Association of the LILRA3 Deletion with B-NHL and Functional Characterization of the Immunostimulatory Molecule

Hui Zhi Low, Sandra Reuter, Michael Topperwien, Nadine Dankenbrink, Dietrich Peest, Gamze Kabalak, Renata Stripecke, Reinhold E Schmidt, Torsten Matthias and Torsten Witte

PLOS ONE, 2013, vol. 8, issue 12, 1-9

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-stimulated lymphocyte proliferation was mediated by monocytes and required both cell contact and soluble factors. Secretion of IL-6, IL-8, IL-1β and IL-10 in the cell supernatant was stimulated by LILRA3. We conclude that LILRA3 is an immunostimulatory molecule, whose deficiency is associated with higher frequency of B-NHL.

Date: 2013
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Persistent link: https://EconPapers.repec.org/RePEc:plo:pone00:0081360

DOI: 10.1371/journal.pone.0081360

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