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Alopecia areata: Pathogenesis, clinical features, diagnosis, and management
Published in Jerry Shapiro, Nina Otberg, Hair Loss and Restoration, 2015
Studies reveal a significant association of HLA-DR11 and DQ3 in patients with AA [5,20,21,33,35–40]. The HLA alleles DQB1*03 (DQ3) and HLA-DRB1*1104 (DR11) appear to be markers of general susceptibility for all forms of AA [5,20,21,33,35–40]. The HLA alleles DRB1*0401 (DR4) and DQB1*0301(DQ7) are markers for more severe long-standing alopecia totalis (AT)/alopecia universalis (AU) [5,20,21]. The investigators [20] suggest that amino acid sequencing of the antigen-binding grooves of these HLA antigens may indicate the structure and identity of the elusive AA target antigens. Other investigators [35] also suggest that DRB3*52a may confer resistance to AA.
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
The docking experiments conducted with HLA-DR11 and HLA-DR15 provided results similar to those obtained with HLA-DR10 except that all three ligands were more promiscuous with respect to the sites where they were predicted to bind (Figure 5(A)). For HLA-DR15, several Ct conformers were predicted to bind inside the antigen-binding cavity to all three sites. A similar result was obtained with the Cb ligand, which was also predicted to bind to all three sites. Most of the conformers of Dv docked to HLA-DR15 were predicted to bind to Site 2 as in HLA-DR10, but a few also bound in or near Site 1. In the experiments conducted with HLA-DR11, all three ligands were predicted to bind to Site 1, Dv and Cb were predicted to bind to Site 2, and Ct and Cb conformers were predicted to bind to Site 3. While the predicted binding of each ligand to multiple sites suggest the structures or surface properties of the cavities in HLA-DR15 and HLA-DR11 must differ sufficiently from those in HLA-DR10 to reduce the selectivity of the ligand’s binding to a single specific site (Figure 5(A)), these results also indicate SH7129 should be fully capable of binding to the antigen-binding pockets of HLA-DR15 and HLA-DR11 when the three ligands are linked together.
Progress towards precision medicine for lupus: the role of genetic biomarkers
Published in Expert Review of Precision Medicine and Drug Development, 2018
Juan-Manuel Anaya, Kelly J. Leon, Manuel Rojas, Yhojan Rodriguez, Yovana Pacheco, Yeny Acosta-Ampudia, Diana M. Monsalve, Carolina Ramirez-Santana
In spite of a strong association between some HLA-DRB1 alleles and SLE, the disease cannot be predicted based only on the HLA genotype [86]. Most genetic studies of SLE have concluded that HLA-DR3, HLA-DR9, HLA-DR15 are strong risk factors for SLE. In contrast, HLA-DR4, HLA-DR11, and HLA-DR14 are considered protective factors [86,87]. In addition, some HLA alleles have also been associated with some subphenotypes, such as LN and cutaneous systemic lupus erythematosus (CSLE) (Table 3) [82,86–101].
Imaging in the diagnosis of idiopathic inflammatory myopathies; indications and utility
Published in Expert Review of Neurotherapeutics, 2019
Shereen Paramalingam, Peter Counsel, Frank L. Mastaglia, Helen Keen, Merrilee Needham
The important MSA antibodies in NAM include anti-signal recognition particle (SRP) and anti-3-hydroxy-3-methlglutaryl-coenzyme A reductase (HMGCR) antibodies. Statin exposed HLA-DR11 carriers have the highest risk of developing anti-HMGCR antibodies, supporting a ‘two-hit phenomenon’ [19] requiring both a primed immune system and environmental exposure for the development of the disease. However, anti-HMGCR antibodies may also occur in statin-naïve patients.