Immunoglobulin E autoantibodies (IgE autoantibodies)

Patient-derived IgE autoantibodies in atopic dermatitis (AD) are a specialized class of Immunoglobulin E that target self-antigens expressed by human keratinocytes (PMID: 15634292). These autoantigens, including proteins such as Hom s 1-5, manganese superoxide dismutase (MnSOD), and thioredoxin, are typically intracellular but become accessible to the immune system following skin barrier disruption or cell damage (PMID: 11803795, PMID: 29520268). Upon binding to these autoantigens, the IgE autoantibodies form immune complexes that can activate mast cells and basophils via the high-affinity IgE receptor (FceRI). This activation leads to the degranulation and release of pro-inflammatory mediators like histamine and cytokines, which perpetuate the chronic skin inflammation and pruritus seen in AD (PMID: 29520268). This autoreactive mechanism is particularly prevalent in patients with severe, recalcitrant disease and is associated with high total serum IgE levels (PMID: 15634292). Therapeutic strategies to address this target include the use of anti-IgE monoclonal antibodies such as omalizumab, which prevent IgE from binding to its receptors, and immunoadsorption techniques that physically remove circulating IgE and autoantibodies (PMID: 29520268). These treatments aim to interrupt the cycle of IgE-mediated autoimmunity and provide clinical benefit for patients who are unresponsive to standard anti-inflammatory therapies.

Other names

Autoreactive IgEAnti-keratinocyte IgEHom s-specific IgEIgE-class autoantibodiesIgE-mediated autoimmunity

Neutralization of circulating Immunoglobulin E to prevent its binding to high-affinity (FceRI) and low-affinity (FceRII/CD23) receptors on effector cells, thereby inhibiting the allergic and inflammatory cascade.