M. Retuerto Guerrero, C. Moriano Morales, I. González Fernández , I. González Fernández
{"title":"Protocolo de tratamiento de los antilinfocitos B en las enfermedades inmunomediadas","authors":"M. Retuerto Guerrero, C. Moriano Morales, I. González Fernández , I. González Fernández","doi":"10.1016/j.med.2025.04.017","DOIUrl":null,"url":null,"abstract":"<div><div>B lymphocytes play a key role in the pathophysiology of systemic autoimmune diseases (SAD), as they not only transform into autoantibody-producing plasma cells, but also secrete proinflammatory cytokines that amplify the immune response. In addition, these lymphocytes act as antigen-presenting cells, which promotes the activation of T lymphocytes and perpetuates the autoimmune process. Aberrant B-cell activation contributes to the formation of immune complexes that, when deposited in different organs and tissues, cause tissue damage, as observed in diseases such as systemic lupus erythematosus, rheumatoid arthritis, and systemic sclerosis. Due to their central role in the pathogenesis of SAD, B-cells have become a key therapeutic target. Therapies targeting these lymphocytes, such as rituximab, have shown efficacy in improving clinical outcomes and reducing systemic inflammation. However, their use entails risks, such as an increase in serious infections due to its immunosuppressive effect and the possible induction of hypogammaglobulinemia, lymphopenia, and neutropenia, which compromises the patient's immune defense. Close monitoring of immunoglobulin levels and the administration of antimicrobial prophylaxis according to the patient's needs is essential.</div></div>","PeriodicalId":100912,"journal":{"name":"Medicine - Programa de Formación Médica Continuada Acreditado","volume":"14 30","pages":"Pages 1842-1846"},"PeriodicalIF":0.0000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medicine - Programa de Formación Médica Continuada Acreditado","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0304541225000903","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
B lymphocytes play a key role in the pathophysiology of systemic autoimmune diseases (SAD), as they not only transform into autoantibody-producing plasma cells, but also secrete proinflammatory cytokines that amplify the immune response. In addition, these lymphocytes act as antigen-presenting cells, which promotes the activation of T lymphocytes and perpetuates the autoimmune process. Aberrant B-cell activation contributes to the formation of immune complexes that, when deposited in different organs and tissues, cause tissue damage, as observed in diseases such as systemic lupus erythematosus, rheumatoid arthritis, and systemic sclerosis. Due to their central role in the pathogenesis of SAD, B-cells have become a key therapeutic target. Therapies targeting these lymphocytes, such as rituximab, have shown efficacy in improving clinical outcomes and reducing systemic inflammation. However, their use entails risks, such as an increase in serious infections due to its immunosuppressive effect and the possible induction of hypogammaglobulinemia, lymphopenia, and neutropenia, which compromises the patient's immune defense. Close monitoring of immunoglobulin levels and the administration of antimicrobial prophylaxis according to the patient's needs is essential.