Pro- and anti-apoptotic CD95 signaling in T cells
<p>Abstract</p> <p>The TNF receptor superfamily member CD95 (Fas, APO-1, TNFRSF6) is known as the prototypic death receptor in and outside the immune system. In fact, many mechanisms involved in apoptotic signaling cascades were solved by addressing consequences and pathways initia...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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BMC
2011-04-01
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| Series: | Cell Communication and Signaling |
| Online Access: | http://www.biosignaling.com/content/9/1/7 |
| _version_ | 1818207510988849152 |
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| author | Janssen Ottmar Paulsen Maren |
| author_facet | Janssen Ottmar Paulsen Maren |
| author_sort | Janssen Ottmar |
| collection | DOAJ |
| description | <p>Abstract</p> <p>The TNF receptor superfamily member CD95 (Fas, APO-1, TNFRSF6) is known as the prototypic death receptor in and outside the immune system. In fact, many mechanisms involved in apoptotic signaling cascades were solved by addressing consequences and pathways initiated by CD95 ligation in activated T cells or other "CD95-sensitive" cell populations. As an example, the binding of the inducible CD95 ligand (CD95L) to CD95 on activated T lymphocytes results in apoptotic cell death. This activation-induced cell death was implicated in the control of immune cell homeostasis and immune response termination. Over the past years, however, it became evident that CD95 acts as a dual function receptor that also exerts anti-apoptotic effects depending on the cellular context. Early observations of a potential non-apoptotic role of CD95 in the growth control of resting T cells were recently reconsidered and revealed quite unexpected findings regarding the costimulatory capacity of CD95 for primary T cell activation. It turned out that CD95 engagement modulates TCR/CD3-driven signal initiation in a dose-dependent manner. High doses of immobilized CD95 agonists or cellular CD95L almost completely silence T cells by blocking early TCR-induced signaling events. In contrast, under otherwise unchanged conditions, lower amounts of the same agonists dramatically augment TCR/CD3-driven activation and proliferation. In the present overview, we summarize these recent findings with a focus on the costimulatory capacity of CD95 in primary T cells and discuss potential implications for the T cell compartment and the interplay between T cells and CD95L-expressing cells including antigen-presenting cells.</p> |
| first_indexed | 2024-12-12T04:30:05Z |
| format | Article |
| id | doaj.art-34bb2e728406439c91e43824da064b51 |
| institution | Directory Open Access Journal |
| issn | 1478-811X |
| language | English |
| last_indexed | 2024-12-12T04:30:05Z |
| publishDate | 2011-04-01 |
| publisher | BMC |
| record_format | Article |
| series | Cell Communication and Signaling |
| spelling | doaj.art-34bb2e728406439c91e43824da064b512022-12-22T00:38:05ZengBMCCell Communication and Signaling1478-811X2011-04-0191710.1186/1478-811X-9-7Pro- and anti-apoptotic CD95 signaling in T cellsJanssen OttmarPaulsen Maren<p>Abstract</p> <p>The TNF receptor superfamily member CD95 (Fas, APO-1, TNFRSF6) is known as the prototypic death receptor in and outside the immune system. In fact, many mechanisms involved in apoptotic signaling cascades were solved by addressing consequences and pathways initiated by CD95 ligation in activated T cells or other "CD95-sensitive" cell populations. As an example, the binding of the inducible CD95 ligand (CD95L) to CD95 on activated T lymphocytes results in apoptotic cell death. This activation-induced cell death was implicated in the control of immune cell homeostasis and immune response termination. Over the past years, however, it became evident that CD95 acts as a dual function receptor that also exerts anti-apoptotic effects depending on the cellular context. Early observations of a potential non-apoptotic role of CD95 in the growth control of resting T cells were recently reconsidered and revealed quite unexpected findings regarding the costimulatory capacity of CD95 for primary T cell activation. It turned out that CD95 engagement modulates TCR/CD3-driven signal initiation in a dose-dependent manner. High doses of immobilized CD95 agonists or cellular CD95L almost completely silence T cells by blocking early TCR-induced signaling events. In contrast, under otherwise unchanged conditions, lower amounts of the same agonists dramatically augment TCR/CD3-driven activation and proliferation. In the present overview, we summarize these recent findings with a focus on the costimulatory capacity of CD95 in primary T cells and discuss potential implications for the T cell compartment and the interplay between T cells and CD95L-expressing cells including antigen-presenting cells.</p>http://www.biosignaling.com/content/9/1/7 |
| spellingShingle | Janssen Ottmar Paulsen Maren Pro- and anti-apoptotic CD95 signaling in T cells Cell Communication and Signaling |
| title | Pro- and anti-apoptotic CD95 signaling in T cells |
| title_full | Pro- and anti-apoptotic CD95 signaling in T cells |
| title_fullStr | Pro- and anti-apoptotic CD95 signaling in T cells |
| title_full_unstemmed | Pro- and anti-apoptotic CD95 signaling in T cells |
| title_short | Pro- and anti-apoptotic CD95 signaling in T cells |
| title_sort | pro and anti apoptotic cd95 signaling in t cells |
| url | http://www.biosignaling.com/content/9/1/7 |
| work_keys_str_mv | AT janssenottmar proandantiapoptoticcd95signalingintcells AT paulsenmaren proandantiapoptoticcd95signalingintcells |