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Review
. 2022 Oct 13:9:1007892.
doi: 10.3389/fmed.2022.1007892. eCollection 2022.

Elevation of IgE in patients with psoriasis: Is it a paradoxical phenomenon?

Leyao Shi  1   2 , Chen Liu  2 , Huabao Xiong  3 , Dongmei Shi  2   4
Affiliations
Review

Elevation of IgE in patients with psoriasis: Is it a paradoxical phenomenon?

Leyao Shi et al. Front Med (Lausanne). .

Abstract

Immunoglobulin E (IgE) elevation is a hallmark of allergic conditions such as atopic dermatitis (AD). The pathogenesis of AD is typically associated with high levels of IL-4 and IL-13 produced by activated T helper 2 (Th2) cells. Psoriasis, on the other hand, is an inflammatory skin disease mainly driven by Th17 cells and their related cytokines. Although the immunopathologic reactions and clinical manifestations are often easily distinguished in the two skin conditions, patients with psoriasis may sometimes exhibit AD-like manifestations, such as elevated IgE and persistent pruritic lesions. Given the fact that the effective T cells have great plasticity to re-differentiate in response to innate and environmental factors, this unusual skin condition could be a consequence of a cross-reaction between distinct arms of T-cell and humoral immunity. Here we review the literature concerning the roles of IgE in the development of AD and psoriasis, showing that elevated IgE seems to be an important indicator for this non-typical psoriasis.

Keywords: Immunoglobulin E; T helper 17 cell; T helper 2 cell; atopic dermatitis; psoriasis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
(1) Mutations of several genes are associated with IgE elevation in atopic dermatitis, including FCER1A, PGM3, FLG and Sequestosome 1/P62, among which Sequestosome 1/ P62 mutation was also observed in psoriasis patients with elevated IgE; (2) Exogenous phenotypes account for 80% of patients with AD, which are characterized by high total serum IgE and allergen-specific IgE. Patients with endogenous types (20%) of AD always exhibit normal IgE levels manifested by the secretion of autoreactive IgE. IgE elevation was observed in a certain percentage of patients with different subtypes of psoriasis; (3) In the pathogenesis of AD, IgE binds to immune and non-immune cells that expressed high-affinity IgE receptors (FcεRI) (e.g., dendritic cells, Langerhans cells, mast cells, basophils, and keratinocytes) to release proinflammatory mediators or to facilitate antigen presentation. In psoriasis, IgE can be bound to the above cells that expressed high-affinity receptors to be involved in the pathogenesis; (4) Anti-IgE treatment is often effective in AD patients, but there are no reports concerning anti-IgE treatment for psoriasis. AD, Atopic dermatitis; IgE, Immunoglobin E; FcεRI, Fc epsilon receptor Iα; PGM3, Phosphoglucomutase 3; FLG, Filaggrin.
Figure 2
Figure 2
(1) An important pathogenesis of AD is the destruction of the skin barrier, which makes it easier for pathogens and allergens to invade and activate Th2. Keratinocytes play an important role in the inflammatory response to AD. Keratinocytes produce thymic stromal lymphopoietin (TSLP) to promote the differentiation of inflammatory Th2 cells. Th2 cells can produce cytokines, including IL-4, IL-13, and IL-31. IL-4 and IL-13 stimulate B cells, to produce IgE antibodies and aggravate skin barrier defects. IL-31 causes itching and stimulates scratching, which in turn damages the skin barrier. In addition, IgE promotes antigen presentation, which tilts the reaction toward Th2 and exacerbates the process. (2) Childhood AD patients, endogenous AD patients, Asian AD patients, etc. also show elevated Th17, thus exhibiting a partial overlap with psoriasis. In addition, certain percentage of psoriasis patients present with AD-like symptoms such as elevated serum IgE and pruritus, which may be due in part to Th17 remaining plastic and shifting to Th2 in response to stimulation mainly by IL-4. In addition, some patients with psoriasis show a shift to an eczematous phenotype following the use of IL-17 inhibitors, which may be due to a suppressed Th17 response and a relatively enhanced Th2 response. IgE produced during this process may act through cells expressing IgE high-affinity receptors. (3) Upon activating by a variety of stimuli, dendritic cells secrete IL-23 and further stimulate Th17 differentiation to produce IL-17. The IL-17/IL-23 axis plays a central role in the pathogenesis of psoriasis. Keratinocytes also play an important role in psoriasis by releasing chemokines to recruit neutrophils. In addition, keratinocytes with high expression of autoantigens may play a role in maintaining the pathological state of psoriasis. AD, Atopic dermatitis; IgE, Immunoglobin E; Th, T helper cells; DC, Dendritic cell; IL, Interleukin.
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