{"title":"免疫耐受:发展和破坏。","authors":"W O Weigle","doi":"10.1080/21548331.1995.11443152","DOIUrl":null,"url":null,"abstract":"<p><p>Loss of tolerance to self-antigens is thought to have a role in a variety of common diseases. Studies in animal models of such diseases as systemic lupus erythematosus have provided new insights into how self-tolerance is broken or bypassed and how it may be restored. These and other experiments also are clarifying how self-tolerance is normally established; the T lymphocyte appears to be the dominant player.</p>","PeriodicalId":77164,"journal":{"name":"Hospital practice (Office ed.)","volume":"30 2","pages":"81-4, 89-92"},"PeriodicalIF":0.0000,"publicationDate":"1995-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/21548331.1995.11443152","citationCount":"14","resultStr":"{\"title\":\"Immunologic tolerance: development and disruption.\",\"authors\":\"W O Weigle\",\"doi\":\"10.1080/21548331.1995.11443152\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Loss of tolerance to self-antigens is thought to have a role in a variety of common diseases. Studies in animal models of such diseases as systemic lupus erythematosus have provided new insights into how self-tolerance is broken or bypassed and how it may be restored. These and other experiments also are clarifying how self-tolerance is normally established; the T lymphocyte appears to be the dominant player.</p>\",\"PeriodicalId\":77164,\"journal\":{\"name\":\"Hospital practice (Office ed.)\",\"volume\":\"30 2\",\"pages\":\"81-4, 89-92\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1995-02-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/21548331.1995.11443152\",\"citationCount\":\"14\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Hospital practice (Office ed.)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/21548331.1995.11443152\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hospital practice (Office ed.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/21548331.1995.11443152","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Immunologic tolerance: development and disruption.
Loss of tolerance to self-antigens is thought to have a role in a variety of common diseases. Studies in animal models of such diseases as systemic lupus erythematosus have provided new insights into how self-tolerance is broken or bypassed and how it may be restored. These and other experiments also are clarifying how self-tolerance is normally established; the T lymphocyte appears to be the dominant player.