scholarly journals HLA-DP, HLA-DQ, and HLA-DR Have Different Requirements for Invariant Chain and HLA-DM

2010 ◽  
Vol 285 (52) ◽  
pp. 40800-40808 ◽  
Author(s):  
Marcel van Lith ◽  
Rosanna M. McEwen-Smith ◽  
Adam M. Benham
Keyword(s):  
Invariant Chain ◽  
Hla Dr ◽  
Hla Dq

First report on the antibody verification of HLA-DR, HLA-DQ and HLA-DP epitopes recorded in the HLA Epitope Registry

2014 ◽  
Vol 75 (11) ◽  
pp. 1097-1103 ◽  
Author(s):  
Rene J. Duquesnoy ◽  
Marilyn Marrari ◽  
Anat R. Tambur ◽  
Arend Mulder ◽  
Luiz Cláudio Demes da Mata Sousa ◽  
...  
Keyword(s):  
First Report ◽  
Hla Dr ◽  
Hla Dq

scholarly journals Cytokines in chronic inflammatory arthritis. IV. Granulocyte/macrophage colony-stimulating factor-mediated induction of class II MHC antigen on human monocytes: a possible role in rheumatoid arthritis.

1989 ◽  
Vol 170 (3) ◽  
pp. 865-875 ◽  
Author(s):  
J M Alvaro-Gracia ◽  
N J Zvaifler ◽  
G S Firestein
Keyword(s):  
Rheumatoid Arthritis ◽  
Class Ii ◽  
Tnf Alpha ◽  
Blood Monocytes ◽  
Ifn Gamma ◽  
Normal Peripheral Blood ◽  
Gm Csf ◽  
Hla Dr ◽  
Class Ii Mhc ◽  
Hla Dq

Granulocyte/macrophage CSF (GM-CSF) has recently been identified in rheumatoid arthritis (RA) synovial effusions. To study a potential role for GM-CSF and other cytokines on the induction of HLA-DR expression on monocytes and synovial macrophages, we analyzed the relative ability of recombinant human cytokines to induce the surface expression of class II MHC antigens on normal peripheral blood monocytes by FACS analysis. GM-CSF (800 U/ml) (mean fluorescence channel 2.54 +/- 0.33 times the control, p less than 0.001) and IFN-gamma (100 U/ml) (5.14 +/- 0.60, p less than 0.001) were the most potent inducers of HLA-DR. TNF-alpha and IL-4 also increased HLA-DR expression, although to a lesser degree [1.31 +/- 0.06 (p less than 0.02) and 1.20 +/- 0.03 (p less than 0.01), respectively]. IL-1 (40 U/ml), IL-2 (10 ng/ml), IL-3 (50 U/ml), IL-6 (100 U/ml), and CSF-1 (1,000 U/ml) did not affect surface HLA-DR density. GM-CSF also increased HLA-DR mRNA expression and surface HLA-DQ expression, but decreased CD14 (a monocyte/macrophage antigen) expression. The effect of GM-CSF on HLA-DR was not mediated by the generation of IFN-gamma in vitro because it was not blocked by anti-IFN-gamma mAb. GM-CSF was additive with IL-4 and low amounts (less than 3 U/ml) of IFN-gamma and synergistic with TNF-alpha. Because we have recently reported that supernatants of cultured RA synovial cells produce a non-IFN-gamma factor that induces HLA-DR on monocytes, we then attempted to neutralize this factor with specific anti-GM-CSF mAb. Four separate synovial tissue supernatants were studied, and the antibody neutralized the HLA-DR-inducing factor in each (p less than 0.01).

INTRACELLULAR AND CELL SURFACE MAPPING OF HLA DR IN THE PRESENCE AND ABSENCE OF THE INVARIANT CHAIN

1997 ◽  
Vol 25 (2) ◽  
pp. 259S-259S ◽  
Author(s):  
Kathy Triantafilou ◽  
Keith M. Wilson ◽  
Nelson Fernandez
Keyword(s):  
Cell Surface ◽  
Invariant Chain ◽  
Surface Mapping ◽  
Hla Dr ◽  
Presence And Absence

Hlamatchmaker-based determination of HLA-DR and HLA-DQ compatibility at the structural level

2003 ◽  
Vol 64 (10) ◽  
pp. S36
Author(s):  
Medhat Z. Askar ◽  
Rene J. Duquesnoy
Keyword(s):  
Structural Level ◽  
Hla Dr ◽  
Hla Dq

scholarly journals Somatic genetics of CDR3 control TCR V-domain rotational probability and germline CDR2 scanning of polymorphic MHC

2021 ◽  
Author(s):  
Joseph Murray
Keyword(s):  
Major Histocompatibility Complex ◽  
T Cell ◽  
Genetic Linkage ◽  
Alpha Helix ◽  
Volumetric Density ◽  
Mhc Ii ◽  
Histocompatibility Complex ◽  
Hla Dr ◽  
Hla Dq ◽  
Relative Affinity

Abstract The mechanism which adapts the T-cell antigen receptor (TCR) within a given major histocompatibility complex (MHC/HLA) genotype is essential for protection against pathogens. Historically attributed to relative affinity, genetically vast TCRs are surprisingly focused towards a micromolar affinity for their respective peptide (p) plus MHC (pMHC) ligands. Thus, the somatic diversity of the TCR with respect to MHC-restriction, and (ultimately) to pathogens, remains enigmatic. Here, we derive a triple integral solution (from fixed geometry) for any given V domain in TCR bound to pMHC. Solved complexes involving HLA-DR and HLA-DQ, where genetic linkage to the TCR is most profound, were examined in detail. Certain V domains displayed rare geometry within this panel—specifying a restricted rotational probability/volumetric density (dV). Remarkably, hydrogen (H) bond charge-relays distinguished these structures from the others; suggesting that CDR3 binding chemistry dictates CDR2 contacts on the opposite MHC-II alpha helix. Together, these data suggest that TCR recapitulate dV and specialise target pMHC recognition, i.e., a dynamics alternative to a relative TCR-affinity based mechanism.

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