Molecular characterization and genetic mapping of class I and class II MHC genes of the domestic cat

1988 ◽  
Vol 27 (6) ◽  
pp. 414-425 ◽  
Author(s):  
Naoya Yuhki ◽  
Stephen J. O'Brien
1986 ◽  
Vol 13 (2-3) ◽  
pp. 241-246 ◽  
Author(s):  
G. Angelini ◽  
G. Fossati ◽  
P. Radice ◽  
A. Longo ◽  
P. Piccioli ◽  
...  

Author(s):  
K. Yamazaki ◽  
G. K. Beauchamp ◽  
L. Thomas ◽  
J. Bard ◽  
E. A. Boyse
Keyword(s):  
Class Ii ◽  
Class I ◽  

1998 ◽  
Vol 48 (2) ◽  
pp. 141-143 ◽  
Author(s):  
Rafael Gongora ◽  
Zofia Zaleska-Rutczynska ◽  
Kimitaka Takami ◽  
F. Figueroa ◽  
Jan Klein
Keyword(s):  
Class Ii ◽  
Class I ◽  

Author(s):  
T. A. Stewart ◽  
D. Liggitt ◽  
S. Pitts ◽  
L. Martin ◽  
M. Siegel ◽  
...  

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.


2020 ◽  
Vol 8 (3) ◽  
pp. 144-156
Author(s):  
Şule KARATAŞ ◽  
Fatma SAVRAN OĞUZ

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


1989 ◽  
Vol 26 (12) ◽  
pp. 1095-1104 ◽  
Author(s):  
Teresa Burke ◽  
Karen Pollok ◽  
William Cushley ◽  
E. Charles Snow

Nature ◽  
1989 ◽  
Vol 342 (6246) ◽  
pp. 180-182 ◽  
Author(s):  
Marianne T. Sweetser ◽  
Lynda A. Morrison ◽  
Vivian L. Braciale ◽  
Thomas J. Braciale
Keyword(s):  
T Cells ◽  
Class Ii ◽  
Class I ◽  

Sign in / Sign up

Export Citation Format

Share Document