6533b831fe1ef96bd12986f3

RESEARCH PRODUCT

Perpetual proliferation of LYT-1 cells requires repetitive signals for IL-2 receptor induction by antigen-presenting cells.

D.v. SteldernAngelika B. Reske-kunzErwin Rüde

subject

Time FactorsCell divisionOvalbuminT cellT-LymphocytesImmunologyReceptors Antigen T-CellLymphocyte ActivationAbsorptionCell LineMiceAntigenmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorAntigensReceptors ImmunologicReceptorAntigen-presenting cellCD40biologyReceptors Interleukin-2HematologyMolecular biologymedicine.anatomical_structureImmunologybiology.proteinInterleukin-2Spleen

description

Abstract T cell lines with specificity for bovine insulin and ovalbumin were maintained by serial stimulation with antigen presented on irradiated syngeneic spleen cells, alternating 3 days later with subculture in IL-2 containing medium (CM). When the cultures were repetitively split in CM, with concomitant dilution of antigen-presenting cells, a gradual loss of proliferative capacity of the cells in the presence of CM was observed. Absorption studies revealed a 20-fold reduction of IL-2 receptors on the surface of T blasts assayed 12 days after antigenic stimulation as compared with day 5 blasts. This decrement in the number of IL-2 acceptor sites reflected an actual decrease in cell surface density of IL-2 receptors. Restimulation of the T blasts with antigen and spleen cells induced both a substantial increase in IL-2 receptor density and responsiveness to CM. Furthermore, the permanent presence of antigen and spleen cells during splitting of the T blasts in CM prevented the loss of responsiveness to IL-2. As an interpretation we propose that the Lyt-1 cells studied here clear their IL-2 receptors from the cell surface after interaction with IL-2. Thus, each new round of replication of the daughter cells would be dependent on induction of IL-2 receptors by activating signals provided by antigen/la structures on accessory cells as well as possibly accessory cell products such as IL-1, rendering Lyt-1 cells sensitive to regulatory influences.

10.1016/s0171-2985(84)80147-3https://pubmed.ncbi.nlm.nih.gov/6425205