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Kwatra, S. Mouse Models of Atopic Dermatitis. Encyclopedia. Available online: (accessed on 15 April 2024).
Kwatra S. Mouse Models of Atopic Dermatitis. Encyclopedia. Available at: Accessed April 15, 2024.
Kwatra, Shawn. "Mouse Models of Atopic Dermatitis" Encyclopedia, (accessed April 15, 2024).
Kwatra, S. (2021, February 22). Mouse Models of Atopic Dermatitis. In Encyclopedia.
Kwatra, Shawn. "Mouse Models of Atopic Dermatitis." Encyclopedia. Web. 22 February, 2021.
Mouse Models of Atopic Dermatitis

The complexity of atopic dermatitis (AD) continues to present a challenge in the appropriate selection of a mouse model because no single murine model completely recapitulates all aspects of human AD. This has been further complicated by recent evidence of the distinct AD endotypes that are dictated by unique patterns of inflammation involving Th1, Th2, Th17, and Th22 axes. A review of currently used mouse models demonstrates that while all AD mouse models consistently exhibit Th2 inflammation, only some demonstrate concomitant Th17 and/or Th22 induction. As the current understanding of the pathogenic contributions of these unique endotypes and their potential therapeutic roles expands, ongoing efforts to maximize a given mouse model’s homology with human AD necessitates a close evaluation of its distinct immunological signature. 

atopic dermatitis eczema mouse models dermatology immunology

1. Introduction

Atopic dermatitis (AD) is a common, relapsing inflammatory skin condition characterized by pruritic, erythematous plaques and papules typically affecting the body’s flexural surfaces. While AD is known to emerge due to barrier dysfunction, aberrant immune activation, and genetic predisposition, a clear understanding of the pathogenesis of its varying clinical presentations remains under investigation. Current knowledge of AD’s multifaceted pathogenesis has been predicated on a diverse array of murine models that have played a pivotal role in delineating the functions of various susceptibility genes and exogenous triggers in the disease process.

However, the heterogeneity of AD disease in humans continues to present a challenge in selecting an appropriate mouse model for preclinical studies, given that no single model fully recapitulates all aspects of human AD. This has been further complicated by the recent identification of immunologically distinct human AD subtypes that occur due to differential inflammatory axis activation [1]. As the roles of these unique inflammatory patterns and their potential therapeutic implications in AD are further clarified, the selection of appropriate mouse models based on downstream immune pathways that modulate these clinically distinct subtypes is especially important in drug validation studies.

2. An Overview of Mouse Models for Atopic Dermatitis

The current repository of AD murine models reflects a broad range of mechanisms used to induce eczematous dermatitis, including the use of exogenous agents, transgenic mice, and inbred mice. Several of these mechanisms, such as mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1) deficiency, fibroblast-specific inhibitor of nuclear factor kappa-beta subunit beta (Ikk2) deficiency, and Matt deficiency, have been only loosely correlated to human AD, and a clear understanding of their pathogenic contributions resulting in AD has yet to be fully delineated [2][3][4]. Nevertheless, the cutaneous inflammation observed in most models demonstrates significant overlap with key features found in human AD lesions, including elevated serum IgE, inflammatory infiltrate consisting of eosinophils, mast cells, and lymphocytes, increased epidermal thickness, hyperkeratosis, parakeratosis, acanthosis, and spongiosis [4][5][6].

More recently, transcriptomic analyses have measured similarities between highly differentially expressed genes in human AD and select murine models using the Meta-analysis derived atopic dermatitis transcriptome (MADAD), with data demonstrating most significant overlap with Adam17fl/flSox9Cre mice (34% overlap) and mice induced with IL-23 (36% overlap) [6][7][8]. This is followed by NC/Nga mice, demonstrating 18% overlap with the human AD transcriptome, and oxazolone-sensitized mice, with 17% overlap [7]. Similarly, gene set enrichment analysis conducted by Nunomura et al. (2019) on Ikk2-deficient (Ikk2∆NES) mice demonstrated a high degree of concordance with human AD in both upregulated (16 of 30) and downregulated (19 of 30) genes [3].

Consistent with the Th2 induction that broadly underscores all human AD endotypes, murine models invariably demonstrate Th2-biased immune response, with elevated levels of Th2-related cytokines: IL-4, IL-5, IL-13, and/or thymic stromal lymphopoietin (TSLP). Eight models (models 1–8) reported exclusively Th2 elevations, while two models (models 9–10) reported Th1 in addition to Th2 activation (Table 1). Four models (models 11–14) reported heightened Th2 and Th17 inflammation, three of which (models 12–14) also reported an increase in Th1-related cytokines (Table 2).

