{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T23:47:26Z","timestamp":1785800846225,"version":"3.56.0"},"reference-count":41,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,8,2]],"date-time":"2011-08-02T00:00:00Z","timestamp":1312243200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cytometry Part B Clinical"],"published-print":{"date-parts":[[2012,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background:<\/jats:title><jats:p>Immunoglobulins (IVIG) have been shown to be useful in adults suffering from sepsis. In contrast, prophylactic and curative IVIG trials failed to show beneficial effects in neonates. We tested the hypothesis that IVIG, have different effects on monocytes from cord blood (CBMO) and peripheral blood monocytes from adults (PBMO) with respect to survival, phenotype, and function.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods:<\/jats:title><jats:p>Mononuclear cells, or purified monocytes, were cultured in 5% human serum, incubated with polyvalent IVIG (1 mg\/ml), stimulated with green fluorescent protein (GFP)\u2010labeled <jats:italic>Escherichia coli<\/jats:italic> (<jats:italic>E. Coli<\/jats:italic>\u2010GFP), Interferon\u2010\u03b3 (IFN\u2010\u03b3, 50 U\/ml), or the T cell mitogen anti\u2010CD3 monoclonal antibody, \u03b1CD3\u2010mAb, (5 \u03bcg\/ml). Phagocytosis, phenotype, T cell proliferation, and apoptosis were assessed by flow cytometry.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results:<\/jats:title><jats:p>IVIG enhanced phagocytosis in PBMO or CBMO when infected directly after isolation, while IVIG had no effect on monocytes cultured 48 h prior to infection. In contrast to PBMO, IVIG inhibited the IFN\u2010\u03b3 mediated up\u2010regulation of CD80, CD86, and HLA\u2010DR on CBMO. In the presence of IVIG, stimulation with \u03b1CD3 in cord blood enhanced deletion, inhibited blast formation and CD28 up\u2010regulation of T cells (<jats:italic>P<\/jats:italic> &lt; 0.05 vs. T cells from adults). IVIG induced monocyte apoptosis, associated with up\u2010regulation of Annexin V and loss of nuclear DNA, which was more pronounced in CBMO. Although phagocytosis induced cell death (PICD) was lower in CBMO (<jats:italic>P<\/jats:italic> &lt; 0.05 vs. PBMO), the addition of IVIG enhanced PICD levels of CBMO to the extent of PBMO.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions:<\/jats:title><jats:p>IVIG inhibits co\u2010stimulatory receptors and functions of CBMO and induces apoptosis. These findings may be of clinical relevance for the failure of IVIG benefit in neonatal sepsis. \u00a9 2011 International Clinical Cytometry Society<\/jats:p><\/jats:sec>","DOI":"10.1002\/cyto.b.20609","type":"journal-article","created":{"date-parts":[[2011,8,2]],"date-time":"2011-08-02T20:49:52Z","timestamp":1312318192000},"page":"26-34","source":"Crossref","is-referenced-by-count":11,"title":["Differential modulation of cord blood and peripheral blood monocytes by intravenous 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