Skip to main content
. 2022 Mar 22;13:824746. doi: 10.3389/fimmu.2022.824746

Figure 4.

Figure 4

The 3S/gp41 peptide regulates PLA2G1B activity in a gC1qR-dependent manner. (A, B) The HIV 3S peptide increases PLA2G1B activity on human Jurkat T cells. [3H]AA-labeled Jurkat T cells were pretreated with 3S gp41 (3S) or scrambled 3S (Scr 3S) peptides (11 µM) for various times (2, 4, or 21 h for A) or 21 h (for B) and incubated alone or with PLA2G1B (200 nM). (C) The gC1qR protein is detected in WT but not in gC1qR-deficient (gC1qR KO) Jurkat T cells by immunoblot. Two different anti-gC1qR mAbs were used (60.11 and 74.5.2), as well as anti-ß-actin mAb as an endogenous control of protein load. (D) The 3S peptide increases PLA2G1B activity on WT but not on gC1qR KO cells. WT and gC1qR KO [3H]-AA-labeled Jurkat T cells were pretreated with 3S or Scr 3S peptides at 11 μM for 21 h. Then, peptide-pretreated cells were incubated with PLA2G1B (200 nM) for 2 h. Results are expressed as the mean ± SEM of a pool of three (A, D) and seven (B) experiments performed in triplicate and as ΔPLA2G1B activity (activity with the 3S peptide minus that with the Scr 3S peptide). The level of [3H]AA released in the cell supernatant was quantified in cpm/mL. *p < 0.05, **p < 0.01 and ***p < 0.001 by two-way ANOVA with Tukey’s correction for multiple comparisons (A, D) or an unpaired t-test (B).