N-Acetyl-D-glucosamine-coated polyamidoamine dendrimer modulates antibody formation via natural killer cell activation
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19303462
DOI
10.1016/j.intimp.2009.03.007
PII: S1567-5769(09)00094-0
Knihovny.cz E-resources
- MeSH
- Acetylglucosamine analogs & derivatives chemistry pharmacology MeSH
- Antigens, Ly immunology metabolism MeSH
- B-Lymphocytes drug effects immunology MeSH
- Killer Cells, Natural drug effects immunology MeSH
- Antibody-Producing Cells drug effects immunology MeSH
- Dendrimers chemistry pharmacology MeSH
- Hemocyanins immunology MeSH
- Immunoglobulins blood MeSH
- Immunologic Factors chemistry pharmacology MeSH
- Rats MeSH
- NK Cell Lectin-Like Receptor Subfamily B immunology metabolism MeSH
- Mice, Inbred BALB C MeSH
- Mice, Inbred C57BL MeSH
- Mice, Inbred DBA MeSH
- Mice MeSH
- Natural Killer T-Cells drug effects immunology MeSH
- Antibody Formation drug effects MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acetylglucosamine MeSH
- Antigens, Ly MeSH
- Dendrimers MeSH
- Hemocyanins MeSH
- Immunoglobulins MeSH
- Immunologic Factors MeSH
- keyhole-limpet hemocyanin MeSH Browser
- Klrb1c protein, mouse MeSH Browser
- NK Cell Lectin-Like Receptor Subfamily B MeSH
N-Acetyl-D-glucosamine-coated polyamidoamine dendrimer (GlcNAc8) was shown previously to exhibit binding affinity to the rat recombinant NKR-P1 molecule (known in mice also as NK1.1) and to induce NK cell-mediated cytotoxicity. In this study, we investigated whether GlcNAc8 modulates antibody formation as activated NK cells were reported to participate in its regulation. C57BL/6 mice treated with GlcNAc8 and intact controls were immunized either with sheep red blood cells (SRBCs), 2,4-dinitrophenylated-lipopolysaccharide (DNP-LPS) or keyhole limpet hemocyanin (KLH) for evaluation of splenic antibody forming cell counts and serum immunoglobulin (Ig) levels. In vitro Ig formation was determined using supernatants of spleen mononuclear cells (SMCs) and CD49b or NK1.1-depleted SMC subpopulations. Serum antigen-specific IgG2a levels were also measured in DBA/2 and BALB/c mice (NK1.1-negative mouse strains on the basis of flow cytometric analysis) which possess different Nkr-p1c gene form than C57BL/6 ones. A significant increase in anti-SRBC IgG forming cells, serum levels of anti-KLH as well as anti-DNP IgG and IgG2a was observed after GlcNAc8 administration in C57BL/6 mice. IgM levels in supernatants of SMCs stimulated in vitro simultaneously with DNP-LPS and GlcNAc8 were significantly mounted compared with supernatants of SMCs primed with the antigen alone, but this enhancement was blocked after depletion of CD49b-positive or NK1.1-positive cells. In DBA/2 and BALB/c mice, GlcNAc8 influenced neither serum levels of anti-KLH nor anti-DNP IgG2a. These results indicate that GlcNAc8-induced upregulation of antibody formation is triggered by NK cell stimulation and depends on expressed NKR-P1 isoforms, particularly NKR-P1C.
References provided by Crossref.org
Nkrp1 family, from lectins to protein interacting molecules
