Phosphorylation of class I but not class II MHC molecules by membrane-localized protein kinase C

1989 ◽  
Vol 26 (12) ◽  
pp. 1095-1104 ◽  
Author(s):  
Teresa Burke ◽  
Karen Pollok ◽  
William Cushley ◽  
E. Charles Snow
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Class Ii ◽  
Class I ◽  
Mhc Molecules ◽  
Kinase C ◽  
Class Ii Mhc

scholarly journals Protein kinase C delta stimulates antigen presentation by Class II MHC in murine dendritic cells

2007 ◽  
Vol 19 (6) ◽  
pp. 719-732 ◽  
Author(s):  
M. Majewski ◽  
T. O. Bose ◽  
F. C. M. Sille ◽  
A. M. Pollington ◽  
E. Fiebiger ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Antigen Presentation ◽  
Class Ii ◽  
Protein Kinase C Delta ◽  
Kinase C ◽  
Class Ii Mhc

Role of protein kinase C and tyrosine kinase activity in IFN-gamma-induced expression of the class II MHC gene

1995 ◽  
Vol 268 (1) ◽  
pp. C127-C137 ◽  
Author(s):  
Y. J. Lee ◽  
R. B. Panek ◽  
M. Huston ◽  
E. N. Benveniste
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Protein Tyrosine Kinase ◽  
Class Ii ◽  
Factor X ◽  
Induced Expression ◽  
Ifn Gamma ◽  
Kinase C ◽  
Class Ii Mhc

Astrocytes are induced by interferon-gamma (IFN-gamma) to express class II major histocompatibility complex (MHC) antigens. Our previous studies demonstrated that IFN-gamma-initiated signaling events important for class II expression include activation of protein kinase C (PKC) and the Na+/H+ antiporter. We have extended these studies and found that protein tyrosine kinase (PTK) activity is also required for class II expression. Treatment of astrocytes with inhibitors specific for PKC and PTK blocked INF-gamma-induced class II gene transcription, mRNA expression, and protein expression. Immunoblotting and immunoprecipitation experiments demonstrated that IFN-gamma induced tyrosine phosphorylation of the p91 component of ISGF3, which is blocked by preincubation of cells with PTK inhibitors. Treatment of astrocytes with IFN-gamma and either PKC and PTK inhibitors changed the mobility and intensity of a nuclear factor, IFN-gamma-enhanced factor X, which binds to the X box of the class II MHC promoter. Taken together, these data provide evidence that activation of both PTK and PKC is required for IFN-gamma-induced expression of the class II gene.

Electron microscopy analysis of degenerating pancreatic ß cells in transgenic mice expressing the MHC Class I antigen Dd

1990 ◽  
Vol 48 (3) ◽  
pp. 548-549
Author(s):  
T. A. Stewart ◽  
D. Liggitt ◽  
S. Pitts ◽  
L. Martin ◽  
M. Siegel ◽  
...  
Keyword(s):  
Type I Diabetes ◽  
Disease Process ◽  
Class Ii ◽  
Class I ◽  
Type I ◽  
Aberrant Expression ◽  
Mhc Molecules ◽  
Endogenous Insulin ◽  
Class Ii Mhc ◽  
Ifn Γ

Insulin-dependant (Type I) diabetes mellitus (IDDM) is a metabolic disorder resulting from the lack of endogenous insulin secretion. The disease is thought to result from the autoimmune mediated destruction of the insulin producing ß cells within the islets of Langerhans. The disease process is probably triggered by environmental agents, e.g. virus or chemical toxins on a background of genetic susceptibility associated with particular alleles within the major histocompatiblity complex (MHC). The relation between IDDM and the MHC locus has been reinforced by the demonstration of both class I and class II MHC proteins on the surface of ß cells from newly diagnosed patients as well as mounting evidence that IDDM has an autoimmune pathogenesis. In 1984, a series of observations were used to advance a hypothesis, in which it was suggested that aberrant expression of class II MHC molecules, perhaps induced by gamma-interferon (IFN γ) could present self antigens and initiate an autoimmune disease. We have tested some aspects of this model and demonstrated that expression of IFN γ by pancreatic ß cells can initiate an inflammatory destruction of both the islets and pancreas and does lead to IDDM.

