scholarly journals Cutting Edge: Permissive MHC Class II Allele Changes the Pattern of Antitumor Immune Response Resulting in Failure of Tumor Rejection

2009 ◽  
Vol 182 (3) ◽  
pp. 1242-1246 ◽  
Author(s):  
Elena N. Klyushnenkova ◽  
Diana V. Kouiavskaia ◽  
Carla A. Berard ◽  
Richard B. Alexander
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


1995 ◽  
Vol 181 (2) ◽  
pp. 619-629 ◽  
Author(s):  
S Baskar ◽  
L Glimcher ◽  
N Nabavi ◽  
R T Jones ◽  
S Ostrand-Rosenberg

Mice carrying large established major histocompatibility complex (MHC) class 1+ sarcoma tumors can be successfully treated by immunization with genetically engineered sarcoma cells transfected with syngeneic MHC class II plus B7-1 genes. This approach is significantly more effective than previously described strategies using cytokine- or B7-transduced tumor cells which are only effective against smaller tumor loads, and which cannot mediate regression of longer-term established tumors. The most efficient tumor rejection occurs if both the class II and B7-1 molecules are coexpressed on the same tumor cell. Immunity induced by immunization with class II+B7-1(+)-transfected sarcoma cells involves CD4+ and CD8+ T cells, suggesting that the increased effectiveness of the transfectants is due to their ability to activate both of these T cell populations.


2006 ◽  
Vol 203 (5) ◽  
pp. 1319-1328 ◽  
Author(s):  
Christopher A. Lazarski ◽  
Francisco A. Chaves ◽  
Andrea J. Sant

DM edits the peptide repertoire presented by major histocompatibility complex class II molecules by professional antigen-presenting cells (APCs), favoring presentation of some peptides over others. Despite considerable research by many laboratories, there is still significant uncertainty regarding the biochemical attributes of class II–peptide complexes that govern their susceptibility to DM editing. Here, using APCs that either do or do not express DM and a set of unrelated antigens, we found that the intrinsic kinetic stability of class II–peptide complexes is tightly correlated with the effects of DM editing within APCs. Furthermore, through the use of kinetic stability variants of three independent peptides, we demonstrate that increasing or decreasing the kinetic stability of class II–peptide complexes causes a corresponding alteration in DM editing. Finally, we show that the spontaneous kinetic stability of class II complexes correlates directly with the efficiency of presentation by DM+ APCs and the immunodominance of that class II–peptide complex during an immune response. Collectively, these results suggest that the pattern of DM editing in APCs can be intentionally changed by modifying class II–peptide interactions, leading to the desired hierarchy of presentation on APCs, thereby promoting recruitment of CD4 T cells specific for the preferred peptides during an immune response.


2010 ◽  
Vol 185 (7) ◽  
pp. 3809-3813 ◽  
Author(s):  
Daniel Kreisel ◽  
Steven B. Richardson ◽  
Wenjun Li ◽  
Xue Lin ◽  
Christopher G. Kornfeld ◽  
...  

2012 ◽  
Vol 60 (1) ◽  
pp. 1 ◽  
Author(s):  
Sarah E. Jobbins ◽  
Claire E. Sanderson ◽  
Joanna E. Griffith ◽  
Mark B. Krockenberger ◽  
Katherine Belov ◽  
...  

The host immune response is an important factor determining the outcome of the host–pathogen–environment interaction. At the gateway between the innate and adaptive immune systems are MHC molecules, which facilitate antigen presentation to T lymphocytes, and initiate the adaptive immune response. Despite their integral role in adaptive immunity, the genes encoding class II MHC molecules have not been examined directly in koalas. Furthermore, indirect historical evidence suggests that this species might lack functional diversity in class II MHC genes, with potential implications for disease susceptibility. We have examined diversity in the β chain genes of the koala class II MHC DA gene family and identified 23 alleles, including several atypical alleles. The levels of diversity observed are consistent with other marsupial and eutherian species, and do not support the paucity of variation suggested by the early literature. These findings are relevant to the conservation management of koalas and provide both a benchmark for maintaining population diversity and a platform for further conservation genetic research in this species.


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