<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>8(12)</volume><submitter>Low HZ</submitter><pubmed_abstract>LILRA3 is the sole soluble member of the LILR family. Previous studies from our group had shown that a 6.7 kb genetic deletion of LILRA3 is associated with MS and Sjögren's syndrome. An impairment of the immune response leads to a predisposition for B-NHL, so we wanted to study whether the deletion of LILRA3 is also a risk factor for B-NHL, as well as the function of LILRA3. We discovered that the frequency of the homozygous LILRA3 deletion was significantly higher in B-NHL (6%) than in blood donors (3%) (P = 0.03). We detected binding of fluorochrome-conjugated recombinant LILRA3 to monocytes and B-cells. Incubation of PBMCs with recombinant LILRA3 induced proliferation of CD8(+) T-cells and NK cells, as determined by CFSE staining. Using a transwell system, we demonstrated that LILRA3-st</pubmed_abstract><journal>PloS one</journal><pagination>e81360</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3867304</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Association of the LILRA3 deletion with B-NHL and functional characterization of the immunostimulatory molecule.</pubmed_title><pmcid>PMC3867304</pmcid><pubmed_authors>Peest D</pubmed_authors><pubmed_authors>Schmidt RE</pubmed_authors><pubmed_authors>Witte T</pubmed_authors><pubmed_authors>Matthias T</pubmed_authors><pubmed_authors>Stripecke R</pubmed_authors><pubmed_authors>Topperwien M</pubmed_authors><pubmed_authors>Dankenbrink N</pubmed_authors><pubmed_authors>Low HZ</pubmed_authors><pubmed_authors>Reuter S</pubmed_authors><pubmed_authors>Kabalak G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Association of the LILRA3 deletion with B-NHL and functional characterization of the immunostimulatory molecule.</name><description>LILRA3 is the sole soluble member of the LILR family. Previous studies from our group had shown that a 6.7 kb genetic deletion of LILRA3 is associated with MS and Sjögren's syndrome. An impairment of the immune response leads to a predisposition for B-NHL, so we wanted to study whether the deletion of LILRA3 is also a risk factor for B-NHL, as well as the function of LILRA3. We discovered that the frequency of the homozygous LILRA3 deletion was significantly higher in B-NHL (6%) than in blood donors (3%) (P = 0.03). We detected binding of fluorochrome-conjugated recombinant LILRA3 to monocytes and B-cells. Incubation of PBMCs with recombinant LILRA3 induced proliferation of CD8(+) T-cells and NK cells, as determined by CFSE staining. Using a transwell system, we demonstrated that LILRA3-st</description><dates><release>2013-01-01T00:00:00Z</release><publication>2013</publication><modification>2025-04-21T16:59:34.798Z</modification><creation>2019-03-26T23:17:24Z</creation></dates><accession>S-EPMC3867304</accession><cross_references><pubmed>24363809</pubmed><doi>10.1371/journal.pone.0081360</doi></cross_references></HashMap>