scholarly journals Impact of negatively charged patches on the surface of MHC class II antigen-presenting proteins on risk of chronic beryllium disease

2007 ◽  
Vol 5 (24) ◽  
pp. 749-758 ◽  
Author(s):  
James A Snyder ◽  
Eugene Demchuk ◽  
Erin C McCanlies ◽  
Christine R Schuler ◽  
Kathleen Kreiss ◽  
...  
Keyword(s):  
Glutamic Acid ◽  
Mhc Class Ii ◽  
Protein Interactions ◽  
Class Ii ◽  
Chronic Beryllium Disease ◽  
Glutamic Acid Residue ◽  
The One ◽  
Class Ii Antigen ◽  
Antigen Presenting ◽  
Beryllium Disease

Chronic beryllium disease (CBD) is a granulomatous lung disease that occurs primarily in workers who are exposed to beryllium dust or fumes. Although exposure to beryllium is a necessary factor in the pathobiology of CBD, alleles that code for a glutamic acid residue at the 69th position of the HLA-DPβ1 gene have previously been found to be associated with CBD. To date, 43 HLA-DPβ1 alleles that code for glutamic acid 69 (E69) have been described. Whether all of these E69 coding alleles convey equal risk of CBD is unknown. The present study demonstrates that, on the one hand, E69 alleloforms of major histocompatibility complex class II antigen-presenting proteins with the greatest negative surface charge convey the highest risk of CBD, and on the other hand, irrespective of allele, they convey equal risk of beryllium sensitization (BeS). In addition, the data suggest that the same alleles that cause the greatest risk of CBD are also important for the progression from BeS to CBD. Alleles convey the highest risk code for E26 in a constant region and for E69, aspartic acid 55 (D55), E56, D84 and E85 in hypervariable regions of the HLA-DPβ1 chain. Together with the calculated high binding affinities for beryllium, these results suggest that an adverse immune response, leading to CBD, is triggered by chemically specific metal–protein interactions.

scholarly journals Influence of MHC CLASS II in Susceptibility to Beryllium Sensitization and Chronic Beryllium Disease

2003 ◽  
Vol 171 (12) ◽  
pp. 6910-6918 ◽  
Author(s):  
Lisa A. Maier ◽  
Dierdre S. McGrath ◽  
Hiroe Sato ◽  
Penny Lympany ◽  
Ken Welsh ◽  
...  
Keyword(s):  
Mhc Class Ii ◽  
Class Ii ◽  
Chronic Beryllium Disease ◽  
Beryllium Disease ◽  
Beryllium Sensitization

Allotransplantation of culture-isolated neonatal rat islet tissue. Absence of MHC class II positive antigen-presenting cells in nonimmunogenic islets

Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 146-151 ◽  
Author(s):  
O. D. Hegre ◽  
R. J. Ketchum ◽  
H. Popiela ◽  
C. R. Eide ◽  
R. M. Meloche ◽  
...  
Keyword(s):  
Mhc Class Ii ◽  
Antigen Presenting Cells ◽  
Class Ii ◽  
Neonatal Rat ◽  
Islet Tissue ◽  
Antigen Presenting

Towards a systems understanding of MHC class I and MHC class II antigen presentation

2011 ◽  
Vol 11 (12) ◽  
pp. 823-836 ◽  
Author(s):  
Jacques Neefjes ◽  
Marlieke L. M. Jongsma ◽  
Petra Paul ◽  
Oddmund Bakke
Keyword(s):  
Antigen Presentation ◽  
Mhc Class I ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Class I ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals Regulation of MHC Class II Antigen Presentation by Sorting of Recycling HLA-DM/DO and Class II within the Multivesicular Body

2001 ◽  
Vol 167 (2) ◽  
pp. 884-892 ◽  
Author(s):  
Marcel van Lith ◽  
Marieke van Ham ◽  
Alexander Griekspoor ◽  
Esther Tjin ◽  
Desiree Verwoerd ◽  
...  
Keyword(s):  
Antigen Presentation ◽  
Mhc Class Ii ◽  
Multivesicular Body ◽  
Class Ii ◽  
Class Ii Antigen ◽  
Mhc Class Ii Antigen

scholarly journals Hierarchy of Susceptibility of Dendritic Cell Subsets to Infection by Leishmania major: Inverse Relationship to Interleukin-12 Production

2002 ◽  
Vol 70 (7) ◽  
pp. 3874-3880 ◽  
Author(s):  
Sandrine Henri ◽  
Joan Curtis ◽  
Hubertus Hochrein ◽  
David Vremec ◽  
Ken Shortman ◽  
...  
Keyword(s):  
Immune Responses ◽  
Mhc Class Ii ◽  
Leishmania Major ◽  
Parasitophorous Vacuole ◽  
Class Ii ◽  
Host Cells ◽  
Interleukin 12 ◽  
Histocompatibility Complex ◽  
T Cell Immune Responses ◽  
Antigen Presenting

ABSTRACT Dendritic cells (DCs) are professional antigen-presenting cells which initiate and regulate T-cell immune responses. Here we show that murine splenic DCs can be ranked on the basis of their ability to phagocytose and harbor the obligately intracellular parasite Leishmania major. CD4+ CD8− DCs are the most permissive host cells for L. major amastigotes, followed by CD4− CD8− DCs; CD4− CD8+ cells are the least permissive. However, the least susceptible CD4− CD8+ DC subset was the best interleukin-12 producer in response to infection. Infection did not induce in any DC subset production of the proinflammatory cytokine gamma interferon and nitric oxide associated with the induction of Th1 responses. The number of parasites phagocytosed by DCs was low, no more than 3 organisms per cell, compared to more than 10 organisms per macrophage. In infected DCs, the parasites are located in a parasitophorous vacuole containing both major histocompatibility complex (MHC) class II and lysosome-associated membrane protein 1 molecules, similar to their location in the infected macrophage. The parasite-driven redistribution of MHC class II to this compartment indicates that infected DCs should be able to present parasite antigen.

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