RT Journal Article
SR Electronic
T1 Expression of CD40 Ligand in CD40-positive Murine Tumors Activates Transcription of the Interleukin-23 Subunit Genes and Produces Antitumor Responses
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 2713
OP 2716
VO 24
IS 5A
A1 WADA, AKIHIKO
A1 TADA, YUJI
A1 SHIMOZATO, OSAMU
A1 TAKIGUCHI, YUICHI
A1 TATSUMI, KOICHIRO
A1 KURIYAMA, TAKAYUKI
A1 TAGAWA, MASATOSHI
YR 2004
UL http://ar.iiarjournals.org/content/24/5A/2713.abstract
AB CD40-positive dendritic cells (DCs) are stimulated with CD40 ligand (CD40L) and subsequently secrete a number of cytokines including interleukin (IL)-23, which is involved in cell-mediated immune responses. Expression of CD40 ligand (CD40L) on tumors can activate host immune systems and produce antitumor effects against the tumors. We examined a possible mechanism of the antitumor responses: tumor cells expressing CD40 can transcribe DCs-derived cytokine genes by the expressed CD40L. For the purpose, CD40-positive A11 and -negative P29 murine lung tumors cells, both of the same origin, were transfected with the CD40L gene (A11/CD40L and P29/CD40L). The growth rate in vitro of A11/CD40L and P29/CD40L cells was not different from that of the respective parent tumors; however, the growth in vivo of A11/CD40L tumors in syngeneic mice was significantly retarded and the growth retardation of P29/CD40L tumors was marginal. Transcription of the p40 and p19 genes, IL-23 subunit genes, was up-regulated in A11/CD40L cells compared with parent A11 cells, whereas this up-regulation was not observed in P29/CD40L cells. Since expression of IL-23 in tumors can produce antitumor effects, the present data suggest that the CD40/CD40L interaction can activate cytokine transcripts in certain tumors and consequently contribute to antitumor responses. Copyright© 2004 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved