Immune surveillance : Paraneoplastic or environmental triggers of autoimmunity
(1997) In Critical Reviews in Immunology 17. p.437-447- Abstract
Autoimmunity associated with tumor cell development seems an important mechanism by which to prevent progression to clinical cancer. In this brief review, tumor autoantigens associated with paraneoplastic syndrome, non-HLA- associated organ-specific autoimmune diseases, and the highly cell-specific autoimmune eradication of the islet beta cells in type I diabetes are compared and discussed. It is suggested that autoreactivity is important in preventing tumor formation; however, it may be at the expense of the development of autoimmune disease. Although the cytotoxic T lymphocytes (CTL) induction by HLA class I has been studied and use in clinical trials, little is understood about the initiation and HLA class II mediated induction of an... (More)
Autoimmunity associated with tumor cell development seems an important mechanism by which to prevent progression to clinical cancer. In this brief review, tumor autoantigens associated with paraneoplastic syndrome, non-HLA- associated organ-specific autoimmune diseases, and the highly cell-specific autoimmune eradication of the islet beta cells in type I diabetes are compared and discussed. It is suggested that autoreactivity is important in preventing tumor formation; however, it may be at the expense of the development of autoimmune disease. Although the cytotoxic T lymphocytes (CTL) induction by HLA class I has been studied and use in clinical trials, little is understood about the initiation and HLA class II mediated induction of an immune response to neoplastic cells. This induction apparently takes place because paraneoplastic disorders are often due to an immune response to the tumor cell resulting in a cross-reactivity with a normally expressed autoantigen on a remote nontumor-associated target cell. The problem of immune surveillance to eradicate neoplasm or downregulate pathological autoimmunity are therefore closely related phenomena. An improved understanding of immune mediated tumor suppression should therefore greatly benefit immunotherapy of type 1 diabetes, and the two areas of research would benefit from an interdisciplinary endeavor.
(Less)
- author
- Lernmark, Åke LU
- publishing date
- 1997-12-29
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- keywords
- Autoantibodies, Autoantigens, Autoimmune polyendocrine syndrome, Breast cancer, Glutamic acid decarboxylase, Insulin-dependent diabetes, Thymoma
- host publication
- Critical Reviews in Immunology
- series title
- Critical Reviews in Immunology
- volume
- 17
- edition
- 5-6
- pages
- 437 - 447
- publisher
- Begell House
- external identifiers
-
- scopus:0013674115
- pmid:9419431
- ISSN
- 1040-8401
- language
- English
- LU publication?
- no
- id
- 73224cba-96b3-4f33-b662-ae0d482be3f0
- date added to LUP
- 2019-07-01 13:19:02
- date last changed
- 2024-07-24 05:04:04
@inproceedings{73224cba-96b3-4f33-b662-ae0d482be3f0, abstract = {{<p>Autoimmunity associated with tumor cell development seems an important mechanism by which to prevent progression to clinical cancer. In this brief review, tumor autoantigens associated with paraneoplastic syndrome, non-HLA- associated organ-specific autoimmune diseases, and the highly cell-specific autoimmune eradication of the islet beta cells in type I diabetes are compared and discussed. It is suggested that autoreactivity is important in preventing tumor formation; however, it may be at the expense of the development of autoimmune disease. Although the cytotoxic T lymphocytes (CTL) induction by HLA class I has been studied and use in clinical trials, little is understood about the initiation and HLA class II mediated induction of an immune response to neoplastic cells. This induction apparently takes place because paraneoplastic disorders are often due to an immune response to the tumor cell resulting in a cross-reactivity with a normally expressed autoantigen on a remote nontumor-associated target cell. The problem of immune surveillance to eradicate neoplasm or downregulate pathological autoimmunity are therefore closely related phenomena. An improved understanding of immune mediated tumor suppression should therefore greatly benefit immunotherapy of type 1 diabetes, and the two areas of research would benefit from an interdisciplinary endeavor.</p>}}, author = {{Lernmark, Åke}}, booktitle = {{Critical Reviews in Immunology}}, issn = {{1040-8401}}, keywords = {{Autoantibodies; Autoantigens; Autoimmune polyendocrine syndrome; Breast cancer; Glutamic acid decarboxylase; Insulin-dependent diabetes; Thymoma}}, language = {{eng}}, month = {{12}}, pages = {{437--447}}, publisher = {{Begell House}}, series = {{Critical Reviews in Immunology}}, title = {{Immune surveillance : Paraneoplastic or environmental triggers of autoimmunity}}, volume = {{17}}, year = {{1997}}, }