Literature DB >> 15350516

Establishment of an ELISA system for determining soluble LAIR-1 levels in sera of patients with HFRS and kidney transplant.

Weiming Ouyang1, Jiangnan Xue, Jingmei Liu, Wei Jia, Zhouli Li, Xin Xie, Xuesong Liu, Jinlong Jian, Qi Li, Yong Zhu, Angang Yang, Boquan Jin.   

Abstract

LAIR-1, the leukocyte-associated Ig-like receptor-1, is a trans-membrane molecule that functions as an inhibitory receptor on natural killer cells, T lymphocytes and monocytes. It has been well known that many trans-membrane receptors can shed from the cell surface and be released into the circulation in soluble form when lymphocytes, endothelials and other immune cells are activated. In many cases, the levels of soluble receptors in the circulation can be used as markers of lymphocyte activation in transplant patients and virus infection patients. To investigate whether LAIR-1 is able to be released into the sera, we developed a sandwich enzyme-linked immunosorbent assay (ELISA) system based on two anti-LAIR-1 monoclonal antibodies (MAb) with different epitope specificities. Using this ELISA, we found that sLAIR-1 existed in the supernatants collected from PMA, PHA or CD3 MAb-stimulated lymphocytes cultures in vitro for the first time. Moreover, we found that LAIR-1 level in serum samples from healthy individuals was 6.2 +/- 3.3 ng/ml, whereas the levels in sera of patients with hemorrhagic fever with renal syndrome (HFRS) and patients 3-7 days after kidney transplant increased to 47.2 +/- 35.9 and 24.4 +/- 16.0 ng/ml, respectively. Furthermore, HFRS patients in oliguric phase showed higher serum sLAIR-1 levels than those in other phases, and transplant patients with rejection showed higher serum sLAIR-1 level than those without rejection. These findings demonstrated that LAIR-1 can be released when lymphocytes are activated, suggesting sLAIR-1 may be used as a predictor for monitoring immune reaction in some virus infections and organ transplants which may be useful in clinical treatment of these diseases.

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Year:  2004        PMID: 15350516     DOI: 10.1016/j.jim.2004.06.005

Source DB:  PubMed          Journal:  J Immunol Methods        ISSN: 0022-1759            Impact factor:   2.303


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