Induction of high‐affinity paf receptor expression during T cell activation

Abstract

Activated human T cells via the CD2 or the CD3 pathways exhibited a higher capacity than resting T lymphocytes to incorporate and metabolize [3H]pafacether (paf) at 37 degrees C. Resting T lymphocytes lacked specific binding capacity for paf, yet high-affinity paf receptors (paf-R) were induced on CD3- or CD2-dependent activation. This up-regulation in the number of paf-R became apparent by day 1 of culture, reached a maximum of about 25,000 sites cell by days 4 to 6 and subsequently declined. Interestingly, human recombinant interleukin-2 in a dose-dependent manner prevented the decrease of high-affinity paf-R expression on T cells. By contrast, the receptor affinity was constant throughout the culture period. Thus, paf-R at different stages of T cell activation were indistinguishable with respect to receptor-ligand interaction, and differed only in their number. Together, these data demonstrate that after activation human T cells develop membrane high-affinity paf-binding sites. They also suggest for the first time that expression of the paf-R are coupled to T cell activation and/or differentiation.

Regulation of G protein-coupled receptor kinase subtypes in activated T lymphocytes. Selective increase of beta-adrenergic receptor kinase 1 and 2.

“…A similar profile of increase has been recently reported for a number of other kinase activities, regulated upon mitogenic stimulation of T lymphocytes (19). A dramatic increase of PAF receptor has been demonstrated on the surface of T lymphocytes 48-72 h after stimulation with mitogen (20). Higher levels of /3ARK may be related to higher levels of PAF receptors, for which a functional role of this kinase has already been suggested by our previous work (5).…”

Levocetirizine Modulates Lymphocyte Activation in Patients With Allergic Rhinitis

“…Hence, agents that have relatively minor effects on lymphocyte activation may ultimately cause major changes in multiple processes coordinated by T cells. Therefore, the suppression of T cell activation by antihistamines observed in this study may be accounted for by the fact that cellular signaling pathways that promote tissue damage in SAR exert positive feedback and increase T cell activation (37,38). By this analysis, drugs that inhibit release of inflammatory metabolites or their biological activity are also expected to exhibit immunosuppressive properties.…”

Microbial Modulation of Host Immunity with the Small Molecule Phosphorylcholine

“…Indeed, even the synthetic oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine, or oxPAPC, molecule, which contains ChoP, has been shown to bind TLR4 and induce IL-8 secretion (81). Interestingly, PAFr has been found on the surface of macrophages as well as B and T cells, raising the possibility that ChoP-mediated immune modulation occurs through PAFr binding (82,83). However, while PAFr is functional on macrophages, it is not on B and T cells, suggesting the presence of additional immune activators responsible for ChoP-dependent effects on the immune system (84).…”