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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Defective antibody-dependent and lectin-induced polymorphonuclear cytotoxicity in patients with myelodysplastic syndromes.

A short-term 51Cr-release assay was employed to investigate polymorphonuclear leukocyte (PMN) antibody-dependent (ADCC) and phytohemaglutinin-induced (PHA-ICC) cytotoxicity against chicken erythrocytes in 28 patients with myelodysplastic syndromes (MDS). MDS patients PMN-mediated ADCC and PHA-ICC were significantly reduced when compared to normal donors. When the patients were subdivided according to the revised FAB classification, a reduction in PHA-ICC from the RAEB group and a progressive impairment of ADCC from RA to RAEB-t patients was observed. These abnormalities may be ascribed to a reduced number of effector cells or to a metabolic impairment of their cytolytic capacity. These PMN functional deficiences may contribute to the increased susceptibility to infectious diseases, irrespective of the presence of granulocytopenia.[1]

References

  1. Defective antibody-dependent and lectin-induced polymorphonuclear cytotoxicity in patients with myelodysplastic syndromes. Fontana, L., De Sanctis, G., Bottari, V., Petti, M.C., Mandelli, F. Haematologica (1990) [Pubmed]
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