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The prevailing concept is that gestational alloimmune liver disease (GALD) is caused by maternal antibodies targeting a currently unknown antigen on the liver of the fetus. This leads to deposition of complement on the fetal hepatocytes and death of the fetal hepatocytes and extensive liver injury. In many cases, the newborn dies. In subsequent pregnancies early treatment of the woman with intravenous immunoglobulin can be instituted, and the prognosis for the fetus will be excellent. Without treatment the prognosis can be severe. Crucial improvements of diagnosis require identification of the target antigen. For this identification, this work was based on two hypotheses: 1. The GALD antigen is exclusively expressed in the fetal liver during normal fetal life in all pregnancies; 2. The GALD antigen is an alloantigen expressed in the fetal liver with the woman being homozygous for the minor allele and the father being, most frequently, homozygous for the major allele. We used three different experimental approaches to identify the liver target antigen of maternal antibodies from women who had given birth to a baby with the clinical GALD diagnosis: 1. Immunoprecipitation of antigens from either a human liver cell line or human fetal livers by immunoprecipitation with maternal antibodies followed by mass spectrometry analysis of captured antigens; 2. Construction of a cDNA expression library from human fetal liver mRNA and screening about 1.3 million recombinants in Escherichia coli using antibodies from mothers of babies diagnosed with GALD; 3. Exome/genome sequencing of DNA from 26 presumably unrelated women who had previously given birth to a child with GALD with husband controls and supplementary HLA typing. In conclusion, using the three experimental approaches we did not identify the GALD target antigen and the exome/genome sequencing results did not support the hypothesis that the GALD antigen is an alloantigen, but the results do not yield basis for excluding that the antigen is exclusively expressed during fetal life., which is the hypothesis we favor.

Purpose A large proportion of the European Union’s tomato crop is discarded during harvesting and there is a valorisation potential to recover proteins from this waste. Methods Cherry tomatoes were segregated into three separate components: juice, pomace (peels and skins), and seeds. The peels and skins, and seeds were separately hydrolyzed with carbohydrases to determine whether protein recovery could be increased. In addition, a strategy to fractionate the seeds was developed using sequential washing of milled tomato seeds, followed by low-speed centrifugation to remove the denser seed hulls and to collect the protein rich kernels remaining in suspension. Results The protein content of the seeds was highest with 27.4% while the peels and skins contained 7.6%. Carbohydrase mediated hydrolysis resulted in a minor increase in protein recovery of 10% from seeds using Filta 02L (cellulase, xylanase and β-glucanase), and the quantity of protein recovered from peels and skins increased by 210% using Tail 157 (pectinase, hemicellulase). The strategy to separate the seeds into two fractions, revealed that a higher proportion of the fibre (65%) was associated with the hull fraction compared with the original seeds (47%). A significant proportion of the fibre in this fraction was composed of lignin although the protein contents between both fractions was similar ranging from 27.4 to 29.9%. Conclusions These results reveal that carbohydrases were quite effective in protein extraction from peels and skins, but not from seeds. An alternative strategy was developed to remove the seed hulls from the milled seeds and to collect a fraction containing protein and dietary fibre where oil could be removed at this stage. Graphical Abstract