Infection of human T-lymphotropic virus type I to astrocytes in vitro with induction of the class II major histocompatibility complex

1988 ◽  
Vol 92 (1) ◽  
pp. 34-39 ◽  
Author(s):  
Mikio Hirayama ◽  
Toshiaki Miyadai ◽  
Takashi Yokochi ◽  
Kazufumi Sato ◽  
Toshihiko Kubota ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Virus Type ◽  
Class Ii ◽  
Type I ◽  
Major Histocompatibility ◽  
T Lymphotropic Virus ◽  
Histocompatibility Complex

scholarly journals 15es JSFM : Prix Master 2017

2018 ◽  
Vol 34 ◽  
pp. 35-38
Author(s):  
Cyrielle Hou ◽  
Yasmine Baba-Amer ◽  
Maximilien Bencze ◽  
Frédéric Relaix ◽  
François Jérôme Authier
Keyword(s):  
Major Histocompatibility Complex ◽  
Nous Avons ◽  
Major Histocompatibility Complex Class ◽  
Class Ii ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Class Ii Transactivator ◽  
Histocompatibility Complex

Les myopathies inflammatoires et dysimmunitaires (DIMs) touchent 14/100 000 personnes dans le monde. Ces pathologies sont classées par des critères immunopathologiques en quatre groupes : (1) polymyosites (PM)/ myosites à inclusions (IBM), (2) dermatomyosites, (3) myopathies nécrosantes auto-immunes et (4) myosites de chevauchement comprenant le syndrome anti-synthétase (ASS). Les ASS et PM/IBM sont caractérisées par la présence d’infiltrats inflammatoires mononucléés. Récemment, nous avons mis en évidence une expression myocytaire du complexe majeur d’histocompatibilité de type 2 (CMH2) dans les muscles de patients atteints d’ASS et d’IBM. L’expression du CMH2 est connue pour être induite par l’interféron-gamma (IFNγ) dans les cellules myogéniques. Or, les lymphocytes T CD8 (LTCD8), cellules productrices d’IFNγ sont retrouvés à proximité des fibres musculaires CMH2 positives. Cette cytokine inhibe la différenciation musculaire in vitro par l’interaction CIITA-myogénine (CIITA : major histocompatibility complex class II transactivator). Les mécanismes impliquant une toxicité musculaire médiée par les lymphocytes dans les DIMs restent inconnus. Les objectifs de ce projet sont dans un premier temps de caractériser les effets de l’IFNγ sur la biologie des cellules musculaires par des approches morphologiques, moléculaires et cellulaires. Puis, d’identifier le rôle de l’IFNγ dans ces myopathies et son impact au cours de la régénération musculaire. Des études préliminaires in vitro ont été réalisées sur des myoblastes humains et murins exposés ou non à l’IFNγ. Nos résultats devraient permettre d’obtenir de meilleures connaissances sur la physiopathologie des DIMs et d’identifier de potentielles nouvelles cibles thérapeutiques.

Abstract 124: Parthenogenetic Stem Cell-derived Cardiomyocytes Express Major Histocompatibility Complex-I only after Inflammatory Stimulation

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Satish Galla ◽  
Michael Didie ◽  
Vijayakumar Muppala ◽  
Ralf Dressel ◽  
Wolfram Hubertus Zimmermann
Keyword(s):  
Major Histocompatibility Complex ◽  
Heart Muscle ◽  
Immunological Response ◽  
Type I ◽  
Major Histocompatibility ◽  
Adrenergic Stimulation ◽  
Mhc I ◽  
Histocompatibility Complex

Background: Pluripotent parthenogenetic stem cells (PSCs) can be directed towards a cardiac fate and utilized in tissue engineered heart repair. In vivo applications of tissue engineered allografts are compromised by expression of mismatching major histocompatibility complex proteins (MHC; encoded in the murine H2 locus). Here we investigated whether PSC-derived cardiomyocytes (CM) express MHC-I. Methods: Mouse PSCs (A3-line from B6D2F1 strain with haploidentical H2K d -locus) expressing a CM-specific neomycin-resistance and GFP were differentiated and purified for CM by addition of G418 (85% purity by FACS for actinin). To simulate heart muscle biology in vitro, we made use of engineered heart muscle (EHM) constructed from PSC-derived CM (75%), growth-inhibited murine embryonic fibroblasts (MEF (25%); NMRI mice), and collagen type I. MHC class-I H2K d (MHC-I) expression was assessed on CM and Non myocytes before EHM assembly and from enzymatically digested EHMs (cultured for 10 days) by FACS. Interferon gamma (IFNγ) was added for 48 h to stimulate MHC-I expression. As a reference, we investigated MHC-I expression in CM from neonatal mice and adult mouse hearts by FACS and by immunofluorescence staining. Results: EHM showed a positive ionotropic response to beta-adrenergic stimulation which could be reduced by muscarinergic stimulation. A3-CM, in contrast to Non myocytes, showed negligible expression of MHC-I (1±0.5% vs. 60±10% positive cells; n=3). EHM culture did not change MHC-I expression in CM. IFNγ treatment resulted in a marked increase of MHC-I-expression in CM monolayer culture (40±6%; n=3) and in EHM (30±8%; n=3). For comparison, 30% (n=2) neonatal CM expressed MHC-I while MHC-I was not detectable in adult CM. Conclusion: PSC-derived CM show a similarly low expression of MHC-I as adult CM and respond with MHC-I upregulation to IFNγ stimulation. This suggests a mature immunological response in PSC-CM with important implications for in vivo applications, i.e., MHC-I matching will likely be a prerequisite for successful allografting of PSC-EHM.

