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Complement receptor type 1 (CR1) deficiency on neutrophils in myelodysplastic syndrome
Author(s) -
Ohsaka Akimichi,
Saionji Katsu,
Watanabe Norimichi,
Yokomichi Hironao,
Sugahara Yuichi,
Nagayama Reizo,
Igari Jun
Publication year - 1994
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1994.tb05042.x
Subject(s) - complement (music) , medicine , myelodysplastic syndromes , complement component 5 , immunology , complement system , biology , antibody , genetics , bone marrow , phenotype , gene , complementation
Summary. We present a patient with myelodysplastic syndromes (MDS) whose neutrophils exhibited defective expression of complement receptor type 1 (CR1). A 73‐year‐old man was admitted with an evolution of MDS from RA into RAEBT according to the FAB classification of MDS. The neutrophil alkaline phosphatase (NAP) score was zero. The surface expression of membrance effector melecules on neutrophils was determined by indirect immunofluorescence using flow cytometry and monoclonal antibodies. The expression of CR1 on neutrophils as identified by staining with CD35 was defective in the patient, and the expression of other complement receptors (CR3 and CR4), Fc receptors and adhesion molecules was normal. CR1 deficiency and defective NAP score on neutrophils in the patient might account for impairment of common storage pool, presumably novel intracellular secretory vesicles.