Related Experiment Videos
IL-1 alpha is produced by T lymphocytes activated via the CD2 plus CD28 pathways
Journal of Immunology (Baltimore, Md. : 1950)
|January 15, 1991
Summary
Combined CD2 and CD28 activation of T cells uniquely induces Interleukin-1 alpha (IL-1 alpha) secretion, promoting sustained T cell proliferation without monocytes. This highlights a novel T cell function in immune regulation and autoimmune processes.
Area of Science:
- Immunology
- Cell Biology
Background:
- Resting T cells activate via the T cell receptor (TCR) complex.
- Surface molecules CD2 and CD28 also mediate T cell activation and proliferation through monoclonal antibodies (mAbs).
Purpose of the Study:
- To investigate the cytokine production profile of T cells activated by CD2 and CD28 co-stimulation.
- To determine if combined CD2 and CD28 activation influences the expression and secretion of specific cytokines, particularly monokines.
Main Methods:
- Purified resting T cells were activated using monoclonal antibodies (mAbs) targeting CD2 and CD28.
- Expression and secretion of cytokines, including IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha, were analyzed.
Main Results:
- Combined CD2 and CD28 activation uniquely induced the expression and secretion of IL-1 alpha, a monokine.
- Neither IL-1 beta nor IL-6 were produced by activated T cells.
- Tumor Necrosis Factor-alpha (TNF-alpha) was transiently expressed by T cells activated by either CD2 or CD28 alone, but showed higher levels and prolonged kinetics with combined CD2 plus CD28 activation.
- Prolonged IL-1 alpha gene expression correlated with monocyte-independent, long-lasting T cell proliferation.
Conclusions:
- Co-stimulation via CD2 and CD28 on T cells leads to the secretion of IL-1 alpha, a cytokine typically associated with monocytes.
- This T cell-derived IL-1 alpha may contribute to sustained T cell proliferation independently of monocytes.
- Secretion of monokines by activated T cells could have regulatory roles in immune responses and potentially contribute to autoimmune diseases.