1999
DOI: 10.1016/s0190-9622(99)70257-4
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Extracorporeal photochemotherapy does not suppress T- or B-cell responses to novel or recall antigens

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Cited by 77 publications
(59 citation statements)
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“…Although these diseases are extremely heterogeneous clinically, they share similar underlying pathophysiological mechanisms and response to immunosuppressive therapies. It is unlikely that ECP induces a generalized immunosuppression because patients, including those undergoing long-term ECP therapy, have no reported higher risk of developing infections or malignancies (9) and respond normally to both novel and recall Ag (10). More recently, it has been suggested that ECP may induce Ag-specific immunomodulation, possibly via regulatory T cells (Tr) (11).…”
mentioning
confidence: 99%
“…Although these diseases are extremely heterogeneous clinically, they share similar underlying pathophysiological mechanisms and response to immunosuppressive therapies. It is unlikely that ECP induces a generalized immunosuppression because patients, including those undergoing long-term ECP therapy, have no reported higher risk of developing infections or malignancies (9) and respond normally to both novel and recall Ag (10). More recently, it has been suggested that ECP may induce Ag-specific immunomodulation, possibly via regulatory T cells (Tr) (11).…”
mentioning
confidence: 99%
“…In fact, patients receiving ECP respond normally to new immune challenges such as exposure to pathogens or vaccines. 61 ECP in patients with GVHD does not result in an increased incidence of malignant relapse, and patients undergoing long-term ECP therapy for CTCL and scleroderma do not develop the infections or secondary malignancies that are associated with conventional immunosuppressants. 62,63 Because intravenous access is required to perform ECP, patients are at risk for catheter-related complications including infection and thrombosis.…”
Section: Discussionmentioning
confidence: 99%
“…Considering the delayed clinical responses observed, mechanisms other than the central role of depleting pathogenic T-cell clones may exist. In light of the facts that the standard schedule involves one to two courses weekly for few weeks [5], and that GVHD-treated patients are still able to respond to immune challenges from pathogens or vaccines [6], the key mechanism appears to be an immunomodulation rather than an immunodepletion. made in humans because these studies do not reflect the pathological history of patients, or immune dysregulation during reconstitution, or chronic immunosuppressive drugs for GVHD prevention, or microbial pressure.…”
Section: Mechanisms Of Action For Ecp: From T Lymphocytes Apoptosis Tmentioning
confidence: 99%