T-LYMPHOCYTES ISOLATED FROM THE HEPATIC GRANULOMAS OF SCHISTOSOME-INFECTED MICE EXPRESS SOMATOSTATIN RECEPTOR SUBTYPE-II (SSTR2) MESSENGER-RNA

Citation
De. Elliott et al., T-LYMPHOCYTES ISOLATED FROM THE HEPATIC GRANULOMAS OF SCHISTOSOME-INFECTED MICE EXPRESS SOMATOSTATIN RECEPTOR SUBTYPE-II (SSTR2) MESSENGER-RNA, The Journal of immunology, 153(3), 1994, pp. 1180-1186
Citations number
35
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
153
Issue
3
Year of publication
1994
Pages
1180 - 1186
Database
ISI
SICI code
0022-1767(1994)153:3<1180:TIFTHG>2.0.ZU;2-Z
Abstract
Schistosomiasis mansoni is a disease characterized by liver and intest inal granulomas. Previous investigations in our laboratory showed that nylon wool-adherent CD4(+) T lymphocytes isolated from murine hepatic schistosome granulomas express receptors for somatostatin 1-14. Moreo ver, somatostatin 1-14 substantially decreased IFN-gamma and IgG2a, bu t not IL-5 secretion by dispersed granuloma cells. This paper extends these observations by defining the somatostatin receptor (SSTR) isofor m most likely expressed by granuloma inflammatory lymphocytes. Amplifi cation of mRNA by reverse transcription PCR shows SSTR1, SSTR2, and SS TR3 mRNA in normal mouse brain and other tissues. Nevertheless, only t he SSTR2 PCR product was amplified from granuloma cell RNA. The nucleo tide sequence of the granuloma SSTR2 PCR product from inflammatory cel ls is identical to the CBA murine brain SSTR2 cDNA sequence. Granuloma -derived T cell lines, FACS-isolated granuloma CD4(+) T cells, thymocy tes, splenocytes, and cloned T cell lines all contain mRNA for SSTR2 b y reverse transcription PCR. Moreover, both SSTR2A and the splice vari ant SSTR2B can be amplified from dispersed granuloma cells, granuloma T cell lines, thymocytes, and splenocytes. This is the first demonstra tion that inflammatory cells produce mRNA for an authentic somatostati n receptor. It is probable that the lymphocyte SSTR2 receptor mediates somatostatin-induced modulation of IFN-gamma secretion.