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The Effects of Thapsigargin and Concanavalin A on Jurkat T‐Cell Interleukin‐2 (IL‐2) Production: A Preliminary Study
Author(s) -
Lee Ruth M,
Jones Ward
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.937.8
Subject(s) - concanavalin a , jurkat cells , thapsigargin , t cell , diacylglycerol kinase , interleukin 2 , protein kinase c , phytohaemagglutinin , microbiology and biotechnology , chemistry , interleukin 4 , endocrinology , medicine , cytokine , biology , biochemistry , receptor , signal transduction , in vitro , immunology , extracellular , immune system
Interleukin‐2 production is a key indicator of T cell activation. Specifically, IL‐2 leads to T cell expansion and signal amplification in vivo. Thus, understanding the control of IL‐2 production is important to T cell differentiation. Previous studies suggest a combination of phorbol myristate acetate (PMA) and Thapsigargin (TG) increase IL‐2 production (Sei and Reich et al. 1995). TG works by mimicking Inositol Tri‐Phosphate (IP3) and PMA works by mimicking Diacylglycerol (DAG). Together, both TG and PMA work to bypass the original pathway and activate Protein Kinase C (PKC). However, PKC will not activate when TG or PMA are used alone. Concanavalin A (ConA) activates T‐Cells by binding to cell‐surface glycoproteins. In addition, ConA and PMA are known to activate IL‐2 production. However, it is unknown whether TG, when paired with ConA, will stimulate production of IL‐2. We proposed that TG and ConA, when used simultaneously, would increase IL‐2 levels. Preliminary ELISA data suggests elevated ConA increases IL‐2 production while high concentrations of TG inhibit ConA induced IL‐2 production. Support or Funding Information All funding came from Viterbo University's Summer Research Fellowship.