Expression of SCM-1 alpha/lymphotactin and SCM-1 beta in natural killer cells is upregulated by IL-2 and IL-12

Citation
B. Hennemann et al., Expression of SCM-1 alpha/lymphotactin and SCM-1 beta in natural killer cells is upregulated by IL-2 and IL-12, DNA CELL B, 18(7), 1999, pp. 565-571
Citations number
13
Categorie Soggetti
Molecular Biology & Genetics
Journal title
DNA AND CELL BIOLOGY
ISSN journal
10445498 → ACNP
Volume
18
Issue
7
Year of publication
1999
Pages
565 - 571
Database
ISI
SICI code
1044-5498(199907)18:7<565:EOSAAS>2.0.ZU;2-W
Abstract
Recruitment of lymphocytes is an important feature of the host immune respo nse against pathogens. However, the mechanisms by which lymphocytes are att racted are not yet fully understood. Recently, the cDNA of a lymphocyte-spe cific chemokine, lymphotactin (Lptn), was isolated from murine and human T cells and was also found to be expressed in murine NK cells and human NK ce ll clones. This study investigated the influence of interleukin (IL)-2 and IL-12 on the expression of Lptn, also known as SCM (single cysteine motif)- 1 alpha, and SCM-1 beta, a 97% homolog of Lptn, in freshly isolated human N K cells and the human NK cell line NK-92, Northern blot analysis and RT-PCR confirmed that nonactivated human NK cells expressed both genes at low lev el. After activation with IL-2 or IL-12, the expression of both Lptn and SC M-1 beta was upregulated within hours. NK-92 cells maintained in medium sup plemented with IL-2 constitutively expressed SCM-1 mRNA, However, after 24 h of IL-2 starvation and subsequent culturing at various 11,-2 concentratio ns, the expression of Lptn/SCM-1 alpha was upregulated in a dose-dependent manner, whereas the expression of SCM-1 beta remained consistently high, Th ese observations indicate that NK cells, in addition to T lymphocytes, expr ess Lptn/SCM-1 alpha and SCM-1 beta after cytokine activation. The upregula tion of these chemokines in NK cells on activation likely acts to increase the number of effector cells reaching the site of an immune response such a s inflammation.