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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >EARLY-ONSET MULTIFOCAL INFLAMMATION IN THE TRANSFORMING GROWTH FACTOR BETA-1-NULL MOUSE IS LYMPHOCYTE MEDIATED
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EARLY-ONSET MULTIFOCAL INFLAMMATION IN THE TRANSFORMING GROWTH FACTOR BETA-1-NULL MOUSE IS LYMPHOCYTE MEDIATED

机译：转化生长因子BETA-1-NULL小鼠中的早期多灶炎症发生是通过淋巴细胞介导的

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摘要

Transforming growth factor beta 1 (TGF beta 1)-null mice die from complications due to an early-onset multifocal inflammatory disorder. We show here that cardiac cells are hyperproliferative and that intercellular adhesion molecule 1 (ICAM-1) is elevated. To determine which phenotypes are primarily caused by a deficiency in TGF beta 1 from those that are secondary to inflammation, we applied immunosuppressive therapy and genetic combination with the severe combined immunodeficiency (SCID) mutation to inhibit the inflammatory response. Treatment with antibodies to the leukocyte function-associated antigen 1 doubled longevity, reduced inflammation, and delayed heart cell proliferation. TGF beta 1-null SCID mice displayed no inflammation or cardiac cell proliferation, survived to adulthood, and exhibited normal major histocompatibility complex II (MHC II) and ICAM-1 levels. TGF beta 1-null pups born to a TGF beta 1-null SCID mother presented no gross congenital heart defects, indicating that TGF beta 1 alone does not play an essential role in heart development. These results indicate that lymphocytes are essential for the inflammatory response, cardiac cell proliferation, and elevated MHC II and ICAM-1 expression, revealing a vital role for TGF beta 1. in regulating lymphocyte proliferation and activation, which contribute to the maintenance of self tolerance.
机译：转化生长因子beta 1（TGF beta 1）无效的小鼠死于因早发性多灶性炎症引起的并发症。我们在这里显示，心脏细胞过度增殖，并且细胞间粘附分子1（ICAM-1）升高。为了确定哪些表型主要是由TGFβ1缺乏引起的，而不是继发于炎症的那些，我们应用了免疫抑制疗法和具有严重联合免疫缺陷（SCID）突变的基因组合来抑制炎症反应。用与白细胞功能相关的抗原1的抗体治疗可使寿命延长一倍，减少炎症，并延迟心脏细胞的增殖。 TGF beta 1空SCID小鼠没有发炎或心肌细胞增殖，存活到成年，并表现出正常的主要组织相容性复合物II（MHC II）和ICAM-1的水平。 TGF beta 1无SCID母亲所生的TGF beta 1无患幼仔没有明显的先天性心脏缺陷，这表明单独的TGF beta 1对心脏发育没有重要作用。这些结果表明，淋巴细胞对于炎症反应，心肌细胞增殖以及MHC II和ICAM-1表达升高至关重要，这揭示了TGF beta 1在调节淋巴细胞增殖和活化中起着至关重要的作用，这有助于维持自身耐受性。

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