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. 2022 Jun 19;11(12):3528. doi: 10.3390/jcm11123528

Figure 2.

Figure 2

Mechanisms of the emerging therapies of bullous pemphigoid. ① Omalizumab prohibits the adherence of IgE antibodies to the basement membrane proteins BP180 and BP230. ② Avdoralimab blocks the subsequent binding of the C5aR on the mast cells to the complements and deters the process of degranulation. ③ In the upstream, dendritic cells release IL-4 and IL-23 which then activate Th2 and Th17 cells, respectively. Ustekinumab, tildrakizumab and ixekizumab are therefore applied to inhibit the cascade. ④ In the blisters, chemokines result in recruitment of multiple innate and adaptive cells of which eosinophils play the pivotal role. Dupilumab, mepolizumab, and bertilimumab targeting the downstream products of eosinophils (IL-4/IL-13, IL-5 and eotaxin) may reduce further blister formation. ⑤ AKST4290 interacts with the receptor of eotaxin CCR3 causing downregulation of the eosinophils. Abbreviations: IgE, immunoglobulin E; IgG, immunoglobulin G; C5aR, C5a receptor; IL, interleukin; Th, T-helper; CCR3, C-C chemokine receptor 3.