scholarly journals Total chemical synthesis, characterization, and immunological properties of an MHC class I model using the TASP concept for protein de novo design

1992 ◽  
Vol 1 (10) ◽  
pp. 1377-1386 ◽  
Author(s):  
G. Tuchscherer ◽  
C. Servis ◽  
G. Corradin ◽  
U. Blum ◽  
J. Rivier ◽  
...  
Keyword(s):  
Chemical Synthesis ◽  
Mhc Class I ◽  
De Novo ◽  
De Novo Design ◽  
Class I ◽  
Immunological Properties

scholarly journals Differentiation-stage specific self-peptides bound by major histocompatibility complex class I molecules.

1993 ◽  
Vol 177 (3) ◽  
pp. 783-790 ◽  
Author(s):  
P E Harris ◽  
F Lupu ◽  
B Hong ◽  
E F Reed ◽  
N Suciu-Foca
Keyword(s):  
Major Histocompatibility Complex ◽  
Mhc Class I ◽  
High Performance ◽  
De Novo ◽  
Interleukin 1 ◽  
Class I ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Differentiation Stage ◽  
Mhc Class I Molecules

We have tested the hypothesis that phenotypic changes of development are accompanied by expression of differentiation-stage specific peptides bound to major histocompatibility complex (MHC) class I molecules. The U937 cell line, when cultured in the presence of phorbol myristate acetate (PMA), undergoes differentiation from monoblasts to macrophage-like cells. The high-performance liquid chromatography profile of peptides eluted from purified human histocompatibility leukocyte antigen class I molecules expressed by U937 treated with PMA differs from that obtained from control, untreated U937 cells. Chemical sequencing of eluted peptides identified a peptide derived from cytomegalovirus in both treated and untreated cells. PMA-treated, but not untreated cells, displayed an additional peptide derived from interleukin 1 beta. Hence, differentiation-induction of U937 is accompanied by the presentation of at least one differentiation-stage specific peptide. Our results indicate that, similar to viral infection, cellular development and transformation is accompanied by the de novo synthesis of proteins which are processed and presented on MHC class I molecules.

scholarly journals Homologies between SARS-CoV-2 and allergen proteins may direct T cell-mediated heterologous immune responses

2020 ◽  
Author(s):  
Kathrin Balz ◽  
Meng Chen ◽  
Abhinav Kaushik ◽  
Franz Cemic ◽  
Vanessa Heger ◽  
...  
Keyword(s):  
T Cell ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
De Novo ◽  
Class Ii ◽  
Cross Reactivity ◽  
Phleum Pratense ◽  
Class I ◽  
T Cell Epitopes ◽  
Allergen Sources

Abstract The outbreak of the new Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) is a public health emergency. Asthma does not represent a risk factor for COVID-19 in several published cohorts. We hypothesized that the SARS-CoV-2 proteome contains T cell epitopes, which are potentially cross-reactive to allergen epitopes. We aimed at identifying homologous peptide sequences by means of two distinct complementary bioinformatics approaches. Pipeline 1 included prediction of MHC Class I and Class II epitopes contained in the SARS-CoV-2 proteome and allergens along with alignment and elaborate ranking approaches. Pipeline 2 involved alignment of SARS-CoV-2 overlapping peptides with known allergen-derived T cell epitopes. Our results indicate a large number of MHC Class I epitope pairs including known as well as de novo predicted allergen T cell epitopes with high probability for cross-reactivity. Allergen sources, such as Aspergillus fumigatus, Phleum pratense and Dermatophagoides species are of particular interest due to their association with multiple cross-reactive candidate peptides, independently of the applied bioinformatic approach. In contrast, peptides derived from food allergens, as well as MHC class II epitopes did not achieve high in silico ranking and were therefore not further investigated. Our findings warrant further experimental confirmation along with examination of the functional importance of such cross-reactive responses.

scholarly journals Oxidative Phosphorylation Induces De Novo Expression of the MHC Class I in Tumor Cells through the ERK5 Pathway

2010 ◽  
Vol 185 (6) ◽  
pp. 3498-3503 ◽  
Author(s):  
Seyma Charni ◽  
Geoffroy de Bettignies ◽  
Moeez G. Rathore ◽  
Juan I. Aguiló ◽  
Peter J. van den Elsen ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Tumor Cells ◽  
Mhc Class I ◽  
De Novo ◽  
Class I

Locus-specific de novo methylation down-regulates MHC class I in S49 lymphomas

1995 ◽  
Vol 43 (1-2) ◽  
Author(s):  
RonaldJ. Rubocki ◽  
BruceE. Berrigan ◽  
SusanL. Speaks ◽  
JamesL. Wisecarver
Keyword(s):  
Mhc Class I ◽  
De Novo ◽  
Class I ◽  
De Novo Methylation

scholarly journals Surface Downregulation of Major Histocompatibility Complex Class I, PE-CAM, and ICAM-1 following De Novo Infection of Endothelial Cells with Kaposi's Sarcoma-Associated Herpesvirus

2003 ◽  
Vol 77 (17) ◽  
pp. 9669-9684 ◽  
Author(s):  
Costin Tomescu ◽  
Wai K. Law ◽  
Dean H. Kedes
Keyword(s):  
Endothelial Cells ◽  
Major Histocompatibility Complex ◽  
Cell Surface ◽  
Mhc Class I ◽  
Immune Evasion ◽  
De Novo ◽  
Lytic Replication ◽  
Class I ◽  
Histocompatibility Complex ◽  
Infected Cells

ABSTRACT Under selective pressure from host cytotoxic T lymphocytes, many viruses have evolved to downregulate major histocompatibility complex (MHC) class I and/or T-cell costimulatory molecules from the surface of infected cells. Kaposi's sarcoma-associated herpesvirus (KSHV) encodes two proteins, MIR-1 and MIR-2, that serve this function during lytic replication. In vivo, however, KSHV exists in a predominantly latent state, with less than 5% of infected cells expressing discernible lytic gene products. Thus, mechanisms of immune evasion that depend on genes expressed only during lytic replication are unlikely to be active in most KSHV-infected cells. As a result, we searched for evidence of similar defensive strategies extant during latency, employing culture systems that strongly favor latent KSHV infection. We measured cell surface levels of immunomodulatory proteins on both primary dermal microvascular endothelial cells (pDMVEC) infected through coculture with induced primary effusion lymphoma cells and telomerase-immortalized DMVEC infected directly with cell-free virus. Employing a panel of antibodies against several endothelial cell surface proteins, we show that de novo infection with KSHV leads to the downregulation of MHC class I, CD31 (PE-CAM), and CD54 (ICAM-I) but not CD58 (LFA-3) or CD95 (Fas). Furthermore, flow cytometry with a fluorescently labeled monoclonal antibody to the latency-associated nuclear antigen (LANA) revealed that downregulation occurred predominantly on KSHV-infected (LANA-positive) cells. Although the vast majority of infected cells displayed this downregulation, less than 1% expressed either immediate-early or late lytic proteins detectable by immunofluorescence. Together, these results suggest that downregulation of immunomodulatory proteins on the surface of target cells may represent a constitutive mode of immune evasion employed by KSHV following de novo infection.

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