过敏性疾病与自体免疫疾病的关联性
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
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