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Analysis of PI (phosphatidylinositol)‐anchoring antigens in a patient of paroxysmal nocturnal hemoglobinuria (PNH) reveals deficiency of 1F5 antigen (CD59), a new complement‐regulatory factor
Author(s) -
Taguchi Ryo,
Funahashi Yasuhiro,
Ikezawa Hiroh,
Nakashima Izumi
Publication year - 1990
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(90)80656-4
Subject(s) - paroxysmal nocturnal hemoglobinuria , cd59 , antigen , decay accelerating factor , immunology , complement component 5 , biology , complement system , antibody
FACS analysis together with PIPLC treatment was applied to Pi‐anchoring antigens such as DAF (decay‐accerelating factor, CD55), 1F5 antigen (CD59), CD14 and CD16 on the cell surfaces of blood cells from a normal adult and a male patient with paroxysmal nocturnal hemoglubinuria (PNH). Through the extensive analysis, this patient proved to be completely defective in 1F5 antigen, a newly found complement‐regulatory protein, on all the blood cells tested. In normal blood cells such as lymphocytes, monocytes and granulocytes, 1F5 antigen was expressed as one of PI‐anchoring proteins. In contrast to most of PNH patients, this patient reserved DAF, CD14 and CD16 at normal levels in his erythrocytes, monocytes and granulocytes. Also, there were no significant differences between the normal adult and the patient in the activities of erythrocyte acetylchol‐inesterase and granulocyte alkaline phosphatase which were also known to be PI‐anchoring enzymes. Thus, deficiency of 1F5 antigen must be deeply related to the clinical symptoms of PNH in this patient.