Anti-neutrophil antibodies in patients with nutritional copper deficiency

Higuchi, Shigenori; Higashi, Akimasa; Nakamura, Takehiko; Yanabe, Y; Matsuda, Ichiro

doi:10.1007/bf01955933

Cited by 21 publications

(12 citation statements)

References 11 publications

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“…In an earlier study, we noted that in patients with severe copper defi ciency antineutrophil antibodies (ANA) were present and some were accompanied by a neutropenia of less than 1.5 x 109/1, and some were without neutropenia. Oral supplementation of copper led to a good recovery [8,9], We describe here our findings in 6 ANA-positive patients with copper deficiency.…”

Section: Introductionmentioning

confidence: 86%

“…The present study was done on 6 serum samples taken from Japa nese patients; 4 were from the patients described in earlier reports [8,9] and 2 were from newly identified patients on a copper-deficient enteral diet for over 12 months. The age of the patients ranged from 15 to 73 years.…”

Section: Patients' Serummentioning

confidence: 99%

“…Antibodies were determined by the indirect immunofluorescence test, according to Verheugt et al [12] with slight modifications as described elsewhere [9]. In brief, normal granulocytes prepared by standard methods [9] or cultured HL-60 cells (1.5 x 106) were incu bated with 10 pi of the patient's serum after prevention of nonspe cific binding with rabbit IgG solution.…”

Section: Detection O F Ana and Anti-hl-60 Cell Antibodiesmentioning

confidence: 99%

“…In brief, normal granulocytes prepared by standard methods [9] or cultured HL-60 cells (1.5 x 106) were incu bated with 10 pi of the patient's serum after prevention of nonspe cific binding with rabbit IgG solution. Following incubation with flu orescein isothiocyanate-labelled goat-antihuman IgG, F(ab')2 anti body, the suspension of granulocytes or HL-60 cells was examined using a flow cytometer.…”

Section: Detection O F Ana and Anti-hl-60 Cell Antibodiesmentioning

confidence: 99%

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Characterization of Antineutrophil Antibodies in Patients with Neutropenia Associated with Nutritional Copper Deficiency

et al. 1995

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Six antineutrophil antibody (ANA)-positive patients with copper deficiency were classified into two groups; those with (group A, n =3) and those without (group B, n = 3) neutropenia. The percent binding of ANA for normal peripheral neutrophils was similar in both groups (8 3.5 ± 7.2 vs. 79.1 ± 10.5%). The percent binding of sera to cultured promyelocytic leukemia cells (HL-60) was increased in group A (from 3.7 ± 3.2 to 12.2 ± 2.3%) but not in group B (from 65.3 ± 21.7 to 40.7 ± 6.3%) after stimulation of HL-60 with DMSO. The stimulated HL-60 cells expressed CD 16 and CD 11b antigens. In the presence of monoclonal antibody for CD 16, the titer of ANA was nil in group A and unchanged in group B. Thus, ANA of patients with neutropenia may recognize mainly the CD 16 antigen, the Fcγ receptor III of neutrophils.

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Section: Introductionmentioning

confidence: 86%

Section: Patients' Serummentioning

confidence: 99%

Section: Detection O F Ana and Anti-hl-60 Cell Antibodiesmentioning

confidence: 99%

Section: Detection O F Ana and Anti-hl-60 Cell Antibodiesmentioning

confidence: 99%

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Characterization of Antineutrophil Antibodies in Patients with Neutropenia Associated with Nutritional Copper Deficiency

et al. 1995

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“…Other potential mechanisms that could result in neutropenia include impaired secretion from the marrow, an early death of progenitor cells in the marrow, reduced life span of the circulating peripheral cells, and redistribution into tissues or organs (16). Higuchi et al (17) detected anti-neutrophil antibodies in the serum of copper-deficient patients, which might indicate a mechanism of neutrophil loss. In addition to a reduced number of circulating neutrophils in copper deficiency, the function of those neutrophils was impaired.…”

Section: Innate Systemmentioning

confidence: 99%

Copper and immunity

Percival

1998

The American Journal of Clinical Nutrition

336

192

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Iron and copper requirements for proliferation and differentiation of a human promyelocytic leukemia cell line (HL‐60)

Sergeant¹,

Johnson²

1995

Journal Cellular Physiology

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Trace mineral deficiencies tend to have profound effects on the integrity of formed blood elements. Anemia and neutropenia are commonly seen in copper (Cu) deficiency. We therefore developed a serum-free medium to examine the trace mineral requirements, in particular iron and Cu, for proliferation and retinoic acid (RA)-induced differentiation of HL-60 cells. This defined medium (DFM) was composed of Iscove's Modified Dulbecco's Medium (IMDM) supplemented with insulin and human apo-transferrin (each at 5 micrograms/ml) and 1.4 microM FeSO4. The iron concentration range for optimal cellular proliferation was narrow (2-3 microM). HL-60 cells could be maintained in DFM for 15 passages with a doubling time of 38-40 hr. The Cu content of IMDM was very low. Thus, by the fourth passage in DFM, the activity of cuproenzymes (cytochrome c oxidase, CCO; and copper-zinc superoxide dismutase, CuZnSOD) began to decline. Supplementation of DFM with CuSO4 (50 nM) restored enzyme activities. Treatment of cells with a Cu chelator (tetrathiomolybdate, 1 microM) rapidly reduced the activities of both CCO and CuZnSOD. Over the Cu concentration range examined (5-350 nM), Cu supplementation had little effect on HL-60 proliferation. Cell retained the ability to differentiate along the granulocytic pathway when treated with RA, but seemed to be less sensitive to the inducing agent except at the highest concentration tested (1 microM). This decreased sensitivity to RA did not seem to be related to the Cu status of the cells but rather to the absence of a component of serum. Indeed, cells grown in DFM regained their sensitivity to RA when allowed to differentiate in IMDM with 5% serum. These data indicate that the processes of growth and terminal differentiation in HL-60 cells are not greatly influenced by Cu. Thus, it seems likely that the insult resulting in neutropenia which is associated with Cu deficiency may occur earlier than the promyelocytic stage. However, the possibility that the mechanisms contributing to neutropenia may be unrelated to primary defects in the biochemistry of neutrophil maturation cannot be ruled out.

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Anti-neutrophil antibodies in patients with nutritional copper deficiency

Cited by 21 publications

References 11 publications

Characterization of Antineutrophil Antibodies in Patients with Neutropenia Associated with Nutritional Copper Deficiency

Characterization of Antineutrophil Antibodies in Patients with Neutropenia Associated with Nutritional Copper Deficiency

Copper and immunity

Iron and copper requirements for proliferation and differentiation of a human promyelocytic leukemia cell line (HL‐60)

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