue injury and subsequent organ fibrosis. When the skin is involved in autoimmune disease, skin fibrosis such as that seen in scleroderma can occur. In this study, we propose that keloid possesses features of autoimmune disease. METHODS: To verify whether keloid possesses features of autoimmune disease, immune cell infiltration and immune complex deposits were detected with immunohistochemical staining and immunofluorescence, respectively, in keloid and normal skin tissues. A routine antinuclear antibody profile was tested in sera from 28 keloid patients and 28 healthy controls. Lastly, the anti-hnRNPA2B1 autoantibody in sera was evaluated by enzyme-linked immunosorbent assay. RESULTS: The numbers of CD1α(+) Langerhans cells, CD3(+) T lymphocytes, CD68(+) macrophages, and CD20(+) B lymphocytes increased in keloid tissues compared to normal skin. IgA, IgM, C3, and C1q deposits were found in keloid tissues but not in normal skin, while anti-hnRNPA2B1 levels in sera from keloid patients were elevated. CONCLUSION: The above findings suggest that keloids have some characteristics that are similar to autoimmune disease and might be mediated by autoimmune responses. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
Authors: Grace C Limandjaja; Taco Waaijman; Sanne Roffel; Frank B Niessen; Susan Gibbs Journal: Arch Dermatol Res Date: 2019-06-11 Impact factor: 3.017
Authors: Franz Rödel; Claudia Fournier; Julia Wiedemann; Felicitas Merz; Udo S Gaipl; Benjamin Frey; Ludwig Keilholz; M Heinrich Seegenschmiedt; Claus Rödel; Stephanie Hehlgans Journal: Front Immunol Date: 2017-05-03 Impact factor: 7.561