Regulation of major histocompatibility complex class II antigen expression by the FRTL-5 rat thyroid cell line

1987 ◽  
Vol 115 (3) ◽  
pp. 481-487 ◽  
Author(s):  
A. P. Weetman ◽  
C. Green ◽  
L. K. Borysiewicz
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Line ◽  
Antigen Expression ◽  
Class Ii ◽  
Thyroid Cell ◽  
Histocompatibility Complex ◽  
Thyroid Cell Line ◽  
Rat Thyroid ◽  
Class Ii Antigen ◽  
Γ Interferon

ABSTRACT We have used the continuously growing FRTL-5 rat thyroid cell line to examine the regulation of major histocompatibility complex (MHC) class II (or la) antigen expression. Of the various stimuli investigated, only the supernatant from activated T cells or recombinant γ-interferon induced Ia expression. All Ia-inducing activity was removed from the T cell supernatant by acid dialysis, suggesting that γ-interferon is the single critical mediator for class II antigen expression. Its action was not TSH dependent but expression of class II antigens increased from the G0-G1 to the S and G2 phases of the cell cycle, so that TSH enhanced Ia expression by its action on cell division. Other agents including lectins, hormones, epidermal growth factor, a calcium ionophore and a phorbol ester did not induce Ia expression. Substances known to inhibit murine macrophage Ia expression (cortisol, prostaglandin E2 and 5-hydroxytryptamine) had no effect on FRTL-5 Ia expression. The use of this thyroid cell line has permitted direct examination of modulators in the absence of any possible effects from contaminating non-thyroid cells present in primary cultures and the results suggest that, of the agents tested, only γ-interferon has significance in the context of Ia antigen expression by the thyroid. J. Endocr. (1987) 115, 481–487

Immune induction of major histocompatibility complex antigens on a human thyroid cell line (SGHTL-34)

1989 ◽  
Vol 2 (3) ◽  
pp. 183-187 ◽  
Author(s):  
S. L. King ◽  
G. St J. Whitley ◽  
S. Page ◽  
S. S. Nussey ◽  
A. P. Johnstone
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Line ◽  
Class Ii ◽  
Class I ◽  
Human Thyroid ◽  
Thyroid Cell ◽  
Histocompatibility Complex ◽  
Thyroid Cell Line ◽  
Class Ii Antigens ◽  
Γ Interferon

ABSTRACT Expression of major histocompatibility complex antigens by epithelial cells may play a role in the aetiology of autoimmune disorders. We have studied the effect of γ-interferon on SGHTL-34, a human thyroid cell line which constitutively expresses class I but not class II antigens. γ-Interferon induced the expression of class II and increased the expression of class I molecules (assessed by flow cytofluorimetry) in a dose-dependent manner. Thyrotrophin or phytohaemagglutinin had no effect on either class I or class II expression. However, a supernatant from phytohaemagglutinin-stimulated peripheral blood mononuclear cells, containing 6400 U γ-interferon/ml, was an effective inducer of both class I and class II antigens. These data clarify earlier studies using primary thyroid cultures, which are contaminated with cells of the immune system.

Expression and modulation of major histocompatibility antigens on murine primary brain tumor in vitro

1991 ◽  
Vol 75 (6) ◽  
pp. 922-929 ◽  
Author(s):  
Aytac Akbasak ◽  
Edward H. Oldfield ◽  
Stephen C. Saris
Keyword(s):  
Major Histocompatibility Complex ◽  
Cell Lines ◽  
Antigen Expression ◽  
Class Ii ◽  
Gamma Interferon ◽  
Class I ◽  
Major Histocompatibility ◽  
Necrosis Factor Alpha ◽  
Histocompatibility Complex ◽  
Class Ii Antigen

✓ Lysis of tumor cells by activated cytotoxic lymphocytes requires their recognition of antigens associated with major histocompatibility complex molecules. The authors studied the constitutive expression of Class I and Class II major histocompatibility complex antigens on mouse brain-tumor cells and the capacity of different cytokines and cytokine combinations to alter this expression in vitro. Cells from the murine glioma 26 (GL26), glioma 261 (GL261), and ependymoblastoma A (EpA) cell lines were established in monolayer culture and treated for 48 hours with either alpha interferon, gamma interferon, tumor necrosis factor alpha, tumor necrosis factor alpha plus gamma interferon, or interleukin-2. They were then analyzed by flow cytometry for baseline and cytokine-altered major histocompatibility complex expression. All cell lines had a similar constitutive major histocompatibility complex pattern with low Class I antigen expression and no detectable Class II antigen expression. Alpha interferon substantially induced and up-regulated Class I antigen expression, but had no effect on Class II antigen expression. Gamma interferon also stimulated up-regulation of Class I antigen expression, generally doubling the anti-Class I antigen fluorescence of treated cells. Its effect on Class II antigen expression was more extensive. In the GL26 and GL261 cell lines, the expression of Class II antigen determinants increased to 12 × and 14 × control values and as many as 75% of cells that had no detectable constitutive expression of Class II antigen expressed this antigen after priming with gamma interferon. The addition of tumor necrosis factor alpha to gamma interferon further increased Class II antigen expression on EpA tumor cells only. Interleukin-2 and tumor necrosis factor alpha alone had no effect on Class I or Class II antigen expression of any cell lines. It is concluded that Class I and Class II antigen expression in mouse glioma cell lines is induced and enhanced after treatment with certain cytokines in vitro. Use of these cell lines to create in situ primary brain tumors in C57BL/6 mice should provide an excellent animal system to study major histocompatibility complex modulation in brain tumor cells and to examine the potential impact of major histocompatibility complex up-regulation on the response of brain tumors to immunotherapy.

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