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Posted in Uncategorized by Hemant Naidu on April 8, 2021

Our study has some weaknesses. First, this is a small first study that may not have been sufficiently motivated for all the analyses. More studies will be needed to continue to reproduce and validate our results. It is likely that we did not find associations in the Euro-American cohort because of its small size. Second, we have not corrected for several tests. However, it is important to note that our hypothesis was based on previous studies and focused exclusively on DRB1. Our final analyses of persistence were all guided by preliminary observations and were not based on an agnostic approach that could result in several test problems. In addition, our results are consistent with many hypothetical AD models that describe a process that begins with external antigens that enter a defective skin barrier that triggers PPA, which in turn activate the cytokine response associated with Th2. A well-known function of MHC Class II molecules is the representation of antigen by IPCs in Th2 cells.

Since AD is a common disease in all races and ethnicities, it can be expected that there is a common mechanism (p.B immunodyseration mediated by MHC). Finally, it is possible that in some of our samples, the HLA-DRB1 aisle assignment was not correct, because for many of our samples, not all ambiguities in the allele have been corrected. In these cases, we have the most likely aisle by default. However, 14 of the subjects (for 23 aisles) that were not fully resolved were also part of the group evaluated by the Omixon software, and for these, the Omixon approach was 100% consistent with this “standard” approach. It is therefore unlikely that this is a major source of errors. The etiology of AD and the manifestation of its classic skin discoveries are often explained on the basis of changes in skin barrier function, immune dysegation and the presence of pressure on the environment. These factors are conceptually modelled as either “outside-in” or “inside-out.” (10) The outside-in model indicates that the transmission of external exposures is through a dysfunctional skin barrier and causes AD symptoms due to immunological activation. In this context, a model antigen crosses a skin barrier that is necessarily defective. The resulting allergic sensitization is manifested in part by high levels of total summary (often increased in atopic, incoherent and AD diseases) and the presence of IgE for certain environmental genes. In contrast, the conceptual inside-out model is based on the idea that the classic epidermal changes found in AD are due to constitutive immunological abnormalities that, in turn, alter the skin barrier that causes AD skin results. (10;11) In this model Immunological activation is proposed based on cytokine responses associated with immune cells of the t-auxiliary type (Th2) that directly promote the defective skin barrier and thus allow the passage of the antigen, resulting in an even more vivid immunological reaction. (10–12) In our research, we interviewed the DRB1 gene, which is part of the HLA II class region, which has been identified in previous major genetic studies as a region of interest for ad.

(29–32) The amino acid variable positions of HLA-DRB1 allele in antigen presents shared domains, as identified by a software tool, were nominally linked to an increased prevalence of AD.