Association of the LILRA3 deletion with B-NHL and functional characterization of the immunostimulatory molecule.
Association of the LILRA3 deletion with B-NHL and functional characterization of the immunostimulatory molecule.
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LILRA3 缺失与 B-NHL 的关联以及免疫刺激分子的功能表征。
DOI:
10.1371/journal.pone.0081360
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Witte T
中科院分区:
文献类型:
--
作者:
Low HZ;Reuter S;Topperwien M;Dankenbrink N;Peest D;Kabalak G;Stripecke R;Schmidt RE;Matthias T;Witte T
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.
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影响因子:
3.7
作者:
Ryu M;Chen Y;Qi J;Liu J;Fan Z;Nam G;Shi Y;Cheng H;Gao GF
通讯作者:
Gao GF
影响因子:
5.8
作者:
Dietrich, J;Nakajima, H;Colonna, M
通讯作者:
Colonna, M
影响因子:
--
作者:
Kabalak, G.;Dobberstein, S. B.;Witte, T.
通讯作者:
Witte, T.
影响因子:
5
作者:
Koch, S;Goedde, R;Witte, T
通讯作者:
Witte, T
影响因子:
4.4
作者:
Cho, Minkwon;Ishida, Koji;Kamogawa-Schifter, Yumiko
通讯作者:
Kamogawa-Schifter, Yumiko