来自Washington大学（UW）儿童医院及地区医疗中心的科学家们通过一项新研究发现，在过敏性疾病——例如过敏性皮炎，也叫湿疹——和自体免疫疾病之间存在特殊的联系。这一研究结果发表在4月1日出版的刊物《自然－免疫学》（Nature Immunology）上。
大约有75%左右的自体免疫疾病发生在女性身上，其中绝大部分是处于分娩期的女性。这些疾病同时还会造成很大一部分的童年期慢性异常等。自体免疫疾病会导致超过80种非常严重的慢性疾病，其中包括神经、胃肠道、内分泌系统的异常，以及皮肤和其它结缔组织、眼睛、血液、和血管疾病等。在所有这些疾病中，其内部的发病机制都是一致的——我们身体的免疫系统（包括B细胞和T细胞）变得失去方向，从而攻击那些本应被保护的器官。
研究主要负责人，来自UW儿童医院的免疫学主任David Rawlings博士表示：“我们的研究结果表明，过敏性疾病和炎症或许会触发自体免疫疾病，因为这些疾病会放松对于新产生的活跃B细胞的控制。而以上过程非常重要，这是由于很多的自体免疫疾病都是由这些B细胞产生的自活跃抗体引起的。”
目前UW的科学家们正在寻找对于B细胞的控制的这种放松究竟发生在哪里。Rawlings最后说：“通过和UW的实验室合作，我们也在寻找治疗这些疾病的药物。现在一种帮助保护肾脏免受自体免疫疾病侵害的药物正在进行动物实验。”
原始出处：http://www.physorg.com/news94837786.html
部分英文原文：
Published online: 1 April 2007; | doi:10.1038/ni1452
Local increase in thymic stromal lymphopoietin induces systemic alterations in B cell development
Alexander Astrakhan1, Miyuki Omori2, 7, Thuc Nguyen3, 7, Shirly Becker-Herman4, 7, Masanori Iseki2, 7, Theingi Aye2, Kelly Hudkins5, James Dooley6, Andrew Farr1, 6, Charles E Alpers5, Steven F Ziegler1, 2 & David J Rawlings1, 4
1 Department of Immunology, University of Washington School of Medicine Seattle, Washington 98195, USA.
2 Benaroya Research Institute, Seattle, Washington 98195, USA.
3 Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA.
4 Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, USA.
5 Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195, USA.
6 Department of Biological Structure, University of Washington School of Medicine, Seattle, Washington 98195, USA.
7 These authors contributed equally to this work.
Correspondence should be addressed to David J Rawlings drawling@u.washington.edu or Steven F Ziegler sziegler@benaroyaresearch.org
Abstract
The cytokine thymic stromal lymphopoietin (TSLP) drives immature B cell development in vitro and may regulate T helper type 2 responses. Here we analyzed the involvement of TSLP in B cell development in vivo with a doxycycline-inducible, keratin 5–driven transgene encoding TSLP (K5-TSLP). K5-TSLP-transgenic mice given doxycycline showed an influx of immature B cells into the periphery, with population expansion of follicular mature B cells, near-complete loss of marginal zone and marginal zone precursor B cells, and 'preferential' population expansion of peritoneal B-1b B cells. These changes promoted cryoglobulin production and immune complex–mediated renal disease. Identical events occurred in mice without T cells, in alternative TSLP-transgenic models and in K5-TSLP-transgenic mice with undetectable systemic TSLP. These observations suggest that signals mediating localized TSLP expression may modulate systemic B cell development and promote humoral autoimmunity.
