Understanding the processes by which certain mucosal pathogens and their products induce regulatory T cells (Tregs) is important in determining mechanisms of pathogenicity and may point toward their use in treating immunological disorders. Accordingly, we have studied the events that follow mucosal administration of the B subunit of E. coli heat-labile enterotoxin (EtxB). EtxB modulates the response to co-administered antigens and can prevent autoimmune disease. Our data show that EtxB translocates across the nasal epithelium, modulating the expression of interleukin-10 (IL-10) and transforming growth factor-β(1) (TGF-β(1)). The modulated microenvironment drives an increase in Forkhead box P3 (Foxp3)-positive T cells, predominantly in the CD4(+)CD25(-) subset. Adoptive transfer experiments showed that enhanced Foxp3 expression was particularly evident in recently activated T cells by concomitant unrelated antigen challenge, and was both TGF-β(1) and IL-10 dependent. This ability to alter T-cell differentiation pathways following mucosal delivery explains how EtxB may modify mucosal immune environments and prevent unwanted pathologies.
In ribosomal protein S12 mutant or L24 mutant the expression of lambdaN gene was depressed at translational level. To study its mechanism the lambdaN gene region of lambdaN -lacZ gene fusion was trimmed from its 5' end to 3' end with DNA exonuclease III (DNA exoIII) in order to alter the TIR (translational initiation region) and the coding region of lambdaN gene. After DNA sequencing 23 species of different lambdaN-lacZ fused genes were obtained. The beta-galactosidase activities of these deletants in ribosomal protein mutant were compared with that in wild type strain. The result indicated that (i) S12 mutant could affect 305 subunit's binding to the TIR of lambdaN gene messenger and cause the difficulty in forming 30s initiation complex and then decrease the efficiency of translational initiation; (ii) in S12 mutant the coding region of lambdaN gene also affected the expression lambdaN gene; (iii) in L24 mutant the inhibition of lambdaN gene expression was not related to translational initiation and the 5' end of the coding region of lambdaN gene, but related to the 3' end of lambdaN gene.
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