Table 2. Mouse models with Th17, Th2, and/or Th1 upregulation.

Model Mechanism Features Immune Profile Comparison to Human AD
(If Applicable)
(11) Ikk2∆NES Conditional Ikk2-deficient mice that do not express Ikk2 in the dermis fibroblasts of the face; develop AD spontaneously. Keratinocyte proliferation, mast cell/eosinophilic infiltrate, increased IgE. Th2 (IL-4, IL-5, IL-9, IL-13, TSLP, and Postn), Th17 (IL-17a)
IL-10/20 family of genes (IL-10, IL-19, IL-20, and IL-24)
No change in Th1 or Th22
Unclear relevance of pathogenesis; Ikk2-deficient humans do not display AD-like phenotype; the role of fibroblasts in AD is not characterized.
No barrier dysfunction; the study reports an increase in filaggrin.
The transcriptomic analysis shows broad similarities with human AD.
(12) MALT-1 knockout MALT1 KO interferes with TCR-induced gene expression, lymphocyte proliferation, and regulatory T cell development, leading to Th2 expansion. Acanthosis, hyperkeratosis, and parakeratotic scaling, as well as CD3+ T cell infiltration. Th1 (IFN-γ)
Th2 (IL-4)
Th17 (IL-17)
Dermatitis is reported in humans with MALT1 deficiency. (Demeyer et al., 2019) [22]
(13) Tmem79/Mattrin mutants No expression of the protein mattrin; Impaired lamellar granular secretory system, leading to dysfunctional stratum corneum. IL-17-dependent acanthosis, orthokeratosis, inflammatory infiltrate. Higher IgE response and TEWL levels in ma/ma after challenge with house dust mite allergen compared to FLG(ft/ft) mice. Th1 (IFN-γ)
Th2 (IL-4)
Th17 (IL-17A)
Matt gene mutation was found to have only a small but significant association in human AD risk. [23][24][25][26]
(14) 2,4-dinitrofluoro-benzene Optimized DNFB dosing/scheduling to induce AD. Lymphocytic and mast cell infiltrate epidermal hypertrophy and edema. Th1 (IFN-γ)
Th2 (IL-4)
Th17 (IL-17A)
DNFB is also used to model other proliferative skin disorders. [27]

TEWL: trans-epidermal water loss. FLG: filaggrin. DNFB: 1-fluoro-2,4-dinitrobenzene.

Ten models noted Th22-related T-cell and cytokine changes in mice: Adam17fl/flSox9Cre, NC/Nga, IL-23-induced, house dust mite (HDM)-induced, ovalbumin (OVA)-induced, chloromethylisothiazonilone or methylisothiazonilone (CMIT/MIT)-primed, oxazolone (OXA)-induced, flaky tail (ft), vitamin D3-induced, and K5-tTA-IL-22 mice (Table 3). These include all models whose transcriptomic homology with human AD have been evaluated: IL-23-induced (37%), Adam17fl/flSox9Cre (34%), NG/Nga (18%), oxazolone-induced (17%), ovalbumin-induced (11%), and ft (4%) mice [7]. On the other hand, Th22 activity was assessed in Ikk2∆NES mice and found to be unchanged in affected animals (Table 2). All models with Th22 induction also exhibited Th17 upregulation, while six (models 17–18, 20, 22–24) also reported Th1 inflammation. Thus, among the models evaluated for this study, six murine models demonstrated broad upregulation of Th1, Th2, Th17, and Th22 inflammation: Adam17fl/flSox9Cre, IL-23-exposed, OXA-induced, OVA-induced, ft, and vitamin D3-induced mice.

Table 3. Th2 and/or Th1, Th17, or Th22 upregulation.

