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Updated: Aug 9, 2026

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
Interleukin-1 induces c-fos and c-jun gene expression in T helper type II cells through different signal transmission
E Muñoz1, A M Zubiaga, B T Huber
1Departamento de Bioquímica y Biología Molecular, Facultad de Medicina de Córdoba, Spain.
Insights
Interleukin-1 (IL-1) activates distinct signaling pathways in D10A cells. These pathways differentially regulate protooncogene expression, involving protein tyrosine kinase and protein kinase C.
Area of Science:
- Immunology
- Molecular Biology
- Cell Signaling
Background:
- Interleukin-1 (IL-1) is a key cytokine involved in immune responses and cellular processes.
- Protooncogene expression, such as c-jun and c-fos, is crucial for cell proliferation and differentiation.
- Understanding IL-1 signaling pathways is vital for comprehending cellular regulation.
Purpose of the Study:
- To elucidate the signal transduction pathways activated by IL-1 in the T helper 2 cell line D10A.
- To investigate the mechanisms underlying IL-1-induced expression of c-jun and c-fos protooncogenes.
Main Methods:
- Utilized the D10A T helper 2 cell line.
- Investigated IL-1 signaling pathways using protein tyrosine kinase inhibitors (tyrphostin) and protein kinase C activators (phorbol esters).
- Analyzed gene transcription and mRNA expression of c-jun and c-fos.
- Examined the role of different Interleukin-1 Receptors (IL-1R) and intracellular cAMP levels.
Main Results:
- IL-1 induced c-jun transcription and mRNA expression via a protein tyrosine kinase-dependent pathway linked to the 80-kDa IL-1R, independent of protein kinase C.
- IL-1-mediated c-fos mRNA expression was dependent on protein kinase C and linked to a distinct, unidentified IL-1R.
- Intracellular cAMP accumulation, generated through the 80-kDa IL-1R, negatively regulated IL-1-induced c-fos expression mediated by protein kinase C.
Conclusions:
- IL-1 modulates c-fos expression in D10A cells through two independent IL-1Rs.
- These distinct IL-1Rs are coupled to different signal transduction pathways, highlighting complex IL-1 regulatory mechanisms.
Abstract:
Interleukin (IL)-1 induces proliferation and expression of several protooncogenes in the T helper 2 cell line D10A. We have analyzed the signal transmission pathways activated by IL-1 in these cells, leading to the expression of c-jun and c-fos. IL-1 induced c-jun gene transcription and mRNA expression by means of a pathway dependent on protein tyrosine kinase activity since tyrphostin, a specific inhibitor of tyrosine kinase, inhibited this induction. This mechanism of transmission signaling was independent of protein kinase C (PKC) and was linked to the 80-kDa IL-1 receptor (IL-1R). In addition, phorbol esters did not induce c-jun mRNA expression, whereas c-fos mRNA expression mediated by IL-1 dependent on PKC; this pathway was linked to a different, still unidentified IL-1R that was functional in the D10A cell line. Accumulation of intracellular cAMP generated by IL-1 through the 80-kDa IL-1R negatively regulated c-fos expression which was induced by IL-1 through PKC activation. We conclude that IL-1 modulates the expression of c-fos in D10A cells by occupying of two independent IL-1R that are linked to different signal transduction pathways.
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