{"title":"Hybridoma SLE autoantibodies: insights for the pathogenesis of autoimmune disease.","authors":"D S Pisetsky","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"3 2","pages":"169-234"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17152376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"T-lymphocyte malignancies: recent advances in the understanding of their biology, diagnosis and treatment.","authors":"D R Parkinson, J W Mier","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"2 1","pages":"59-121"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Immunopathology of pemphigus vulgaris, bullous pemphigoid and related bullous dermatoses.","authors":"H P Patel, G J Anhalt, T T Provost, L A Diaz","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"2 2","pages":"157-86"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17430317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Allergic reactions to industrial chemicals.","authors":"K G McGrath, C R Zeiss, R Patterson","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"2 1","pages":"1-58"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17410605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"HLA and disease.","authors":"F C Grumet","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"2 1","pages":"123-55"},"PeriodicalIF":0.0,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17470385","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Complement may play a primary or exacerbating factor in the production of urticaria and/or angioedema. As we have seen, the absence of inhibitor proteins, such as ClINH, C3bINA, or Carboxypeptidase N Anaphylatoxin Inactivator) can permit small amounts of active complement fragments, liberated "normally" through the action of nonspecific effector pathways, to produce generalized urticaria or angioedema. Abnormal degrees of complement activation, produced by circulating immune complexes, cryoglobulins, paraproteins, may also cause angioedema and/or urticaria. Autoimmune diseases, lymphoreticular malignancy, infections, drug reactions, and syndromes currently termed idioipathic may be associated with urticaria and angioedema due to pathologic complement activation. Direct effects of complement on blood vessels, either by anaphylatoxins or by the deposition of complement fixing immune complexes, may produce the vascular permeability requisite to these syndromes. Secondary effects, produced by the recruitment of inflammatory cells and/or the liberation of other vasoactive mediators from these cells may also occur. Finally, complement may act in a potent synergistic fashion with mediators such as prostaglandins to produce vascular permeability. Current studies, using antigenic, hemolytic, and immunofluorescent techniques for detecting complement involvement have identified a relatively limited number of syndromes in which complement is involved. It is anticipated that the use of more sensitive assays for anaphylatoxins, such as radioimmunoassay, neutrophil aggregation, and others, coupled with an understanding of the potential synergism between these and other mediators, will lead to the recognition of a wider role for complement in urticaria and angioedema.
{"title":"The role of complement in urticaria and angioedema.","authors":"J A Gelfand","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Complement may play a primary or exacerbating factor in the production of urticaria and/or angioedema. As we have seen, the absence of inhibitor proteins, such as ClINH, C3bINA, or Carboxypeptidase N Anaphylatoxin Inactivator) can permit small amounts of active complement fragments, liberated \"normally\" through the action of nonspecific effector pathways, to produce generalized urticaria or angioedema. Abnormal degrees of complement activation, produced by circulating immune complexes, cryoglobulins, paraproteins, may also cause angioedema and/or urticaria. Autoimmune diseases, lymphoreticular malignancy, infections, drug reactions, and syndromes currently termed idioipathic may be associated with urticaria and angioedema due to pathologic complement activation. Direct effects of complement on blood vessels, either by anaphylatoxins or by the deposition of complement fixing immune complexes, may produce the vascular permeability requisite to these syndromes. Secondary effects, produced by the recruitment of inflammatory cells and/or the liberation of other vasoactive mediators from these cells may also occur. Finally, complement may act in a potent synergistic fashion with mediators such as prostaglandins to produce vascular permeability. Current studies, using antigenic, hemolytic, and immunofluorescent techniques for detecting complement involvement have identified a relatively limited number of syndromes in which complement is involved. It is anticipated that the use of more sensitive assays for anaphylatoxins, such as radioimmunoassay, neutrophil aggregation, and others, coupled with an understanding of the potential synergism between these and other mediators, will lead to the recognition of a wider role for complement in urticaria and angioedema.</p>","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"1 2","pages":"257-309"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17817774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Disorders of human leukocyte chemotaxis.","authors":"K M Lohr, R Snyderman","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"1 1","pages":"67-118"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17817772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Immunologic responses to insulin can be manifested by both laboratory animals immunized with insulin as a known modifiable model antigen and by patients receiving heterologous insulin as a mainstay of therapy for insulin dependent diabetes mellitus. The use of purified insulin as a model antigen for the study of cellular interactions, T cell antigen recognition, and the mechanism and specificity of Ir gene action in experimental animals has given us great insight into the potential workings of these complex functions. In humans with IDDM, immune cofactors may play a role in both the pathogenesis of disease as well as the obvious complications of therapy. Intense study of cellular, genetic, biochemical, and immunologic parameters in these patients with IDDM may provide us with unique insights into the complex regulatory interactions between the immunologic and endocrine-metabolic systems.
{"title":"Immunologic reactivity to insulin: animal models and clinical syndromes.","authors":"L J Rosenwasser","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Immunologic responses to insulin can be manifested by both laboratory animals immunized with insulin as a known modifiable model antigen and by patients receiving heterologous insulin as a mainstay of therapy for insulin dependent diabetes mellitus. The use of purified insulin as a model antigen for the study of cellular interactions, T cell antigen recognition, and the mechanism and specificity of Ir gene action in experimental animals has given us great insight into the potential workings of these complex functions. In humans with IDDM, immune cofactors may play a role in both the pathogenesis of disease as well as the obvious complications of therapy. Intense study of cellular, genetic, biochemical, and immunologic parameters in these patients with IDDM may provide us with unique insights into the complex regulatory interactions between the immunologic and endocrine-metabolic systems.</p>","PeriodicalId":77692,"journal":{"name":"Clinical immunology reviews","volume":"1 2","pages":"311-35"},"PeriodicalIF":0.0,"publicationDate":"1981-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17817775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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