Model Mechanism Features Immune Profile Comparison to Human AD
(If Applicable)
(15) K5-tTA-IL-22 mice Transgenic mice with inducible expression of IL-22 in the skin Thickening of the epidermis and dermis, spongiosis, hyperkeratosis, inflammatory cell infiltration (eosinophils, lymphocytes, macrophages, Langerhans cells, and mast cells), and dermal collagen accumulation Th2 (IL-4, IL-13)
Th17 (IL-17)
Th22 (IL-22)
Decreased IL-1 (low IFN-γ)
Spontaneous AD formation (pathogenesis undetermined) Moderate epidermal hyperplasia with elongation of rete ridges, hyperkeratosis, increased mast cells, and eosinophils, increased IgE Th2 (IL-4, IL-5)Th17/Th22 (IL-17A, IL-22) 18% homology with human AD transcriptome [29][30][31]
(17) IL-23 injection in CCR2-deficient mice IL-23 injection stimulates IL-22-dependent dermal inflammation and acanthosis; CCR2 blockade shunts immune response toward Th2 and away from Th1. Acanthosis, hyperkeratosis, increased epidermal thickness, tissue eosinophilia. Th1 (IFN-γ)
Th2 (IL-13)
Th17/Th22 (IL-17A, IL-22)
37% homology with human AD transcriptome [32]
(18) Adam17fl/fl Sox9Cre Adam17 deficiency in Sox9-expressing tissue causes dysbiosis, leading to AD. Increased TEWL, eczematous skin lesions, increased IgE, mononuclear infiltrate. Dysbiosis with increased colonization of S. aureus. Th1
Th2 (CCL17)
34% homology with human AD transcriptome.
Adam17 deficiency in humans leads to AD-like phenotype.
(19) House dust mite allergen (HDM) Epicutaneous sensitization to HDM Epidermal hyperplasia, spongiosis, lymphocytic infiltrate, elevated serum IgE Th2 (IL-4, IL-5, IL-13)- BALB/c and C57BL/6 miceTh17 (IL-17)
Th22 (IL-22)- C57BL/6 mice
(20) Ovalbumin (OVA) with mechanical barrier disruption Tape-stripping followed by sensitization with topical or inhaled OVA. Epidermal and dermal thickening with increased collagen deposition, infiltration of CD4+ T cells, and eosinophils, increased IgE. Th1 (IFN-γ)
Th2 (IL-4, IL-5, IL-13), Th17 (IL-17)- topical OVA Th17 (IL-17)- inhaled OVA
Th22 (IL-22)
11% homology with human AD transcriptome. [29][34][35]
(21) Chloromethyl-isothiazonilone (CMIT), methylisothia-zonilone (MIT) and Ovalbumin CMIT/MIT with OVA leads to a more pronounced Th2 and Th17 response than OVA alone. Increased TEWL, increased serum IgE, mast cell infiltrate. Th2 (TSLP, IL-4, IL-6, IL-13)
Th17 (IL-17A)
Ability to differentially enhance Th17 to replicate certain endotypes. [29][36]
(22) Spontaneous recessive mouse mutant flaky tail (ft) Expression of truncated profilaggrin with functionally absent filaggrin. Diffuse orthokeratotic hyperkeratosis, acanthosis, infiltrating lymphocytes, eosinophils, mononuclear cells, increased TEWL. Th1 (IFN-γ)
Th2 (IL-4, IL-5, IL-13), Th17 (IL-17) upon percutaneous allergen exposure with OVA
Th22 (IL-22)
Differences in immune upregulation depending on mouse strain: C57BL/6: Th1. BALB/c: Th2/Th17
Filaggrin is the only functionally characterized gene in human AD.
4% homology with human AD transcriptome.
(23) Oxazolone (OXA) Chronic exposure to OXA (vs. allergic contact dermatitis). Dermal infiltration of Th2 lymphocytes, mast cells, eosinophils, elevated IgE, epidermal hyperplasia, decreased expression of filaggrin, loricrin, and involucrin. Decreased stratum corneum ceramide content, decreased stratum corneum hydration, transepidermal water loss, and impaired lamellar body secretion. Th1 (IFN-γ)
Th2 (IL-4, IL-13)
Th17 (IL-17)
Th22 (IL-22)
17% homology with human AD transcriptome. [29][34][39][40]
(24) Vitamin D3 administration Vitamin D3 or its analog MC903 (calcipotriol) induces overexpression of TSLP Epidermal hyperplasia, dermal inflammatory infiltrate of eosinophils, CD3, CD4, CD11c, mast cells Th1/Th2 mixed (TSLP, IL-4, IL-5, IL-13, IL-31, IL-10, IL-8, IFN-γ, TNF)
Th17 (IL-17)
Th22 (IL-22)

Three models are notable for outlining methods that may aid in selectively modulating inflammation: OVA with CMIT/MIT exposure, ft mice, and HDM-induced mice [28][36][37][38]. While ovalbumin commonly to induce eczema in mice, Go et al. (2020), found that mice sensitized with CMIT/MIT before OVA displayed an augmented Th17 reaction than mice exposed to OVA alone [36]. Likewise, Fallon et al. (2009) demonstrated higher Th17 activation in BALB/c mice harboring the (ft) mutation compared to C57BL/6 mice [37]. Similarly, among models that demonstrate Th22 upregulation, the HDM-induced model allows for selective suppression of Th22 response with the use of BALB/c instead of C57BL/6 mice [28]. Although these methods demonstrate the potential for modeling multiple endotypes within a single genetic strain, both OVA-induced and ft mice share the least homology with the human AD transcriptome, at 11% and 4%, respectively [7], while the transcriptomic homology of the HDM-induced model has not been evaluated.

