China
Africa
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HLA-DR and -DQ Serotyping
Published in M. Kam, Jeffrey L. Bidwell, Handbook of HLA TYPING TECHNIQUES, 2020
In Zimbabweans DR11 is the most frequent DR type and is present at over twice the level found in the other panels; DR2 and DR3 are present at frequencies of over 20%, while DR4 and DR7 are only found at about one half the values found in the other groups. The frequency of DR13 is relatively high in the Zimbabweans, while the other split of DR6-DR14 was not detected. HLA-DR13 is also present in the Indian panel at a frequency of almost 20%, but direct comparisons cannot be made with the Saudis and the Chinese, because when these groups were typed reagents to differentiate between and positively identify DR12, DR13, and DR14 were not available locally.
The small molecule antibody mimic SH7139 targets a family of HLA-DRs expressed by B-cell lymphomas and other solid cancers
Published in Journal of Drug Targeting, 2020
Rod Balhorn, Monique Cosman Balhorn, Karuppiah Balakrishnan, Robert B. Rebhun
In the IHC assays conducted in this study, SH7129 exhibited very strong binding to its target as evidenced by its detection on the surface of the PBMCs expressing certain HLA-DRs even after thirteen buffer washes and two incubations (Table 2 and Figures 2 and 4). These results are consistent with the affinity of SH7129 reported previously for HLA-DR10 expressing Raji lymphoma cells (Kd ∼ 23pM) [22]. Although SH7129 is only 1/60th the size of an antibody, its affinity for HLA-DR7, HLA-DR9, HLA-DR10, HLA-DR11, HLA-DR12, HLA-DR13, HLA-DR15 and HLA-DR16 is similar to the best therapeutic monoclonal antibodies, which typically bind to their antigens with nM to pM affinities [97]. The observed lack of staining of PBMCs expressing HLA-DR1, HLA-DR3, HLA-DR4, HLA-DR8 and HLA-DR14 is most likely due to sequence differences predominantly in Site 2 that prevent Dv binding and to changes in Site 3 that block Cb binding. SH7129 may still bind to these HLA-DRs, but its affinity may not be high enough to remain bound under the stringent washing conditions used in our IHC assay. A one thousand-fold reduction in SHAL affinity would be expected if the sequence or structural changes eliminated the ability of one ligand to bind to HLA-DR. Bidentate SHALs containing only two ligands typically bind to their target protein with affinities in the nanomolar range. Picomolar affinities have only been observed with tridentate SHALs containing three ligands or with bis-bidentate SHALs that bind bivalently to two neighbouring HLA-DRs [22].
Does a familial subtype of complex regional pain syndrome exist? Results of a systematic review
Published in Canadian Journal of Pain, 2019
S. Modarresi, E. Aref-Eshghi, D. M. Walton, J. C. MacDermid
One mechanism proposed to explain the genesis of CRPS is genetics, which, if accurate, can mean that a familial subtype of this syndrome exists. Human genetic studies have revealed associations between CRPS and several major histocompatibility complex alleles. These include human leukocyte antigen (HLA)-DR6, HLA-DR13, HLA-DR2, HLA-DQ1, HLA-B62, and HLA-DQ8,8–12 as well as a polymorphism in tumor necrosis factor alpha promotor gene.13 A report of the involvement of HLA-1 in the spontaneous development of CRPS provides evidence of an interaction between severity of nerve damage and genetic factors in CRPS susceptibility.14 Genome-wide expression profiling using the whole blood has shown that HLA-A29.1, matrix metallopeptidase 9, alanyl aminopeptidase, histidine decarboxylase, granulocyte colony-stimulating factor 3 receptor, and signal transducer and activator of transcription 3 genes were highly expressed in those with CRPS compared to healthy controls.15 These findings support a genetic component, indicating that hereditary factors might play a role in the susceptibility to CRPS.