Abstract

Aim Autoantibodies against desmoglein-1 (Dsg1) and Dsg3 molecules are the hallmarks for pemphigus foliaceus (PF) and pemphigus vulgaris (PV), respectively. Overall, PF susceptibility (DRB1 * 01:01/ * 01:02, DQA1 * 01/ * 01:02/ * 03 and DQB1 * 05:01) and protection (DRB1 * 07:01/ * 11:01/ * 13:01, DQA1 * 05 and DQB1 * 03:01) alleles were distinct from susceptibility (DRB1 * 04:02/ * 08:04/ * 14:01, DQA1 * 03:01 and DQB1 * 03:02/ * 05:03) and protection (DRB1 * 07:01, DQB1 * 06:02) alleles observed for Brazilian PV patients. We performed an in silico study to evaluate desmoglein peptide binding sites for HLA class II molecules in PF and PV patients. Methods HLA class II dimers were tested as anchors for 15-length amino acid peptides from Dsg1 or Dsg3 proteins. The NetMHCIIpan software version 3.0 was used for prediction results, considering thresholds for: (i) strong (IC50) 50.000 nM and (ii) weak (IC50) 500.000 nM binding peptides. Results PF and Dsg1: The number of strong/weak binders was greater for DRB1 susceptibility molecules in comparison to DRB1 protection molecules. The DQA1 * 05:01/DQB1 * 03:01 and DQA1 * 05:10/DQB1 * 03:01 protection dimers presented higher number of weak binders compared to strong binders, while DQA1 * 01:02/DQB1 * 05:01 and DQA1 * 03:01/DQB1 * 05:01 susceptibility dimers showed no strong binders. PV and Dsg1: DRB1 * 08:04 exhibited greater strong/weak binders than other susceptibility molecules, and DQA1/DQB1 dimers did not present strong binders. PF and Dsg3: Results were closely similar to those reported for Dsg1; however protection molecules exhibit greater weaker binders. PV and Dsg3: Susceptibility and protection HLA molecules presented almost weak binders to Dsg3. Conclusion Overall, HLA-DRB1 molecules, particularly in PF, exhibited stronger binding peptides for Dsg1 protein. DRB1 molecules presented greater strong binders as compared to DQA1/DQB1 dimers in both pemphigus.

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