Expression of the complement receptors cr1 and cr3 and the type iii fcγ receptor on neutrophils from newborn infants and from fetuses with rh disease

Expression of the complement receptors cr1 and cr3 and the type iii fcγ receptor on neutrophils from newborn infants and from fetuses with rh disease


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ABSTRACT ABSTRACT: Developmental defects in neutrophil function, including diminished expression of plasma membrane receptors, may play an important role in the susceptibility of the newborn


infant to infection. We used monoclonal antibodies and flow cytometry to study the expression of complement receptor type one (CR1), complement receptor type three (CR3), and Fcγ receptor


type three (FcRIII) on neutrophils from six fetuses with Rh disease, 10 preterm infants, nine term infants, and nine adults. Expression of the complement receptors on unstimulated cells was


similar for all groups, but significant diffences in complement receptor expression were observed after stimulation with _N_-formyl-methionyl-leucyl-phenylalanine (FMLP). Fetal, preterm, and


term infant neutrophils expressed less CR3 than FMLP-stimulated neutrophils of adults [61 ± 2, 48 ± 4, and 66 ± 4% (mean ± SEM) of the mean for adults, _p_ < 0.05]. FMLP-stimulated CR1


expression for these groups was 61 ± 6, 73 ± 6, and 91 ± 9% of the adult mean (_p_ < 0.05, fetal _versus_ term infant and adult). Expression of both CR3 and CR1 increased with


postconceptional age in the infants (_r_2 = 0.49, _p_ < 0.001 for CR3; _r_2 = 0.23, _p_ < 0.05 for CR1). Neutrophils of the preterm and term infants expressed less FcRIII than adult


neutrophils (68 ± 10 and 77 ± 7% of the adult mean, _p_ < 0.05, for FMLP-stimulated cells), whereas fetal neutrophil FcRIII expression did not differ from that of the adult. The


fluorescence distributions showed a peak for eosinophils that was distinct from the FMLP-stimulated neutrophil peak, allowing separate analysis for the two cell types. Eosinophils


constituted an unexpectedly large proportion of granulocytes in fetuses with Rh disease, averaging 61% of granulocytes in seven specimens at 20 to 26 wks gestation and 37% in 11 specimens at


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EXPRESSION IN HUMAN MYELOID CELLS UNDERGOING APOPTOSIS AND DIFFERENTIATION Article Open access 19 August 2022 ARTICLE PDF AUTHOR INFORMATION AUTHORS AND AFFILIATIONS * Departments of


Pediatrics, University of Pennsylvania School of Medicine, Children's Hospital of Philadelphia and Pennsylvania Hospital, Philadelphia, 19104, Pennsylvania Jeffrey B Smith, Donald E


Campbell, Richard A Polin, Steven D Douglas, Ben-zion Garty & Mary Catherine Harris * Obstetrics and Gynecology, University of Pennsylvania School of Medicine, Children's Hospital


of Philadelphia and Pennsylvania Hospital, Philadelphia, 19104, Pennsylvania Abraham Ludomirsky * Department of Pediatrics, UCLA School of Medicine, UCLA Center for the Health Sciences, Los


Angeles, 90024, California Jeffrey B Smith Authors * Jeffrey B Smith View author publications You can also search for this author inPubMed Google Scholar * Donald E Campbell View author


publications You can also search for this author inPubMed Google Scholar * Abraham Ludomirsky View author publications You can also search for this author inPubMed Google Scholar * Richard A


Polin View author publications You can also search for this author inPubMed Google Scholar * Steven D Douglas View author publications You can also search for this author inPubMed Google


Scholar * Ben-zion Garty View author publications You can also search for this author inPubMed Google Scholar * Mary Catherine Harris View author publications You can also search for this


author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Smith, J., Campbell, D., Ludomirsky, A. _et al._ Expression of the


Complement Receptors CR1 and CR3 and the Type III Fcγ Receptor on Neutrophils from Newborn Infants and from Fetuses with Rh Disease. _Pediatr Res_ 28, 120–126 (1990).


https://doi.org/10.1203/00006450-199008000-00009 Download citation * Received: 01 January 1989 * Accepted: 27 March 1990 * Issue Date: 01 August 1990 * DOI:


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