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CD95/Fas, Non-Apoptotic Signaling Pathways, and Kinases
Matthieu Le Gallo1,2,3, Amanda Poissonnier1,2,3, Patrick Blanco4,5
1Centre Eugène Marquis, Rennes, France.
Frontiers in Immunology
|October 13, 2017
Summary
Soluble CD95L, elevated in triple-negative breast cancer and lupus, drives disease severity by activating non-apoptotic pathways. This promotes metastasis and T cell accumulation in inflamed tissues.
Area of Science:
- Immunology
- Molecular Biology
- Oncology
Background:
- Endothelial cells in inflammation and cancer regulate organ access.
- CD95L is overexpressed on endothelial cells in cancer and lupus.
- CD95 and CD95L are implicated in immune homeostasis, autoimmune disorders, and cancer.
Purpose of the Study:
- To discuss the roles of CD95 in modulating immune functions.
- To highlight the non-apoptotic signaling pathways induced by CD95.
- To explore the contribution of CD95L to disease severity in cancer and autoimmune disorders.
Main Methods:
- Analysis of CD95L expression in cancer and lupus patient samples.
- Investigation of soluble CD95L (s-CD95L) in serum.
- Examination of CD95-mediated non-apoptotic signaling pathways.
Main Results:
- Soluble CD95L is overexpressed in serum from patients with triple-negative breast cancer or SLE.
- Elevated s-CD95L contributes to disease severity by activating non-apoptotic pathways.
- s-CD95L promotes metastatic dissemination and T cell accumulation in inflamed organs.
Conclusions:
- CD95 plays a critical role in modulating immune functions primarily through non-apoptotic signaling.
- CD95L, particularly its soluble form, is a key mediator of disease severity in conditions like breast cancer and SLE.
- Targeting CD95-mediated non-apoptotic pathways may offer therapeutic strategies for cancer and autoimmune diseases.
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