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Extracorporeal Photochemotherapy (Photopheresis) Induces Apoptosis in Lymphocytes: A Possible Mechanism of Action of PUVA Therapy
Author(s) -
Enomoto Dory N. H.,
Schellekens Peter T. A.,
Yong SiLa,
Berge Ineke J. M.,
Mekkes Jan R.,
Bos Jan D.
Publication year - 1997
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1997.tb01895.x
Subject(s) - photopheresis , apoptosis , puva therapy , extracorporeal photopheresis , dna fragmentation , psoralen , methoxsalen , medicine , immunology , mechanism of action , programmed cell death , dna , biology , pathology , psoriasis , biochemistry , in vitro , disease , lymphoma , graft versus host disease
— The mechanism of action of psoralen plus UVA (PUVA) and photopheresis is not entirely understood. These therapies are assumed to be immunomodulating partly by gradually decreasing leukocyte viability. We investigated whether this delayed form of cell death was due to apoptosis. Untreated and treated (PUVA exposed) leukocytes obtained from six patients with systemic sclerosis and (untreated) leukocytes from healthy control individuals were studied. Qualitative gel electrophoresis and quantitative in situ nick translation analysis of DNA fragmentation was performed. Apoptosis of the treated cells did occur (gel electrophoresis) after 24 h. At t = 0 h, immediately after exposure to PUVA, there was no evidence of DNA fragmentation in the treated cells. The percentage of treated cells undergoing apoptosis was 20–55% at t = 24 h ( in situ nick translation). The untreated leukocytes of the patients and the healthy individuals showed no distinctive rise in apoptotic cells. Apoptosis of the leukocytes after PUVA or photopheresis treatment might be a mechanism of action and might explain the therapeutic response.

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