CIITA Activates The Expression Of MHC Class II Genes In Mouse T Cells

Below is result for CIITA Activates The Expression Of MHC Class II Genes In Mouse T Cells in PDF format. You can download or read online all document for free, but please respect copyrighted ebooks. This site does not host PDF files, all document are the property of their respective owners.

Expression of the retinoblastoma protein RbAp48 in exocrine

However, it is undetermined whether MHC class II express-ing epithelial cells can function as APCs. We frequently observed MHC class II molecule expression on the exo-crine gland cells in RbAp48-Tg mice, but not in WT mice ( Fig. 3 A ). These molecules play a pivotal role in the induc-tion and regulation of immune responses by virtue of

Yin and yang interplay of IFN-γ in inflammation and

(yin) and activates a regulatory process through various genes and pathways to reach the cool point, resulting in shift of the dividing line toward the reduction of inflammation (enlarge-ment of yin area, mutually compressing its opposite). CIITA, MHC class II specific transac-

Class II Transactivator Regulates the Expression of Multiple

CIITA (a major histocompatibility complex [MHC] class II transactivator) has been shown to be required for the expression of MHC class II genes in both B cells and interferon y-inducible cells. Here we demonstrate that CIITA not only activates MHC class II genes but also genes required for antigen presentation.

Toxoplasma gondii TgIST co-opts host chromatin repressors

nonhematopoietic and hematopoietic cells with tachyzoites, regardless of their genotypes, impedes the IFN-γ stimulated STAT1-mediated gene expression program, hence preventing expression of MHC class II molecules, IRF1, iNOS/Nos2, class II transactivator (CIITA), interferon-inducible GTPases, and chemokines (CXCL9 and CXCL10; Scharton-Kersten

RegulationofClassIMajorHistocompatibilityComplex (MHC

classical (H-2K) and nonclassical (Tla) MHC-I expression by T/B lymphocytes, natural killer (NK) cells, and myeloid-mono-cytic lineages. As a comparison, CIITA did not affect mouse MHC-Iexpression.Nlrc5/ splenocytesandbonemarrow-de-rivedmacrophageswereabletoup-regulateMHC-Iinresponse to IFN- ; however, the absolute levels of MHC-I expression

Chromosomal clustering of genes controlled by the aire

intrathymic cell migration: for example, major histocompatibility complex class I and class II gene products and certain chemokine genes are targets of aire-regulated transcription. autoimmunity microarray T cell tolerance thymus gene expression I n organisms that possess an adaptive immune system, the

Immunity, Vol. 10, 377 386, March, 1999, Copyright 1999 by

A Novel Role for the Major Histocompatibility Complex Class II Transactivator CIITA in the Repression of IL-4 Production genes (Chin et al., 1994; Chang and Flavell, 1995). In addition, introduction of the CIITA gene driven by a con-stitutive promoter is sufficient to activate MHC class II genes in plasmacytoma cells or mouse T cells, where

EXTENDED REPORT FGF2 induces RANKL gene expression as well as

IL1β through inhibition of CIITA transcription. HLA-DR induced by IFNγ is not affected by IL1β in hBM-MSC, but is suppressed in articular chondrocytes and lung fibroblasts. Conclusions RANKL expression and IL1β regulated MHC-class II, both induced via activation of the ERK1/2 signalling pathway, are specific for progenitor hBM-MSC

Chromosomal Clustering of Genes Controlled by the Aire

intrathymic cell migration: for example, major histocompatibility complex class I and class 11 gene products and certain chemokine genes are targets of aire-regulated transcription. autoimmunity I microarray I T cell tolerance I thymus I gene expression In organisms that possess an adaptive immune system, the

Tumor-mediated down-regulation of MHC class II in DC

expression of MHC class II but also in their capacity for antigen presentation to T cells. MHC class II down regulation is due to the blockage of GM-CSF-inducible CIITA type I expression It is widely known that the expression of MHC class II is under the control of cell-type-specific CIITA transactivators [17]. To deter-

Immunity, Vol. 4, 167 178, February, 1996, Copyright 1996 by

and dendritic cells, which takeup, process, and present ing a factor called CIITA can complement MHC class II antigens to CD4 T cells. The expression of MHC class expression in these cells and that the defect in BLS-2 II on B cells is required for the collaboration between B cells and RJ2.2.5 is caused by a mutation in a splice

Review SOCS1 and SOCS3 in the control of CNS immunity

STATs promote expression of immune molecules by bind-ing to cis-elements in the promoters of target genes and activating transcription. Along with many proinflamma-tory targets, STATs also induce SOCS1 and SOCS3, which feed back to negatively regulate JAK/STAT signaling (Figure 2). Expression of SOCS1 and SOCS3 is regulated

Inflammasomes Fighting the enemy from within (Inflamasomas

genes have been characterized dividing them in 4 groups (15-16): a) the CIITA subfamily/NLRA, comprising one member containing a CARD domain, the signaling molecule CIITA (class II major histocompatibility complex transactivator) which activated the transcription of the MHC class II genes;

