scholarly journals Effect of Herbal Medicines on Cytokine-Induced Cytotoxicity and Major Histocompatibility Complex (MHC) Class II Antigen Expression in Rat Thyroid Cells

2004 ◽  
Vol 27 (3) ◽  
pp. 371-374 ◽  
Author(s):  
Yun-Hee Shon ◽  
Hee-Soon Lee ◽  
Cheorl-Ho Kim ◽  
Jong-Kook Lim ◽  
Byung-Hun Jeon ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Herbal Medicines ◽  
Antigen Expression ◽  
Class Ii ◽  
Thyroid Cells ◽  
Histocompatibility Complex ◽  
Rat Thyroid ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals Alternative Endogenous Protein Processing via an Autophagy-Dependent Pathway Compensates for Yersinia-Mediated Inhibition of Endosomal Major Histocompatibility Complex Class II Antigen Presentation

2010 ◽  
Vol 78 (12) ◽  
pp. 5138-5150 ◽  
Author(s):  
Holger Rüssmann ◽  
Klaus Panthel ◽  
Brigitte Köhn ◽  
Stefan Jellbauer ◽  
Sebastian E. Winter ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Antigen Presentation ◽  
Mhc Class Ii ◽  
Virulence Factors ◽  
Antigen Processing ◽  
Class Ii ◽  
T Cell Response ◽  
Histocompatibility Complex ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

ABSTRACT Extracellular Yersinia pseudotuberculosis employs a type III secretion system (T3SS) for translocating virulence factors (Yersinia outer proteins [Yops]) directly into the cytosol of eukaryotic cells. Recently, we used YopE as a carrier molecule for T3SS-dependent secretion and translocation of listeriolysin O (LLO) from Listeria monocytogenes. We demonstrated that translocation of chimeric YopE/LLO into the cytosol of macrophages by Yersinia results in the induction of a codominant antigen-specific CD4 and CD8 T-cell response in orally immunized mice. In this study, we addressed the requirements for processing and major histocompatibility complex (MHC) class II presentation of chimeric YopE proteins translocated into the cytosol of macrophages by the Yersinia T3SS. Our data demonstrate the ability of Yersinia to counteract exogenous MHC class II antigen presentation of secreted hybrid YopE by the action of wild-type YopE and YopH. In the absence of exogenous MHC class II antigen presentation, an alternative pathway was identified for YopE fusion proteins originating in the cytosol. This endogenous antigen-processing pathway was sensitive to inhibitors of phagolysosomal acidification and macroautophagy, but it did not require the function either of the proteasome or of transporters associated with antigen processing. Thus, by an autophagy-dependent mechanism, macrophages are able to compensate for the YopE/YopH-mediated inhibition of the endosomal MHC class II antigen presentation pathway for exogenous antigens. This is the first report demonstrating that autophagy might enable the host to mount an MHC class II-restricted CD4 T-cell response against translocated bacterial virulence factors. We provide critical new insights into the interaction between the mammalian immune system and a human pathogen.

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

scholarly journals REOVIRUS INDUCTION OF MHC CLASS II ANTIGEN IN RAT THYROID CELLS

Endocrinology ◽  
1989 ◽  
Vol 124 (1) ◽  
pp. 543-545 ◽  
Author(s):  
David S. Neufeld ◽  
Michael Platzer ◽  
Terry F. Davies
Keyword(s):  
Mhc Class Ii ◽  
Class Ii ◽  
Thyroid Cells ◽  
Rat Thyroid ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals γδ+ T Cells Regulate Major Histocompatibility Complex Class II (IA and IE)-Dependent Susceptibility to Coxsackievirus B3-Induced Autoimmune Myocarditis

1999 ◽  
Vol 73 (7) ◽  
pp. 5630-5636 ◽  
Author(s):  
S. A. Huber ◽  
J. E. Stone ◽  
D. H. Wagner ◽  
J. Kupperman ◽  
L. Pfeiffer ◽  
...  
Keyword(s):  
T Cells ◽  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Γδ T Cells ◽  
Class Ii ◽  
Histocompatibility Complex ◽  
Cvb3 Infection ◽  
Cardiac Lesions ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

ABSTRACT Coxsackievirus B3 (CVB3) infection induces myocardial inflammation and myocyte necrosis in some, but not all, strains of mice. C57BL/6 mice, which inherently lack major histocompatibility complex (MHC) class II IE antigen, develop minimal cardiac lesions despite high levels of virus in the heart. The present experiments evaluate the relative roles of class II IA and IE expression on myocarditis susceptibility in four transgenic C57BL/6 mouse strains differing in MHC class II antigen expression. Animals lacking MHC class II IE antigen (C57BL/6 [IA+ IE−] and ABo [IA− IE−]) developed minimal cardiac lesions subsequent to infection despite high concentrations of virus in the heart. In contrast, strains expressing IE (ABo Eα [IA− IE+] and Bl.Tg.Eα [IA+ IE+]) had substantial cardiac injury. Myocarditis susceptibility correlated to a Th1 (gamma interferon-positive) cell response in the spleen, while disease resistance correlated to a preferential Th2 (interleukin-4-positive) phenotype. Vγ/Vδ analysis indicates that distinct subpopulations of γδ+ T cells are activated after CVB3 infection of C57BL/6 and Bl.Tg.Eα mice. Depletion of γδ+ T cells abrogated myocarditis susceptibility in IE+ animals and resulted in a Th1→Th2 phenotype shift. These studies indicate that the MHC class II antigen haplotype controls myocarditis susceptibility, that this control is most likely mediated through the type of γδ T cells activated during CVB3 infection, and finally that different subpopulations of γδ+ T cells may either promote or inhibit Th1 cell responses.

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