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A protein released by natural killer cells and cytotoxic T lymphocytes that causes lysis of target cells by forming pores in their membranes.

References in periodicals archive ?
Natural killer cells are also cytotoxic by releasing proteins called perforin that form holes in the cell membrane where granzymes enter to destroy the virus inside the cell.
Interferon gamma, perforin, and Fas ligand have been implicated as mechanisms involved in fixed drug reactions.
Moreover, immunohistochemistry showed reactivity for CD99 while the blasts were negative for plasma cell marker, CD138, Langerhans cell marker, CD1a, cytotoxic T cell marker, perforin, pan-B marker, and pax5.
FHL-2 is a result of mutations to the perforin 1 ( PRF1 ) gene, which can occur at numerous sites on the gene.[1]
This is a perforin inhibitor, which stops the killer T-cells from forming pores and thus safeguards the LSECs from attack.
Ganoderma lucidum stimulates NK cell cytotoxicity by inducing NKG2D/NCR activation and secretion of perforin and granulysin.
This vaccine encodes an immunogen and a cytolytic protein (perforin), and has been shown to be significantly more immunogenic than a canonical DNA vaccine (which encodes an alternative immunogen) when delivered via the intradermal route.
Activated CAR T-cells release perforin and granzymes that attack tumour cells directly.
Among the studied genes, perforin and TIM-3 have performed highly in terms of diagnostic accuracy in the mentioned cross-sectional studies (8,10,12,13).
The cells that express perforin regardless of CD8 presence may have a role in controlling the infection.
The most common immunophenotype is a cytotoxic T-cell phenotype (positive for CD3, T-cell receptor [beta] [TCR-[beta]], CD7, and cytotoxic molecules granzyme B, perforin, and TIA-1).
Furthermore, Tregs suppress the pro-inflammatory functions of Teff, such as Th17 ([CD4.sup.+] [RORC2.sup.+]) lymphocytes through various mechanisms such as the local consumption of IL-2; secretion of anti- inflammatory cytokines such as IL-10, IL-35, and TGF-[beta]; inhibition of antigenic presentation; transformation of ATP and ADP to adenosine by surface ectoenzymes (CD39 and CD73), and the controlled release of perforin and granzyme.