Summary. Iron is required for monocyte/macrophage differentiation of HL-60 leukaemia cells. Differentiation requires induction of the cyclin-dependent kinase inhibitor p21 (WAF1/CIP1), and cell cycle arrest at the G1/S checkpoint. With iron depletion, p21 induction and differentiation are blocked. To establish the roles of iron and p21 in normal monocyte/macrophage differentiation, we examined generation of dendritic cells (DCs) and macrophages from peripheral monocytes. Monocytes were cultured with interleukin 4 and granulocyte-macrophage colonystimulating factor (GM-CSF), then treated with lipopolysaccharide to produce DCs or with M-CSF to produce macrophages. Iron deprivation was induced by desferrioxamine (DF). Monocyte-derived DCs had characteristic phenotype and morphology, and stimulated proliferation of naïve allogeneic T lymphocytes. In contrast, DCs generated under iron deprivation were phenotypically undifferentiated and did not stimulate T cells. Similarly, macrophages expressed a characteristic phenotype and morphology, and phagocytosed latex beads, but macrophages generated under iron deprivation failed to develop a mature phenotype and had impaired phagocytosis. Iron deprivation blocked induction of p21 (WAF1/CIP1) expression in both DC and macrophage cultures. Furthermore, p21 antisense oligonucleotides, but not sense oligonucleotides, inhibited both DC and macrophage differentiation. These data indicate that a key role of iron in haematopoiesis is to support induction of p21 which, in turn, is required for DC and macrophage differentiation.

ErrataThe authors of the paper entitled ÔDifferentiation of functional dendritic cells and macrophages from human peripheral blood monocyte precursors is dependent on expression of p21 (WAF1/CIP1) and requires ironÕ published in volume 117, pp. 727-734, have pointed out two errors in the Materials and methods section, as follows:Page 728, column 2, lines 11-12, the primer sequences for PCR should read: 5¢-GAACTTCGACTTTGTCACCGAG-3¢ and 5¢-ATCCCCAGCCGGTTCTGACATGGC-3¢.Page 728, column 2, lines 16-17, the sequence and text should read: 5¢-ATCCCCAGCCGGTTCTGACATGGC-3¢ corresponding to bp )3 to bp +21 relative to ATG.The authors of the paper entitled ÔIdentification of a novel promoter mutation in the human pyruvate kinase (PK) L/R gene of a patient with severe haemolytic anaemiaÕ published in the British Journal of Haematology volume 105, pp. 596-598, have pointed out an error in the reported sequence of the pyruvate kinase promoter of a deficient patient.The paper described the identification of a promoter mutation )249delA in the human pyruvate kinase (PK) L/R gene of a German patient with severe haemolytic anaemia due to PK deficiency. In further analyses with blood from the patient and his parents, which is now available, it was discovered that the sequence of the PK promoter of the deficient patient as reported was incorrect. The mutation named )249delA was, in fact, a )248T delete PK promoter polymorphism. The DNA from the family also contained two other PK promoter mutations, previously reported by van Solinge et al. In cooperation with Professor E. Beutler, The Scripps Research Institute, La Jolla, USA, we worked on elucidating the correct structure. He re-examined and confirmed our results by sequence analysis and allelespecific oligonucleotide hybridization. The results of all three PK positions are as follows:Mother: )324 T/A )248Tdel/wt )83 G/C Father: )324 T/T 248Twt/wt )83 G/G Patient: )324 T/A )248Tdel/wt )83 G/C Consequently, the conclusion drawn from our RT-PCR analysis (Fig. 2) has to be modified. Our current understanding is that the )248Tdel mutation is not of functional significance and, instead, the )83 G/C mutation is responsible for the reduction in mRNA synthesis. This was corroborated by reporter gene assays using the different mutated PK promoters in front of the gene for secreted alkaline phosphatase (SEAP). Only the promoter construct harbouring the )83 G/C mutation reduced the activity of the SEAP gene in K562 cells. These errors have, however, no consequence for the patient.The authors of the paper entitled ÔTrisomy 3 in two paediatric post-transplant lymphomasÕ published in volume 117, pp. 558-562, wish to point out that Fig. 4(B) was reproduced without the relevant modifications. The revised figure is shown below.