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BioMed Research International
Volume 2015, Article ID 293512, 8 pages
Research Article

Decreased Splenic T-Lymphocytes in Apolipoprotein M Gene Deficient Mice

1Department of Cardiothoracic Surgery, Third Affiliated Hospital of Soochow University, Changzhou 213003, China
2Comprehensive Laboratory, Third Affiliated Hospital of Soochow University, Changzhou 213003, China
3Division of Clinical Chemistry and Pharmacology, Department of Laboratory Medicine, Lund University, 221 85 Lund, Sweden

Received 16 July 2015; Revised 23 September 2015; Accepted 28 September 2015

Academic Editor: Fabrizio Montecucco

Copyright © 2015 Zhigang Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Spleen T-lymphocytes, especially CD4+ T-cells, have been demonstrated to be involved in broad immunomodulation and host-defense activity in vivo. Apolipoprotein M gene (apoM) may have an important role in the regulation of immunoprocess and inflammation, which could be hypothesized to the apoM containing sphingosine-1-phosphate (S1P). In the present study we demonstrate that the splenic CD4+ T-lymphocytes were obviously decreased in the apoM gene deficient (apoM−/−) mice compared to the wild type (apoM+/+). Moreover, these mice were treated with lipopolysaccharide (LPS) and it was found that even more pronounced decreasing CD4+ T-lymphocytes occurred in the spleen compared to the apoM+/+ mice. The similar phenomena were found in the ratio of CD4+/CD8+ T-lymphocytes. After administration of LPS, the hepatic mRNA levels of tumor necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) were markedly increased; however, there were no statistical differences observed between apoM+/+ mice and apoM−/− mice. The present study demonstrated that apoM might facilitate the maintenance of CD4+ T-lymphocytes or could modify the T-lymphocytes subgroups in murine spleen, which may further explore the importance of apoM in the regulation of the host immunomodulation, although the detailed mechanism needs continuing investigation.