Toll-Like Receptor 2-Dependent Extracellular Signal-Regulated

16); suppression of class II major histocompatibility complex (MHC-II) expression and, hence, presentation of antigens to CD4 T cells (17 21); and regulation of cytokines expressed by macrophages, e.g., the induction of interleukin-10 (IL-10), which has immune-suppressive functions (22 24). Regulation of some macrophage functions, such as

[Frontiers in Bioscience 9, 2373-2387, September 1, 2004

the endosomal compartments. Expression of MHC class II molecules is tightly regulated by MHC class II transactivator (CIITA) on professional APC, primarily DC, macrophage-lineage cells and B cells. Recent advances in MHC class II gene regulation involve studies in chromatin remodeling, histone acetylation-deacetylation of the SW1/SNF complexes


transcription of MHC class I genes is dependent on the TFIID component TAF1 and its AT activity (2, 3). In response to inflammatory signals, the inflammatory mediator IFN in-duces the transcriptional co-activator CIITA. CIITA mediates increases class I transcription and induction of de novo tran-scription of MHC class II genes. In contrast to

Combination Gene Therapy with CD86 and the MHC Class II

MHC class II expression in most cells; however, in the Line 1 lung carcinoma model system, CIITA activates MHC class I and well as class II. Here we show that CD86 is very effective in inducing a

Components of the IFN-γ Signaling Pathway in Tumorigenesis

g&ene or the MHC class II genes. The MHC class II gene response to IFN- γ requires expression of the retinoblas-t oma (Rb) protein (see below), which is mutated in m any human tumors. Rb gene expression is not known t o be required for any other portion of the IFN-γ sig-naling pathway. Apoptosis Exposure of cells to IFN-γ can result in

Interferon-γ converts human microvascular indoleamine 2,3

DM, but express few, if any, IFN-γ induced genes other than those involved in MHC class II synthesis and expression (Figure 1B). We had previously shown that CIITA transduction in ECs can, like IFN-γ, induce MHC class II molecules and confer the ability to activate alloreactive CD4+ T cells (13), but this is the first

Bacterial Meningitis: The Role of Transforming Growth Factor

duced septic shock in the mouse [29]. T he effect of TGF-also includes down-regulation of CD14 and binds the lipid A moiety of lipopolysaccharide, lipoteichoic acid and mycobacterial lipoarabinomannan. It is of note that CD14 activates the c-Jun N-terminal kinase, which is in-volved in expression of TNF- , a major mediator of sep-

Activation of target-tissue immune-recognition molecules by

normal expression of major histocompatibility complex (MHC) class I and aberrant expression of MHC class II antigens on the surface of cells in the affected tissue (1 4). Abnormal expression of MHC molecules on normal, nonim-mune cells can present antigens to T cells (5), which leads to T cell activation, a loss in self-tolerance, and the

Selective Abrogation of Major Histocompatibility Complex

MHC class II (MHCII) * molecules play a pivotal role in the induction and regulation of the immune response. They are specialized for the presentation of peptides to the TCRs of CD4 T cells. The engagement of MHCII pep-tide complexes by the TCRs of CD4 T cells is a pivotal interaction in the adaptive immune system because it regu-

NLRC5 Functions beyond MHC I Regulation What Do We Know So Far?

histocompatibility complex class II (MHC II) genes by acting as a transactivator on MHC II promoter region where it binds to indirectly, by interaction with an accessory DNA-binding protein

Antagonistic crosstalk between type I and II interferons and

gene products such as CIITA and class II MHC. We also initially investigated upregulation of MHC-II expression by infected or uninfected bone marrow derived macrophages (BMM) in response to stimulation with IFNg. Similar to M. tuberculosis, wildtype L. monocytogenes infection suppressed MHC-II upregula-tion. Using stably transfected RAW264.7

Forkhead transcription factor FOXO3a mediates interferon‐γ

expression of class II major histocompatibility complex (MHC II) genes. Interferon-c (IFN-c) activates MHC II transcription via the assembly of an enhanceosome centred on class II trans-activator (CIITA). In the pre-sent study, we investigated the role of the forkhead transcription factor FOXO3a in IFN- c-induced MHC II transcription in

Fixad avhandling 250718 - ki

suggesting that caspase-2 suppresses normal expression of the complex. Surprisingly, antigen-presenting cells from caspase-2-/-mice did not display any differences in surface distribution of the MHC II, indicating that the transport of MHC II from the cell interior to the exterior was somehow impaired.

Brucella abortus down‐regulates MHC class II by the IL‐6

g-inducible genes, including MHC-II, FcgR type I (CD64), CIITA, and IRF-1 genes [16 19]. The regulation of MHC-II gene expression is primarily at the level of transcription, and the CIITA transcription factor is the master regulator required for both constitutive and IFN-g-in-ducible MHC-II expression [20 25].