scholarly journals Acetylation by PCAF Enhances CIITA Nuclear Accumulation and Transactivation of Major Histocompatibility Complex Class II Genes

2000 ◽  
Vol 20 (22) ◽  
pp. 8489-8498 ◽  
Author(s):  
Charalambos Spilianakis ◽  
Joseph Papamatheakis ◽  
Androniki Kretsovali
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Transcriptional Activation ◽  
Trichostatin A ◽  
Class Ii ◽  
Nuclear Accumulation ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex

ABSTRACT The class II transactivator (CIITA), the master regulator of the tissue-specific and interferon gamma-inducible expression of major histocompatibility complex class II genes, synergizes with the histone acetylase coactivator CBP to activate gene transcription. Here we demonstrate that in addition to CBP, PCAF binds to CIITA both in vivo and in vitro and enhances CIITA-dependent transcriptional activation of class II promoters. Accordingly, E1A mutants defective for PCAF or CBP interaction show reduced ability in suppressing CIITA activity. Interestingly, CBP and PCAF acetylate CIITA at lysine residues within a nuclear localization signal. We show that CIITA is shuttling between the nucleus and cytoplasm. The shuttling behavior and activity of the protein are regulated by acetylation: overexpression of PCAF or inhibition of cellular deacetylases by trichostatin A increases the nuclear accumulation of CIITA in a manner determined by the presence of the acetylation target lysines. Furthermore, mutagenesis of the acetylated residues reduces the transactivation ability of CIITA. These results support a novel function for acetylation, i.e., to regulate gene expression by stimulating the nuclear accumulation of an activator.

scholarly journals Interferon (IFN) beta acts downstream of IFN-gamma-induced class II transactivator messenger RNA accumulation to block major histocompatibility complex class II gene expression and requires the 48-kD DNA-binding protein, ISGF3-gamma.

1995 ◽  
Vol 182 (5) ◽  
pp. 1517-1525 ◽  
Author(s):  
H T Lu ◽  
J L Riley ◽  
G T Babcock ◽  
M Huston ◽  
G R Stark ◽  
...  
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class Ii ◽  
Messenger Rna ◽  
Class Ii ◽  
Type I ◽  
Major Histocompatibility ◽  
Mrna Accumulation ◽  
Class Ii Transactivator ◽  
Ifn Gamma ◽  
Histocompatibility Complex

Interferon (IFN) gamma, a cardinal proinflammatory cytokine, induces expression of the gene products of the class II locus of the major histocompatibility complex (MHC), whereas IFN-alpha or -beta suppresses MHC class II expression. The mechanism of IFN-beta-mediated MHC class II inhibition has been unclear. Recently, a novel factor termed class II transactivator (CIITA) has been identified as essential for IFN-gamma-induced MHC class II transcription. We studied the status of IFN-gamma-induced CIITA messenger RNA (mRNA) accumulation and CIITA-driven transactivation in IFN-beta-treated cells and used cell lines that had defined defects in the type I IFN response pathway to address the roles of IFN signaling components in the inhibition of MHC class II induction. IFN-beta treatment did not suppress IFN-gamma-induced accumulation of CIITA mRNA. After cells were stably transfected with CIITA, endogenous MHC class II genes were constitutively expressed, and MHC class II promoters, delivered by transfection, were actively transcribed in CIITA-expressing cells. Expression of these promoters was significantly impaired by pretreatment with IFN-beta. These results suggest that IFN-beta acts downstream of CIITA mRNA accumulation, and acts in part by reducing the functional competence of CIITA for transactivating MHC class II promoters. IFN stimulated gene factor 3 (ISGF3) gamma was essential for IFN-beta to mediate inhibition of MHC class II induction, regardless of whether MHC class II transcription was stimulated by IFN-gamma or directly by CIITA expression. Results of these experiments suggest that inhibition of MHC class II in IFN-beta-treated cells requires expression of gene(s) directed by the ISGF3-IFN-stimulated response element pathway, and that these gene product(s) may act by blocking CIITA-driven transcription of MHC class II promoters.

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