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ABSTRACT: To synthesize and identify the hapten and complete antigens for Zearalenone for the purpose of preparation of anti-Zearalenone antibodies.
Zearalenone and carboxymethoxylamine hemihydrochloride were incubated to synthesize the hapten ZEN-oxime. The ZEN-oxime was identified by thin layer chromatography (TLC), high performance liquid chromatographic (HPLC) and liquid chromatography-tandem mass spectrometry (LC-MSn). The ZEN-oxime was further conjugated to bovine serum albumin (BSA) or ovalbumin (OVA) to form the complete antigens by NHS ester method. The complete antigens were identified by ultraviolet spectrum, 2, 4, 6-trinitrobenzene sulfonicacid method (TNBS) and immunological analysis.
The results indicated that the hapten and complete antigens were prepared successfully.
The hapten and complete antigens for Zearalenone have been successfully synthesized and identified by several methods, which enables further preparation of anti-Zearalenone antibodies.
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 09/2011; 27(9):975-8.
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ABSTRACT: Sialic-acid-binding immunoglobulin-like lectins, siglecs, are important immune receptors expressed widely in mammals. A unique feature of siglecs is their ability to bind sialylated glycans and transmit signals to immune cells. The CD33-related siglecs (CD33rSiglecs) form a major subfamily of the siglecs, containing a large, rapidly evolving group of genes that expanded in mammals through an inverse duplication event involving a primordial cluster of siglec genes over 180 million years ago. Humans express a much larger set of CD33rSiglecs than mice and rats, a feature that can be explained by a dramatic loss of CD33rSiglec genes in rodents. Most CD33rSiglecs have immune receptor tyrosine-based inhibitory motifs and signal negatively. Interestingly, novel DAP-12-coupled 'activating' CD33rSiglecs have been identified, such as siglec-14 and siglec-16, which are paired with the inhibitory receptors, siglec-5 and siglec-11, respectively. The evolution of these activating receptors may have been driven in part by pathogen exploitation of inhibitory siglecs, thereby providing the host with additional pathways by which to combat these pathogens. Inhibitory siglecs seem to play important and varied roles in the regulation of host immune responses. For example, several CD33rSiglecs have been implicated in the negative regulation of Toll-like receptor signalling during innate responses; siglec-G functions as a negative regulator of B1-cell expansion and appears to suppress inflammatory responses to host-derived 'danger-associated molecular patterns'. Recent work has also shown that engagement of neutrophil-expressed siglec-9 by certain strains of sialylated Group B streptococci can suppress killing responses, thereby providing experimental support for pathogen exploitation of host CD33rSiglecs.
Immunology 11/2010; 132(1):18-26. · 3.32 Impact Factor
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ABSTRACT: The CD33-related sialic acid binding Ig-like lectins (CD33rSiglecs) are predominantly inhibitory receptors expressed on leukocytes. They are distinguishable from conserved Siglecs, such as Sialoadhesin and MAG, by their rapid evolution. A comparison of the CD33rSiglec gene cluster in different mammalian species showed that it can be divided into subclusters, A and B. The two subclusters, inverted in relation to each other, each encode a set of CD33rSiglec genes arranged head-to-tail. Two regions of strong correspondence provided evidence for a large-scale inverse duplication, encompassing the framework CEACAM-18 (CE18) and ATPBD3 (ATB3) genes that seeded the mammalian CD33rSiglec cluster. Phylogenetic analysis was consistent with the predicted inversion. Rodents appear to have undergone wholesale loss of CD33rSiglec genes after the inverse duplication. In contrast, CD33rSiglecs expanded in primates and many are now pseudogenes with features consistent with activating receptors. In contrast to mammals, the fish CD33rSiglecs clusters show no evidence of an inverse duplication. They display greater variation in cluster size and structure than mammals. The close arrangement of other Siglecs and CD33rSiglecs in fish is consistent with a common ancestral region for Siglecs. Expansion of mammalian CD33rSiglecs appears to have followed a large inverse duplication of a smaller primordial cluster over 180 million years ago, prior to eutherian/marsupial divergence. Inverse duplications in general could potentially have a stabilizing effect in maintaining the size and structure of large gene clusters, facilitating the rapid evolution of immune gene families.
Immunogenetics 05/2009; 61(5):401-17. · 2.93 Impact Factor
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ABSTRACT: Sialic acid binding immunoglobulin-like lectins (Siglec) are important components of immune recognition. The organization of Siglec genes in different species is consistent with rapid selection imposed by pathogens. We studied SIGLEC11 genes in human, rodent, dog, cow and non-human primates. The lineages of SIGLEC11 genes in these species have undergone dynamic gene duplication and conversion, forming a potential inhibitory (SIGLEC11)/activating (SIGLEC16) receptor pair in chimpanzee and humans. A cDNA encoding human Siglec-16, currently classed as a pseudogene in the databases (SIGLECP16), is expressed in various cell lines and tissues. A polymorphism screen for the two alleles (wild type and four-base pair deletion, 4bpDelta) of SIGLEC16 found their frequencies to be 50% amongst the UK population. A search for donor sequences for SIGLEC16 revealed a subfamily of activating Siglec with charged transmembrane domains predicted to associate with ITAM-encoding adaptor proteins. In support of this, Siglec-16 was expressed at the cell surface in the presence of DAP12, but not the FcRgamma chain. Using antisera specific to the cytoplasmic tail of Siglec-16, we identified Siglec-16 expression in CD14(+) tissue macrophages and in normal human brain, cancerous oesophagus and lung. This is the first activating human Siglec receptor found to have functional and non-functional alleles within the population.
European Journal of Immunology 08/2008; 38(8):2303-15. · 5.10 Impact Factor
