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
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.