Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2013 Sep 23;210(10):2119–2134. doi: 10.1084/jem.20130252

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2013 Yang et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

PMC Copyright notice

Figure 2. — PFKFB3 induction is suppressed in RA T cells. Naive CD4 (CD4⁺CD45RO⁻) T cells were isolated from RA patients and age-matched controls and stimulated with anti-CD3/CD28 microbeads for 3 d. Glycolysis-related gene transcripts were quantified by qPCR (A, n = 3). Kinetics of the expression of PFKFB3 in T cells following TCR ligation were monitored by RT-PCR over 12 d (B, 6 RA patients and 6 healthy controls) or by Western blotting over 4 d (C). Naive CD4 T cells were stimulated with either anti-CD3/CD28 microbeads or 20 ng/ml PMA and 200 µg/ml ionomycin and PFKFB3 transcript levels were monitored over 72 h in six samples. PMA/ionomycin-induced PFKFB3 transcripts from 5 RA patients and 6 controls are shown (D). Protein levels of PFKFB3 were quantified by Western blotting. Representative data for 2 patients and 2 controls are shown. Quantification of band densities from five independent experiments in 10 patients and 10 control samples are given as mean ± SEM (E). Expression of PFKFB3 in CD4⁺CD45RO⁺ memory T cells was quantified in 10 controls and 5 RA patients by RT-PCR (F). Activation-induced up-regulation of PFKFB3 was compared in control T cells, RA T cells, and SLE T cells on day 3 after TCR ligation. PFKFB3 mRNA levels were determined by RT-PCR in n = 16 RA patients, n = 33 controls, and n = 11 SLE patients. Results are given as mean ± SEM (G). PFKFB3 transcripts quantified by qPCR on day 3 after T cell stimulation were correlated with RA disease activity (DAS28; r² = 0.020, P = 0.306; H). Expression of AMPK family members and mTOR was determined by qPCR and Western blotting, respectively. Data from 6 RA patients and 6 age-matched controls are presented as mean ± SEM and representative immunoblots are shown (I). Transcripts of PFKFB1, 2, and 4 were quantified by qPCR over 6 d (J). Activation-induced up-regulation of PFKFB1, 2, and 4 were compared in control and RA T cells (n = 8 each) on day 3 after TCR ligation. Results are given as mean ± SEM (K). *, P < 0.05; **, P < 0.01; ***, P < 0.001; n.s., non-significant.