TY - JOUR
T1 - Differential cytokine regulation of MHC class II and thyroglobin mRNAs in rat thyroid cells
AU - Graves, P.
AU - Neufeld, D. S.
AU - Davies, T. F.
PY - 1989/5
Y1 - 1989/5
N2 - We have previously demonstrated that recombinant γ-interferon (γIF) inhibits thyroid cell proliferation in vitro. We now demonstrate differential regulation of thyroid cell genes by recombinant γIF, as evidenced by data obtained measuring thyroglobulin (Tg) mRNA and MHC class II α-chain mRNA transcripts. Using the rat thyroid cell clone 1B-6, derived from FRTL-5 cells, γIF markedly increases MHC class II (RT1.D) α-chain transcripts in proliferating cells. Simultaneously, Tg mRNA transcript levels are markedly inhibited, even in the presence of TSH and insulin-like growth factor I (as insulin), known stimulators of Tg mRNA. Similar data were obtained for both FRTL-5 and FRTL parent cell lines. Furthermore, using probes to the 5' region of the rat Tg gene we recognized not just a 9.0-kilobase (kb) mRNA, but also an additional 1.1-kb message in all proliferating thyroid cell cultures, suggesting truncation or alternative splicing of the Tg mRNA. Both the 9.0-and 1.1-kb mRNAs were inhibited by γIF. These data add further complexity to the cytokine regulation of thyroid cell gene expression and advise caution in making the assumption that thyroid cells may be efficient thyroid antigen-presenting cells in thyroid autoimmune disease.
AB - We have previously demonstrated that recombinant γ-interferon (γIF) inhibits thyroid cell proliferation in vitro. We now demonstrate differential regulation of thyroid cell genes by recombinant γIF, as evidenced by data obtained measuring thyroglobulin (Tg) mRNA and MHC class II α-chain mRNA transcripts. Using the rat thyroid cell clone 1B-6, derived from FRTL-5 cells, γIF markedly increases MHC class II (RT1.D) α-chain transcripts in proliferating cells. Simultaneously, Tg mRNA transcript levels are markedly inhibited, even in the presence of TSH and insulin-like growth factor I (as insulin), known stimulators of Tg mRNA. Similar data were obtained for both FRTL-5 and FRTL parent cell lines. Furthermore, using probes to the 5' region of the rat Tg gene we recognized not just a 9.0-kilobase (kb) mRNA, but also an additional 1.1-kb message in all proliferating thyroid cell cultures, suggesting truncation or alternative splicing of the Tg mRNA. Both the 9.0-and 1.1-kb mRNAs were inhibited by γIF. These data add further complexity to the cytokine regulation of thyroid cell gene expression and advise caution in making the assumption that thyroid cells may be efficient thyroid antigen-presenting cells in thyroid autoimmune disease.
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U2 - 10.1210/mend-3-5-758
DO - 10.1210/mend-3-5-758
M3 - Article
C2 - 2502713
AN - SCOPUS:0024517093
SN - 0888-8809
VL - 3
SP - 758
EP - 762
JO - Molecular Endocrinology
JF - Molecular Endocrinology
IS - 5
ER -