华盛顿大学(University of Washington)的研究人员发现过敏性疾病如：湿疹(eczema)，与自体免疫疾病(autoimmune diseases)的关联性，此研究发表于4月1日的Nature Immunology期刊。
大约有75%的自体免疫疾病好发于女性，特别是在育龄期(childbearing years)的女性，另外也有一大部分的儿童慢性疾病，也属于这类型的自体免疫疾病。严重的慢性自体免疫疾病会出现在各种不同的组织或器官，包括：神经、肠胃道、内分泌系统、皮肤、结缔组织、眼睛、血液及血管等。David Rawlings医师表示：「这份研究暗示着过敏与发炎反应疾病会导致身体消灭瑕疵B细胞的机制失效，以致于这些B细胞会持续产生攻击自身细胞、组织或器官的抗体，进而导致自体免疫疾病。」
研究人员目前正努力找寻瑕疵B细胞消灭机制失效的关键，并试图研发可以克服这些问题的解药，Rawlings医师说：「目前在动物模式试验中，已开发了一种药物能预防肾脏方面的自体免疫疾病。」
(资料来源 : Bio.com)
部分英文原文：
Nature Immunology
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
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.
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Department of Immunology, University of Washington School of Medicine Seattle, Washington 98195, USA.
Benaroya Research Institute, Seattle, Washington 98195, USA.
Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA.
Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195, USA.
Department of Pathology, University of Washington School of Medicine, Seattle, Washington 98195, USA.
Department of Biological Structure, University of Washington School of Medicine, Seattle, Washington 98195, USA.
These authors contributed equally to this work.
Correspondence to: David J Rawlings1,4 e-mail: drawling@u.washington.edu
Correspondence to: Steven F Ziegler1,2 e-mail: sziegler@benaroyaresearch.org
