Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In man, three distinct classes of receptors for the Fc fragments of IgG (FcRI, II, III) have been defined. The FcRI has a Mr of about 72 kDa, binds human IgG-coated E, and is recognized by mAb such as 32. The FcRII has a Mr of 40 kDa, binds murine IgG1-coated E, and reacts with the mAb IV.3 and CIKM5, which recognize CDw32 moieties. Lastly, the FcRIII has a Mr of 50 to 70 kDa and is recognized by anti-CD16 mAb. In the present study we have shown that i) only murine IgG1-coated E form rosettes with 49 +/- 1.5% (mean +/- SEM, n = 9) of CD1a+ epidermal cells (EC) (which represent Langerhans and indeterminate cells) and that ii) the mAb anti-FcRII CIKM5 prevents this rosette formation. Among the mAb reacting with the three different types of FcR, only those recognizing FcRII i) stain about 55 +/- 1.5% (mean +/- SEM, n = 9) of the CD1a+ EC and ii) reveal the presence of dendritic cells in epidermal sheets obtained by suction blister. Under the electron microscope i) apparently all the cells forming rosettes or reacting with the gold-labeled anti-FcRII mAb (CIKM5 or the F(ab) fragment of IV.3) contained Birbeck granules and ii) the gold-labeled mAb were internalized in unfixed Langerhans cells by receptor-mediated endocytosis and accumulated in lysosomes. Labeling by the anti-FcRII mAb of the CD1a+ cells in suspension disappears after 48 h of culture. All these observations strongly suggest that CD1a+ EC express only the FcRII. This conclusion was confirmed by immunoprecipitation experiments, whereas no specific immunoprecipitate was noted with the anti-FcRI or anti-FcRIII mAb, the anti-FcRII mAb immunoprecipitated a protein of Mr 40 kDa.
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PMID:Human epidermal Langerhans cells express only the 40-kilodalton Fc gamma receptor (FcRII). 214 Mar 93

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 Fc gamma 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 differences 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 less than 0.05]. FMLP-stimulated CR1 expression for these groups was 61 +/- 6, 73 +/- 6, and 91 +/- 9% of the adult mean (p less than 0.05, fetal versus term infant and adult). Expression of both CR3 and CR1 increased with postconceptional age in the infants (r2 = 0.49, p less than 0.001 for CR3; r2 = 0.23, p less than 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 less than 0.05, for FMLP-stimulated cells), whereas fetal neutrophil FcRIII expression did not differ from that of the adult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of the complement receptors CR1 and CR3 and the type III Fc gamma receptor on neutrophils from newborn infants and from fetuses with Rh disease. 214 35

This study measured Fc gamma receptor (FcR) expression on polymorphonuclear leukocytes (PMN) and monocytes from extremely premature infants. Flow cytometry was used to quantitate FcRIII [cluster of differention (CD) 16], FcRII (CD32), FcRI (CD64), CD14, and CD67 proteins on the PMN surface. Sixty-four premature infants with a mean gestational age +/- SD of 26 +/- 2 wk (birth weight = 847 +/- 217 g), 12 infants born at term (gestational age = 38 +/- 1 wk), and 37 adults were studied. Premature infants' PMN expressed less FcRIII, measured as mean log channel fluorescence (MCF), than did term infants or adults (MCF = 4.7 +/- 1.4, 6.1 +/- 1.0, and 8.8 +/- 1.8, respectively, p < 0.050). Premature infants also had a lower proportion of FcRIII-positive PMN than term infants or adults (mean +/- SEM = 0.83 +/- 0.02 versus 0.92 +/- 0.04 and 0.96 +/- 0.01, respectively, p < 0.050). FcRIII expression on PMN was positively associated with cell isolation procedures (p = 0.004), birth weight (p = 0.004), and postnatal age (p = 0.032). Premature infants also had lower PMN expression of FcRII when compared with adults and term infants (MCF = 2.4 +/- 0.6 versus 3.0 +/- 0.7 and 3.1 +/- 0.3, p < 0.050). Both premature and term infants had fewer FcRII positive PMN than did adults (mean +/- SEM = 0.90 +/- 0.09 and 0.89 +/- 0.07 versus 0.99 +/- 0.00, p < 0.050). Premature infants' monocytes also expressed significantly less FcRIII (MCF = 2.4 +/- 0.6 versus 3.4 +/- 0.9, p = 0.047) and FcRII (2.1 +/- 0.5 versus 2.9 +/- 0.6, p = 0.01) compared with adults. We conclude that extremely premature infants have decreased expression of FcRIII and FcRII on both their PMN and monocytes when compared with adults. The decrease in PMN FcRIII expression appears related to birth weight and chronologic age.
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PMID:Cell-surface expression of immunoglobulin G receptors on the polymorphonuclear leukocytes and monocytes of extremely premature infants. 768 16