New ideas in thyroid autoimmunity.
Endocrine epithelial cells do not normally express human leukocyte antigen (HLA) class II molecules, but do so in a variety of autoimmune diseases. This finding suggests the hypothesis that such inappropriate class II-positive expression may enable these cells to present autoantigens and thus contri...
| Main Authors: | , , , , |
|---|---|
| Format: | Journal article |
| Language: | English |
| Published: |
1987
|
| _version_ | 1797096977121411072 |
|---|---|
| author | Pujol-Borrell, R Todd, I Londei, M Feldmann, M Bottazzo, G |
| author_facet | Pujol-Borrell, R Todd, I Londei, M Feldmann, M Bottazzo, G |
| author_sort | Pujol-Borrell, R |
| collection | OXFORD |
| description | Endocrine epithelial cells do not normally express human leukocyte antigen (HLA) class II molecules, but do so in a variety of autoimmune diseases. This finding suggests the hypothesis that such inappropriate class II-positive expression may enable these cells to present autoantigens and thus contribute to autoimmune pathogenesis. Indeed, class II-positive thyrocytes can present both exogenous antigenic peptides and intrinsic autoantigens to the appropriate T cells. Class II expression by thyrocytes can be induced by interferon-gamma, and is positively and negatively regulated by thyroid-stimulating hormone and epidermal growth factor, respectively. Furthermore, heterogeneity of thyrocyte class II subregion expression appears to be related to the nature of the inducing stimulus. The complexity of regulatory signals is underlined by findings in type I diabetes: islet beta cells aberrantly express class II in this disease, but class II cannot be induced in normal beta cells by interferon-gamma. |
| first_indexed | 2024-03-07T04:49:10Z |
| format | Journal article |
| id | oxford-uuid:d45f02a1-d6f9-4f37-adbc-3216b13365ab |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T04:49:10Z |
| publishDate | 1987 |
| record_format | dspace |
| spelling | oxford-uuid:d45f02a1-d6f9-4f37-adbc-3216b13365ab2022-03-27T08:17:54ZNew ideas in thyroid autoimmunity.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:d45f02a1-d6f9-4f37-adbc-3216b13365abEnglishSymplectic Elements at Oxford1987Pujol-Borrell, RTodd, ILondei, MFeldmann, MBottazzo, GEndocrine epithelial cells do not normally express human leukocyte antigen (HLA) class II molecules, but do so in a variety of autoimmune diseases. This finding suggests the hypothesis that such inappropriate class II-positive expression may enable these cells to present autoantigens and thus contribute to autoimmune pathogenesis. Indeed, class II-positive thyrocytes can present both exogenous antigenic peptides and intrinsic autoantigens to the appropriate T cells. Class II expression by thyrocytes can be induced by interferon-gamma, and is positively and negatively regulated by thyroid-stimulating hormone and epidermal growth factor, respectively. Furthermore, heterogeneity of thyrocyte class II subregion expression appears to be related to the nature of the inducing stimulus. The complexity of regulatory signals is underlined by findings in type I diabetes: islet beta cells aberrantly express class II in this disease, but class II cannot be induced in normal beta cells by interferon-gamma. |
| spellingShingle | Pujol-Borrell, R Todd, I Londei, M Feldmann, M Bottazzo, G New ideas in thyroid autoimmunity. |
| title | New ideas in thyroid autoimmunity. |
| title_full | New ideas in thyroid autoimmunity. |
| title_fullStr | New ideas in thyroid autoimmunity. |
| title_full_unstemmed | New ideas in thyroid autoimmunity. |
| title_short | New ideas in thyroid autoimmunity. |
| title_sort | new ideas in thyroid autoimmunity |
| work_keys_str_mv | AT pujolborrellr newideasinthyroidautoimmunity AT toddi newideasinthyroidautoimmunity AT londeim newideasinthyroidautoimmunity AT feldmannm newideasinthyroidautoimmunity AT bottazzog newideasinthyroidautoimmunity |