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诱导非化脓性后遗症的细菌引起的多克隆B细胞激活。

Polyclonal B-cell activation by bacteria that induce nonsuppurative sequelae.

作者信息

Gross W L

机构信息

I. Medizinische Universitäts-Klinik, Kiel, Federal Republic of Germany.

出版信息

Rheumatol Int. 1989;9(3-5):205-11. doi: 10.1007/BF00271882.

Abstract

The polyclonal B cell activation (PBA) process induced by Klebsiella pneumoniae K34 (klebs) and Yersinia enterocolitica 03 (yers) was investigated. Both heat-inactivated bacteria and their cell wall biostructures (klebsM, muriene, protein I etc.) stimulate human blood B cells to differentiate into immunoglobulin-secreting cells without prior proliferation and without T cells. Klebs-activated B cells secrete mainly IgM and to a lesser degree IgG (mainly IgG2). The PBA process was regulated by CD4+ cells and monocytes, but not by CD8+ cells. While interleukin 2 is able both to induce proliferation and to enhance differentiation in klebs-activated B cell cultures, the low-molecular-weight B cell growth factor (BCGF) did not lead to a significant amount of 3H-thymidine uptake. In addition, in klebs-activated B cell cultures various anti-polynucleotide autoantibodies and the 16/6 idiotype were detectable. Thus, bacteria that induce nonsuppurative sequelae (e.g. klebs, yers) can use several mechanisms to overcome tolerance in their host.

摘要

研究了肺炎克雷伯菌K34(klebs)和小肠结肠炎耶尔森菌03(yers)诱导的多克隆B细胞激活(PBA)过程。热灭活细菌及其细胞壁生物结构(klebsM、muriene、蛋白I等)均可刺激人血B细胞分化为分泌免疫球蛋白的细胞,无需预先增殖且无需T细胞参与。klebs激活的B细胞主要分泌IgM,少量分泌IgG(主要是IgG2)。PBA过程受CD4 +细胞和单核细胞调节,但不受CD8 +细胞调节。虽然白细胞介素2既能诱导klebs激活的B细胞培养物增殖,又能增强其分化,但低分子量B细胞生长因子(BCGF)不会导致大量的3H - 胸腺嘧啶核苷摄取。此外,在klebs激活的B细胞培养物中可检测到各种抗多核苷酸自身抗体和16/6独特型。因此,诱导非化脓性后遗症的细菌(如klebs、yers)可利用多种机制克服宿主中的耐受性。

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