華盛頓大學(xué)(University of Washington)的研究人員發(fā)現(xiàn)過敏性疾病如：濕疹(eczema),，與自體免疫疾病(autoimmune diseases)的關(guān)聯(lián)性,，此研究發(fā)表于4月1日的Nature Immunology期刊,。
大約有75%的自體免疫疾病好發(fā)于女性,，特別是在育齡期(childbearing years)的女性,，另外也有一大部分的兒童慢性疾病,，也屬于這類型的自體免疫疾病,。嚴重的慢性自體免疫疾病會出現(xiàn)在各種不同的組織或器官，包括：神經(jīng),、腸胃道,、內(nèi)分泌系統(tǒng)、皮膚,、結(jié)締組織,、眼睛、血液及血管等,。David Rawlings醫(yī)師表示：「這份研究暗示著過敏與發(fā)炎反應(yīng)疾病會導(dǎo)致身體消滅瑕疵B細胞的機制失效,，以致于這些B細胞會持續(xù)產(chǎn)生攻擊自身細胞、組織或器官的抗體,，進而導(dǎo)致自體免疫疾病,。」
研究人員目前正努力找尋瑕疵B細胞消滅機制失效的關(guān)鍵,，并試圖研發(fā)可以克服這些問題的解藥,，Rawlings醫(yī)師說：「目前在動物模式試驗中，已開發(fā)了一種藥物能預(yù)防腎臟方面的自體免疫疾病,?！?/p>
(資料來源 : 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: [email protected]
Correspondence to: Steven F Ziegler1,2 e-mail: [email protected]