Existing drug validation studies that evaluated the effects of FDA-approved and investigational therapies in select models provide insight into their translational utility (Table 4). Corticosteroids tested against NC/Nga mice and OXA-challenged mice led to improvements in histopathologic features of AD, while also reducing the expression of Th2 cytokines in NC/Nga mice and Th2/Th17-related cytokines in OXA-challenged mice [42]. Calcineurin inhibitors tacrolimus and pimecrolimus have been tested widely against NC/Nga, OXA-challenged, Ikk2∆NES, DNFB-challenged, and HDM-induced mice [3][43][44], with models demonstrating variable response to the indicated compounds in terms of histopathologic improvements. While treatment with tacrolimus and pimecrolimus led to reductions in Th2 and Th17 activity, inflammatory cytokine suppression was not evaluated in all tested models. Conversely, 2,4-dinitrofluoro-benzene (DNFB)-challenged and HDM-induced mice showed minimal inflammatory improvement with cyclosporine treatment, with the former demonstrating partial suppression of IL-13 and TNF-α upregulation [45]. Crisaborole and Compd3, which act via PDE4 inhibition, demonstrated efficacy against calcipotriol-induced AD lesions, demonstrating reductions in TSLP expression and skin swelling [46][47]. Novel Janus kinase (JAK) inhibitors have also been studied broadly in numerous models, including NC/Nga, Ikk2∆NES, DNFB-challenged, HDM-induced, and human skin-grafted mice [44][45][48][49]. Mice treated with JAK inhibitors delgocitinib and tofacitnib led to broad inhibition of Th2-related cytokines, as well as improvements in clinical severity and barrier function [44][45][48][49].

Table 4. The effect of select FDA-approved or investigational agents on specific models.

Model Therapeutic Agent Class Effects on Mice Reference
NC/Nga Dexamethasone Corticosteroid Reduction of Th2- (IL-4, IL-5) and Th17-related (IL-17A) cytokines. Reduction in tissue swelling and immune cell infiltration. [42]
NC/Nga Delgocitinib (JTE-052) JAK inhibitor Improved clinical score, decreased TEWL, restoration of hygroscopic amino acids needed for stratum corneum hydration [48]
NC/Nga Tacrolimus Calcineurin inhibitor Reduction of Th1- (IFN-γ), Th2- (IL-5, IL-13), Th17-related (IL-17) cytokines [44]
MC903 (calcipotriol) Crisaborole PDE4 inhibitor Reduction in ear thickness and skin swelling. [46]
MC903 (calcipotriol) Compd3 Novel PDE4 inhibitor Reduction in TSLP expression [47]
Oxazolone-challenged Pimecrolimus Methylprednisolone Calcineurin inhibitor
Decrease in TEWL and increased stratum corneum hydration
Reduced expression of IL-1α, TNF-α, PAR-2, and TSLP
Ikk2∆NES Tacrolimus
Calcineurin inhibitor JAK inhibitor Stat3 inhibitor Partial decrease in the infiltration of leukocytes and eosinophils; partial decrease in epidermal swelling. [3]
DNFB-challenged Cyclosporine Calcineurin inhibitor Partial suppression of IL-13 and TNF-α upregulation. No effect on inflammatory changes. [45]
DNFB-challenged Delgocitinib (JTE-052) JAK inhibitor Reduction in IL-4, IL-13, and TNF-α expression. Reduction in acanthosis, spongiosis, and inflammatory infiltrate. [45]
House dust mite allergen Cyclosporine Calcineurin inhibitor No effect on ear thickness [45]
House dust mite allergen Delgocitinib (JTE-052) JAK inhibitor Reduction in ear thickness with greater efficacy than cyclosporine. [45]
House dust mite allergen Tofacitinib JAK inhibitor Diminished IL-1β, TNF-α, TSLP, IL-4, IL-13 [49]
Human skin graft model Delgocitinib (JTE-052) JAK inhibitor Increased FLG protein expression [48]

JAK: Janus kinase.


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