The main aim of this study has been to determine the effect of selected non-steroidal anti-inflammatory drugs (NSAIDs) - depending on their selectivity to cyclooxygenase (COX) 1 and 2 - on the activation-induced CD25 expression on CD4 and CD8 T cells. Lymphocytes obtained from lymph nodes of mice were treated with acetylsalicylic acid (ASA; a preferential COX-1 inhibitor), ketoprofen (KET; a non-selective COX inhibitor) and robenacoxib (ROB; a selective COX-2 inhibitor) in concentrations reflecting their plasma levels achieved in vivo at therapeutic doses and in ten-fold lower concentrations. The cells were activated with concanavalin A. In contrast to KET and ROB, ASA had no effect on the activation-induced CD25 expression on CD4 and CD8 T cells, nor did it affect the counts of CD4 and CD8 activated effector (aTeff) and resting (Trest) T cells. Both KET and ROB caused a depletion of CD8 aTeff cells, and additionally KET induced a loss of CD8 Trest cells. Moreover, ROB, but not the other drugs, reduced the activation-induced CD25 expression on CD4 T cells. This suggests that non-selective COX inhibitors and selective COX-2 inhibitors may weaken the effector T cell response by producing a negative effect on the count of aTeff cells. Furthermore, the results seem to imply that ASA and KET have certain potential to induce Foxp3 expression in CD25CD8 and CD25CD4 T cells, respectively. However, all the observed changes were very weakly manifested and therefore it is not certain whether they have clinical importance, despite the statistical significance determined.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6745551PMC
http://dx.doi.org/10.5114/ceji.2019.87058DOI Listing

Publication Analysis

Top Keywords

activation-induced cd25
16
cd25 expression
16
cd4 cd8
16
cd8 cells
12
expression cd4
12
cells
10
selected non-steroidal
8
non-steroidal anti-inflammatory
8
anti-inflammatory drugs
8
non-selective cox
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!