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First-pass extracted concept

Fas receptor

Candidate: concept label1 source documents3 linked claims
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Aliases

Apo-1, CD95, Fas

Extracted Explainers

What the tool is doing

Fas/CD95 is the receptor component of the pathway discussed throughout the review. The abstract frames Fas-sensitive target T cells as susceptible to apoptosis triggered by FasL.

Source 1DOIPubMed

Resources required

Use of this concept requires a system in which Fas expression or Fas sensitivity is relevant. The abstract also references Fas-blocking monoclonal antibody as a way to interrupt the pathway.

Source 1DOIPubMed

What problem it solves

It helps explain how FasL-expressing cells can trigger apoptosis in target immune cells and thereby contribute to immune regulation or tumor escape.

Source 1DOIPubMed

What it does not solve

The abstract does not establish Fas as a standalone engineering tool or therapeutic modality. It also notes that downregulation of Fas was not required in the reported myeloma setting.

Source 1DOIPubMed

Alternatives

The abstract contrasts this mechanism with other tumor contexts where Fas downregulation or intrinsic Fas insensitivity had been implicated.

Source 1DOIPubMed

Evidence Snippets

The title explicitly names Fas (Apo-1/CD95), and the abstract discusses the Fas receptor/ligand system and Fas-sensitive target T cells.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1comparative mechanism summarysupports1998Source 1DOIPubMed

The review states that, in Fas-sensitive multiple myeloma cell lines, downregulation of Fas or intrinsic insensitivity to Fas-mediated signaling were not prerequisites for the reported evasive mechanism.

Claim 2mechanistic interference summarysupports1998Source 1DOIPubMed

Blocking Fas on target T cells or neutralizing FasL on myeloma cells protects target T cells from programmed cell death, supporting Fas/FasL-mediated signaling as the effector pathway in the described myeloma system.

Claim 3review scope summarysupports1998Source 1DOIPubMed

The review presents Fas/FasL signaling as a mechanism involved in immune privilege and also as a potential tumor immune escape strategy.