Regulation of RANTES promoter activation in alveolar epithelial cells after cytokine stimulation

Abstract

. Regulation of RANTES promoter activation in alveolar epithelial cells after cytokine stimulation.

Differential Regulation of Chemokines by IL-17 in Colonic Epithelial Cells

“…IL-17 inhibits expression of Th1-recruiting chemokines and simultaneously increases the expression of chemokines specific for Th17 and other immune cell types. Taken together with the earlier observations that the IFN-␥ positively regulates expression of chemokines that recruit Th1 cells (30,63) and negatively regulates the Th17-chemotactic chemokine CCL20 (9), these results suggest that expression of IL-17 at the site of inflammation would promote recruitment of Th17 and inhibit or delay recruitment of Th1 cells, whereas conversely the expression of IFN-␥ would promote the recruitment of Th1 and inhibit the recruitment of Th17 cells.…”

Transcriptional Mechanisms Regulating Alveolar Epithelial Cell-specific CCL5 Secretion in Pulmonary Tuberculosis

“…For example, in IL-1␤-stimulated astrocytoma cells (56) and T cells (26), deletions to 400 base pairs have little effect on CCL5 promoter activity. This was also the situation in alveolar epithelial cells stimulated by either RSV or TNF␣, where a Ϫ220 deletion of the CCL5 promoter retained near wild type activity (54,55). …”

“…Site-specific analysis revealed that the ⌬TRE3/4 region was the most critical, and independent or concurrent mutation of TRE1/2 did not further reduce promoter-reporter activity. This is a stimulus-specific effect of CoMTB because the minimal CCL5 promoter truncated at Ϫ220 base pairs retained activity similar to a full-length promoter of Ϫ974 base pairs in cytokine-and RSV-stimulated epithelial cells (54,55). In addition, there is cell specificity because in an astrocytoma line, a CCL5 promoter with a Ϫ278 deletion was activated to a similar extent to a full-length promoter by IL-1␤ in part as a consequence of translocation of p50/p65 but not c-rel-containing NF B complexes (56).…”

Unphosphorylated STAT3 accumulates in response to IL-6 and activates transcription by binding to NFκB

“…RANTES promoter deletion and mutation reporter constructs were gifts from Dr. Antonella Casola, University of Texas Medical Branch, Galveston, TX (Casola et al 2002). Further deletions of these luciferase reporter constructs were performed by PCR, by introducing KpnI and NheI sites, followed by subcloning to the same restriction sites of the pGL2-basic vector, to generate pGL2-974 (−974 ∼ −1), pGL2-220 (−220 ∼ −1), pGL2-195 (−195 ∼ −1), pGL2-120 (−120 ∼ −1), pGL2-del (−974 ∼ −120), pGL2-CRE-m (5Ј-AAACT GATGAGCTCACTCTA-3Ј to 5Ј-AAACTtcTtAtagacCgCTA -3Ј), pGL2-ISRE-m (5Ј-TTTCAGTTTTCTTTTCC-3Ј to 5Ј-TT TCAGTaaaCTaaaCC-3Ј), and pGL2-NF B-m (5Ј-TTTTGGAAA CTCCCCTTAGGGGATGCCCT-3Ј to 5Ј-TTTTGGcAcCTtaa CgTA cGCCATGCatT-3Ј), respectively (Casola et al 2002). Note that the RANTES promoter sequence used has two B sites and that both were mutated.…”