Effect of macrophages on the translocation of protein kinase C in concanavalin a-stimulated lymphocytes

✍ Scribed by Deborah S. Grove; Andrea M. Mastro

• Publisher: John Wiley and Sons
• Year: 1989
• Tongue: English
• Weight: 732 KB
• Volume: 138
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041380317

✦ Synopsis

Thv concanavalin A (Con A)-induced prolifcmtion of lymph node lymphocytes is deperidrnt on the prcwnce of rnacrophages. When lymphocytes are depleted of macrophages, Con A is no longcr rnitogenic. Either 12~0-tetradecanoylptinrbol-1 '%acetate (Tt'A), interleukin 1 (ILl), or rr~~icroph~~gcs in conibination with Con A can restore proliferation. To rstahlish where the proliferation process is blocked in the absence of rnacrophages, an rarly step in the signalling pathway, the activation of protein kinase C, was exarriined. It was found that although Con A caused translocation of protein kinas? C: from the cytosol to the mcmbrane of lymph node cells, when the lymph node cells were depleted of rnacrophages and cxposcd to Con A, this translocation of protein kinase (7 did not ucvur~ Instead, protein kinaw C activity decreased in the membrane fraction and incrrascd in the cytosol. O n the other hand, TPA caused translocation of protein kinase C (PKC) from thv cytosol to the membrane reg,wdless of the presence of macrophages.

However, the marrophagc product, IL 1, alone or in combination with Con A did not cause translocation of protein kinase C. In recon5titutioti experirnent, in which lymph node cells were depleted of macrophages and then macrophages were added back, the d d i t i o n of Con A again lead to translocation of protein kinase C from the cytosol to the membrane. This cornhination also restored cell proliferation. Therefore, the Con A induced PKC translocation in T lymphocytes is macrophage mediated. TPA ovrrromrs the macrophage requirement by directly activaing PKC, while IL1 appears to act at <I diffrrcmt step in proliferation.