MHC Sınıf I ve MHC Sınıf II Gen Düzenlenmesi

2020 ◽  
Vol 8 (3) ◽  
pp. 144-156
Author(s):  
Şule KARATAŞ ◽  
Fatma SAVRAN OĞUZ
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Gene Regulation ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Regulation Mechanisms

Introduction: Peptides obtained by processing intracellular and extracellular antigens are presented to T cells to stimulate the immune response. This presentation is made by peptide receptors called major histocompatibility complex (MHC) molecules. The regulation mechanisms of MHC molecules, which have similar roles in the immune response, especially at the gene level, have significant differences according to their class. Objective: Class I and class II MHC molecules encoded by MHC genes on the short arm of the sixth chromosome are peptide receptors that stimulate T cell response. These peptides, which will enable the recognition of the antigen from which they originate, are loaded into MHC molecules and presented to T cells. Although the principles of loading and delivering peptides are similar for both molecules, the peptide sources and peptide loading mechanisms are different. In addition, class I molecules are expressed in all nucleated cells while class II molecules are expressed only in Antigen Presentation Cells (APC). These differences; It shows that MHC class I is not expressed by exactly the same transcriptional mechanisms as MHC class II. In our article, we aimed to compare the gene expressions of both classes and reveal their similarities and differences. Discussion and Conclusion: A better understanding of the transcriptional mechanisms of MHC molecules will reveal the role of these molecules in diseases more clearly. In our review, we discussed MHC gene regulation mechanisms with presence of existing informations, which is specific to the MHC class, for contribute to future research. Keywords: MHC class I, MHC class II, MHC gene regulation, promoter, SXY module, transcription

Role of Class-II Major Histocompatibility Complex (MHC)-Antigen–Positive Donor Leukocytes in Transfusion-Induced Alloimmunization to Donor Class-I MHC Antigens

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 690-694
Author(s):  
K.J. Kao ◽  
M.L.U. del Rosario
Keyword(s):  
Immune Response ◽  
Peripheral Blood ◽  
Class Ii ◽  
Class I ◽  
Mononuclear Leukocytes ◽  
Class I Mhc ◽  
Mhc Antigens ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Mhc Antigen

It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens. However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2d) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2k) were used as transfusion recipients. Antibody development to donor class-I H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2d antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2b) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2b antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens.

scholarly journals 115 CYTOLOGICAL ANALYSIS OF HEPATIC GENE EXPRESSION AND IMMUNOLOGICAL RESPONSE OF MHC ANTIGENS IN MOUSE AMNIOTIC EPITHELIAL CELLS

2005 ◽  
Vol 17 (2) ◽  
pp. 208
Author(s):  
T. Mitani ◽  
T. Nagai ◽  
D. Suzuki ◽  
Y. Ukida ◽  
H. Kato ◽  
...  
Keyword(s):  
Class Ii ◽  
Class I ◽  
Hepatic Gene Expression ◽  
Rt Pcr ◽  
Mhc Antigens ◽  
Mhc Molecules ◽  
Hepatic Cells ◽  
Class Ii Mhc ◽  
Class Ii Mhc Antigens ◽  
Ifn Γ

Human amniotic epithelial cells (hAECs) have been reported to have unique properties. They express almost no class I and class II MHC antigens and lack response to interferon-γ (IFN-γ) which mediates the expression of those MHC molecules. Moreover, hAECs express some genes characteristic of hepatic cells. Therefore, hAECs seem to have multipotency and are expected to substitute for hepatic tissues in part. We aimed to develop the experimental model for investigating AECs in mice (mAECs). In this study, we examined the induction of MHC molecules by IFN-γ and the hepatic gene expression in mAECs. Murine amniotic membranes were collected from C57BL/6J females at 17.5 days of gestation. They were digested by 0.03% hyaluronidase followed by 0.2% collagenase treatment. Dissociated mAECs were cultured on dishes in DMEM supplemented with 10% FBS at 37°C under 5%CO2 in air. Embryonic fibroblasts (EFs) collected from C57BL/6J fetuses at 13.5 dpc were cultured in the same condition as mAECs. In Experiment I, the effect of IFN-γ on induction of MHC molecules in mAECs was examined. mAECs and EFs cultured in the presence or absence of IFN-γ at 1 × 103 U mL−1 for 72 h were recovered and incubated with FITC-conjugated antibodies against mouse H-2 MHC class I or I-A/I-E MHC class II antigens. The cells were analyzed by flow cytometry. In Experiment II, the expression of the genes in mAECs was examined by RT-PCR. mRNA was purified from adult liver, EFs, fresh mAECs, and mAECs cultured for 5 days. As the genes characteristic for hepatic cells, HNF-3α, HNF-3β, HNF-3γ, HNF-4, transthyretin (TTR), albumin, α-fetoprotein (AFP), glucose-6-phosphatase (G6P), and asialoglycoprotein receptor-1 (Asgr1) were examined. In Experiment I, cell-surface expression of class I and class II MHC antigens in response to IFN-γ was observed weakly in mAECs as compared to EFs, suggesting different property in hAECs which lack the expression of those antigens. In Experiment II, RT-PCR analysis showed that all of the genes except G6P were expressed in fresh mAECs. However, the expression of transcription factors such as HNF-3α, HNF-3β, HNF-4, and TTR, serum proteins such as albumin and AFP, and Asgr1 decreased after in vitro culture, contrary to the case of hAECs in which, for example, albumin appeared after cultivation. In conclusion, it was evident that mAECs have quite different properties, both in the inductivity of MHC molecules and the expression of hepatic genes, from hAECs. This work was supported by Wakayama Prefecture Collaboration of Regional Entities for the Advancement of Technological Excellence of the JST, and by a Grant-in-Aid for the 21st Century COE Program of the Japan MEXT.