Differential Regulation of Constitutive Major

the regulation of MHC class I genes (11). MHC class II transactivator (CIITA), a global regulator for MHC class II molecules, is also involved in the constitutive and IFN-g induced expression of MHC class I genes through site a (12, 13). Two sets of molecules involved in antigen processing and presentation are also essential for cell

Interferon-γ Induces Major Histocompatibility Class II

activates major histocompatibility class II (MHC II) gene transcription through similar transcription regulatory pro-teins, RFX5 and CIITA, in fibroblast cells.11 13 However, little is known about the expression and the mechanism of regulation of collagen and MHC II genes by IFN- in SMCs. MHC II molecules are surface glycoproteins that play a

Expression of MHC class II molecules in different cellular

expressed ubiquitously and are also present in MHC-II-negative cells, CIITA expression can only be detected in MHC-II-positive cell types and tissues (Steimle et al., Introduction 1993, 1994). CIITA and MHC-II expression are not only The level of major histocompatibility class II (MHC-II) qualitatively but also quantitatively correlated (L.Otten,

BLIMP1α, the master regulator of plasma cell differentiation

also inhibits class switch recombination (CSR) by silenci n g genes essential for CSR and/or somatic hy-permutation (SHM) (e.g. KU70, KU86, DNA-PKCs and AID) (ref.37-39,35). CIITA is also repressed by BLIMP1 ( ref.40,35), which leads to the down-regula-tion of MHC class II genes and antigen presentation in plasm a cells41.

NEUROSCI ENC 3 4 A new villain in et al neuronal death

NLRs, CIITA acts mainly as a transcription factor to promote the expression of other genes, including serving as the master regu-lator of MHC gene expression. MHC presents peptides from either intracellular (MHC class I) or extracellular (MHC class II) proteins to adaptive immune cells. CIITA induces the expression of MHC class II genes to initiate

Nod-Like Receptors in Host Defence and Disease at the

Apr 28, 2021 LRRs [16]. CIITA has been recognized as the master regulator of Major Histocompatibil-ity Complex (MHC) class II molecule (MHC-II) expression since it controls the differential expression of MHC-II genes [17]. CIITA also plays a role in human MHC class I (MHC-I) expression, a function that is not observed in mice [18].

Induction of IFN- enables Listeria monocytogenes to suppress

genes is up-regulated by IFN- , including those coding for class II MHC proteins (MHCII) and the transcriptional acti-vator of MHCII, CIITA (Reith et al., 2005). IFN- is produced in abundance by L. monocytogenes antigen-specific CD4+ and CD8+ T cells (Zenewicz and Shen, 2007; Harty and Badovinac, 2008). However, within the first

Activation of Target-Tissue Immune-Recognition Molecules by

normal expression of major histocompatibility complex (MHC) class I and aberrant expression of MHC class II antigens on the surface of cells in the affected tissue (1-4). Abnormal expression of MHC molecules on normal, nonim-mune cells can present antigens to T cells (5), which leads to T cell activation, a loss in self-tolerance, and the

A role for STAT3 and cathepsin S in IL‐10 down‐regulation of

the CIITA expression, which is an essential factor for control-ling the expression of many IFN- -induced genes including MHC-II [6, 7], Ii [8, 9], and HLA-DM [8, 10]. All of these gene products participate in antigen processing and presenta-tion, and their inductions are via activation of the JAK/STAT pathway [11, 12].

Chapter 6 Antigen Presentation to T lymphocytes

Human leukocyte antigen (HLA), H-2 (mouse) MHC class I HLA-A, -B, -C MHC class II HLA-DR, -DP, DQ When cells are treated with IFN, expression of MHC class I, proteasome, tapasin and TAP genes is increased Expression of classical MHC class II, Ii, DM, DO is

NLRP12 Regulates Anti-viral RIG-I Activation via Interaction

inflammasome. The most prominent examples are CIITA and NLRC5, which respectively act as master transcriptional activa-tors that regulate class II and I major histocompatibility complex (MHC) gene expression (Kufer and Sansonetti, 2011; Ting et al., 2010). Most relevant to this work, several NLR proteins have

University of Groningen Novel insights in the pathogenesis of

Complete loss of classical HLA class II expression has been observed in 48% of EBV- cases and 30% of EBV+ cases and is an adverse prognostic factor [4]. Approximately 15% of the cHL cases have a translocation involving the MHC class II transactivator (CIITA) gene locus, which is the master regulator of HLA class II expression [5].

Macrophage activation revisited

adaptable cells, able to [email protected] their behavior in response to diverse signals from other cells and the extracellular matrix. A recent worksimp ~ provided tn- sights into current research on these remarkable cells. phage expression of human major histocompotibility comp!e~ (MHC) HI.A-DR, interleukin 1.13 (IL-113),