Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-6
pubmed:abstractText
The neonatal FcR (FcRn) regulates IgG and albumin homeostasis, mediates maternal IgG transport, takes active part in phagocytosis, and delivers Ag for presentation. We have previously shown that overexpression of FcRn in transgenic (Tg) mice extends the half-life of mouse IgG by reducing its clearance. In this paper, we demonstrate that immunization of these mice with OVA and trinitrophenyl-conjugated human IgG results in a 3- to 10-fold increase of Ag-specific IgM and IgG in serum. The IgM increase was unexpected because FcRn does not bind IgM. Our results showed that the affinity of the Ag-specific IgG was at least as good in Tg mice as in the wild-type (wt) controls, implying appropriate affinity maturation in both groups. Influenza vaccination produced a 2-fold increase in the amount of virus-specific Ab in Tg animals, which proved twice as efficient in a hemagglutination inhibition assay as was the case in wt controls. After immunization, Tg mice displayed significantly larger spleens containing a higher number of Ag-specific B cells and plasma cells, as well as many more granulocytes and dendritic cells, analyzed by ELISPOT and flow cytometric studies. The neutrophils from these Tg mice expressed the Tg FcRn and phagocytosed IgG immune complexes more efficiently than did those from wt mice. These results show that FcRn overexpression not only extends the IgG half-life but also enhances the expansion of Ag-specific B cells and plasma cells. Although both effects increase the level of Ag-specific IgG, the increase in immune response and IgG production seems to be more prominent compared with the reduced IgG clearance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
186
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
959-68
pubmed:meshHeading
pubmed-meshheading:21148035-Animals, pubmed-meshheading:21148035-Antibody Affinity, pubmed-meshheading:21148035-B-Lymphocyte Subsets, pubmed-meshheading:21148035-Cattle, pubmed-meshheading:21148035-Chickens, pubmed-meshheading:21148035-Epitopes, B-Lymphocyte, pubmed-meshheading:21148035-Gene Expression Regulation, pubmed-meshheading:21148035-Histocompatibility Antigens Class I, pubmed-meshheading:21148035-Humans, pubmed-meshheading:21148035-Immunity, Maternally-Acquired, pubmed-meshheading:21148035-Immunoglobulin G, pubmed-meshheading:21148035-Immunoglobulins, pubmed-meshheading:21148035-Male, pubmed-meshheading:21148035-Mice, pubmed-meshheading:21148035-Mice, Inbred BALB C, pubmed-meshheading:21148035-Mice, Transgenic, pubmed-meshheading:21148035-Plasma Cells, pubmed-meshheading:21148035-Protein Binding, pubmed-meshheading:21148035-Receptors, Fc, pubmed-meshheading:21148035-Up-Regulation
pubmed:year
2011
pubmed:articleTitle
Neonatal FcR overexpression boosts humoral immune response in transgenic mice.
pubmed:affiliation
Department of Immunology, Institute of Biology, Faculty of Science, Eötvös Loránd University, Budapest, Hungary.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't