scholarly journals Phagocytosis of the Malarial Pigment, Hemozoin, Impairs Expression of Major Histocompatibility Complex Class II Antigen, CD54, and CD11c in Human Monocytes

1998 ◽  
Vol 66 (4) ◽  
pp. 1601-1606 ◽  
Author(s):  
Evelin Schwarzer ◽  
Massimo Alessio ◽  
Daniela Ulliers ◽  
Paolo Arese
Keyword(s):  
Immune Response ◽  
Protein Kinase C ◽  
Major Histocompatibility Complex ◽  
Protein Kinase ◽  
Class Ii ◽  
Fc Receptor ◽  
Human Monocytes ◽  
Major Histocompatibility ◽  
Kinase C ◽  
Histocompatibility Complex

ABSTRACT In Plasmodium falciparum malaria, large proportions of resident macrophages and circulating monocytes and leukocytes contain massive amounts of the malarial pigment, hemozoin. Previous studies have shown that important functions (e.g., the generation of the oxidative burst, the ability to repeat phagocytosis, and protein kinase C activity) were severely impaired in hemozoin-loaded monocytes. Expression of membrane antigens directly involved in the immune response and in the phagocytic process, and/or under protein kinase C control, in hemozoin-loaded human monocytes was studied. Expression of major histocompatibility complex (MHC) class II after gamma interferon stimulation was blocked in hemozoin-loaded monocytes at the protein expression and gene transcription levels but was preserved in control monocytes loaded with opsonized latex beads or anti-D(Rho)-immunoglobulin G (IgG)-opsonized human erythrocytes. Expression of CD54 (intracellular adhesion molecule 1) and CD11c (p150,95 integrin) was also decreased in hemozoin-loaded monocytes. Expression of MHC class I, CD16 (low-affinity Fc receptor for aggregated IgG), CD32 (low-affinity Fc receptor for aggregated IgG), CD64 (high-affinity receptor for IgG), CD11b (receptor for complement component iC3b [CR3]), CD35 (receptor for complement components C3b and C4b [CR1]), and CD36 (non-class-A scavenger receptor) was not specifically affected by hemozoin loading. These results suggest that hemozoin loading may contribute to the impairment of the immune response and the derangement of antigen presentation reported in previous studies of P. falciparum malaria.

Role of Class-II Major Histocompatibility Complex (MHC)-Antigen–Positive Donor Leukocytes in Transfusion-Induced Alloimmunization to Donor Class-I MHC Antigens

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 690-694 ◽  
Author(s):  
K.J. Kao ◽  
M.L.U. del Rosario
Keyword(s):  
Immune Response ◽  
Peripheral Blood ◽  
Class Ii ◽  
Class I ◽  
Mononuclear Leukocytes ◽  
Class I Mhc ◽  
Mhc Antigens ◽  
Mhc Molecules ◽  
Class Ii Mhc ◽  
Mhc Antigen

Abstract It has been shown that peripheral-blood mononuclear leukocytes (MNL) are responsible for transfusion-induced alloimmunization to donor major histocompatability complex (MHC) antigens. However, it is not known which subset of MNL is responsible for this immune response. Because elimination of class-II MHC antigen-positive passenger leukocytes effectively prolongs the survival of allografts, it has been hypothesized that class-II positive MNL are responsible for immunizing transfusion recipients to donor MHC antigens. To test this hypothesis, two different approaches were used. First, we compared the alloantigenicity of BALB/c mice (H-2d) peripheral blood MNL before and after depletion of class-II positive cells. CBA mice (H-2k) were used as transfusion recipients. Antibody development to donor class-I H-2 antigens was determined by flow cytometry and enzyme-linked immunoassay. After four weekly transfusions of MNL depleted for class-II positive cells, only 25% of recipient mice developed antibodies to donor H-2d antigens. In contrast, all mice transfused with control MNL became immunized. Second, we studied the alloantigenicity of peripheral MNL from C57BL/6 mice (H-2b) with homozygous deficiency of class-II MHC molecules in H-2 disparate recipient mice. After transfusions with class-II MHC molecule-deficient MNL, 0% of BALB/c, 40% of C57BR, and 25% of CBA-recipient mice developed antibodies to donor H-2b antigen. All control recipient mice were immunized. The antibody activities of the controls were also higher than those in the treatment group who became immunized. Thus, our study shows that class-II MHC antigen-positive MNL play a significant role in transfusion-induced alloimmunization to donor class-I MHC antigens. The results also support the hypothesis that direct antigen presentation by donor class-II positive MNL to the immune system of transfusion recipients is critical for the initiation of humoral immune response to donor MHC antigens.

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