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Updated: Mar 2, 2026
Real-time Live Imaging of T-cell Signaling Complex Formation
Published on: June 23, 2013
Scaffold protein JLP mediates TCR-initiated CD4+T cell activation and CD154 expression
Qi Yan1, Cheng Yang1, Qiang Fu1
1Department of Nephrology, Renmin hospital of Wuhan University, Wuhan, China.
Insights
Scaffold protein JLP is crucial for CD4+ T-cell activation and CD154 expression. JLP deficiency impairs T-cell proliferation and IL-2 production by affecting calcium influx and NF-AT activation.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- CD4+ T-cell activation and CD154 expression are vital for immune responses.
- Scaffold protein JLP regulates cellular functions but its role in T-cells is unknown.
Purpose of the Study:
- To investigate the role of JLP in CD4+ T-cell activation and CD154 expression.
- To elucidate the signaling pathways affected by JLP deficiency in T-cells.
Main Methods:
- Expression analysis of JLP in mouse immune tissues and CD4+ T cells.
- Functional assays on CD4+ T cells from JLP-deficient and wild-type mice.
- Analysis of T-cell proliferation, cytokine production, surface molecule expression, and signaling pathways (NF-AT, Ca2+, MAPK, NF-κB, AP-1).
Main Results:
- JLP is expressed in mouse immune tissues and CD4+ T cells.
- JLP deficiency impairs T-cell proliferation, IL-2 production, and CD154 induction.
- JLP deficiency affects TCR-induced Ca2+ influx and NF-AT activation, but not MAPK, NF-κB, or AP-1 pathways.
- Expression of CD25, CD69, and TCR remains unaffected.
Conclusions:
- JLP plays a critical role in regulating CD4+ T-cell responses to TCR stimulation.
- JLP mediates TCR-initiated Ca2+/NF-AT activation, impacting T-cell function.
- JLP is a key regulator of adaptive immunity through its role in T-cell activation.
Abstract:
CD4+ T-cell activation and its subsequent induction of CD154 (CD40 ligand, CD40L) expression are pivotal in shaping both the humoral and cellular immune responses. Scaffold protein JLP regulates signal transduction pathways and molecular trafficking inside cells, thus represents a critical component in maintaining cellular functions. Its role in regulating CD4+ T-cell activation and CD154 expression, however, is unclear. Here, we demonstrated expression of JLP in mouse tissues of lymph nodes, thymus, spleen, and also CD4+ T cells. Using CD4+ T cells from jlp-deficient and jlp-wild-type mice, we demonstrated that JLP-deficiency impaired T-cell proliferation, IL-2 production, and CD154 induction upon TCR stimulations, but had no impacts on the expression of other surface molecules such as CD25, CD69, and TCR. These observed impaired T-cell functions in the jlp-/- CD4+ T cells were associated with defective NF-AT activation and Ca2+ influx, but not the MAPK, NF-κB, as well as AP-1 signaling pathways. Our findings indicated that, for the first time, JLP plays a critical role in regulating CD4+ T cells response to TCR stimulation partly by mediating the activation of TCR-initiated Ca2+/NF-AT.
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