This article covers the dermatological science of atopic dermatitis and skincare management principles. It does not constitute medical diagnosis or treatment advice. Consult a dermatologist for clinical diagnosis and prescription therapies.
If you are searching for what filaggrin is, how filaggrin deficiency causes atopic dermatitis, or what skincare approaches address AD at the barrier level — this guide covers the complete science from genetic basis through clinical management, with protocol architecture backed by dermatological research.
Atopic dermatitis (AD) is a chronic inflammatory skin condition fundamentally rooted in barrier dysfunction caused by filaggrin deficiency — either genetic (FLG gene mutations) or acquired (reduced filaggrin expression). Filaggrin is the primary protein component of the stratum corneum's natural moisturising factors (NMF) — hygroscopic molecules that attract and retain water. When filaggrin is deficient, NMF is depleted, stratum corneum hydration falls, transepidermal water loss (TEWL) increases, and the barrier becomes permeable to irritants and allergens. This barrier disruption triggers inflammatory responses and heightened immune reactivity characteristic of AD. Clinical presentation ranges from mild xerosis (dry skin) to severe, widespread inflammation.
- Atopic dermatitis is fundamentally a barrier defect, not purely an inflammatory disease. Filaggrin deficiency — either genetic or acquired — is the root cause in most cases.
- Filaggrin is cleaved into natural moisturising factors that retain water in the stratum corneum. Without it, skin loses hydration → TEWL increases → barrier becomes permeable to irritants → inflammation results.
- FLG gene mutations account for ~20-30% of AD cases and increase risk severity and persistence. However, AD is genetically heterogeneous — other barrier genes and acquired factors also contribute.
- Topical skincare cannot correct genetic mutations, but it can compensate for filaggrin deficiency by delivering replacement NMF components and barrier lipids that prevent flares and reduce disease burden.
- The most effective AD skincare protocol combines: (1) gentle, non-ionic cleansing, (2) immediate post-bathing emollient application to trap water, (3) formulations delivering NMF replacements (urea, amino acids, glycerol), and (4) ceramides + cholesterol + fatty acids in physiological ratios.
- Avoiding flare triggers — harsh surfactants, hot water, allergen contact, stress, infections — is as important as active barrier repair in long-term AD management.
- What is atopic dermatitis and how does it differ from sensitive skin?
- Filaggrin: the protein that holds moisture in skin
- FLG mutations and genetic basis of AD
- The barrier dysfunction hypothesis of atopic dermatitis
- Natural moisturising factors (NMF) and why they matter
- The immune component of AD — beyond barrier defects
- AD flare triggers and how to manage them
- Clinical diagnosis and severity assessment (EASI, SCORAD)
- Skincare protocols for AD barrier management
- Key ingredients for AD — NMF replacement and lipid restoration
- Cleansing and bathing strategies for AD
- Frequently asked questions
Atopic dermatitis is commonly framed as an inflammatory disease — and the visible symptoms of redness, itch, and lesions are certainly inflammatory. But this framing misses the essential starting point: before inflammation appears, there is a barrier defect. That defect is filaggrin deficiency.
For decades, the dominant model of AD focused on immune dysregulation — the heightened Th2 responses, the elevated IgE, the inflammatory cytokine production that characterizes the disease. But modern barrier biology research, particularly studies of FLG mutations, revealed that the barrier defect is often primary, and immune activation secondary. In other words: the barrier breaks first, irritants and allergens enter through the broken barrier, and the immune system reacts to those perceived threats with inflammation.
This distinction matters profoundly for skincare strategy. If AD is purely an inflammatory disease, the primary intervention is immune modulation (corticosteroids, calcineurin inhibitors, newer biologics). If AD is fundamentally a barrier disease with secondary immune consequences, then supporting the barrier — preventing further water loss, replacing missing lipids, reducing irritant ingress — becomes the foundation, and immune therapy becomes a secondary layer.
The evidence supports both: AD has barrier components AND immune components. Effective management addresses both. This guide covers the barrier side in depth, because that is the skincare lever — the mechanism by which topical products can meaningfully reduce disease burden.
What Is Atopic Dermatitis and How Does It Differ From Sensitive Skin?
Atopic dermatitis is a chronic inflammatory skin condition defined by specific clinical and diagnostic criteria, distinct genetic and immunological underpinnings, and measurable pathophysiological markers. It is not a diagnosis of exclusion or a subjective report of discomfort — it is a medical condition with established nosology.
The Hanifin-Rajka criteria (1980), still widely used, require pruritis (itch) plus three or more of the following: early age of onset, history of atopic disease (asthma, allergic rhinitis), dry skin, visible inflammation on flexural surfaces (face, neck, hands, feet, intertriginous areas), history of non-infectious dermatitis, IgE reactivity, and elevated serum IgE. The UK Working Group criteria emphasize pruritis plus three or more of: onset before age 2, history of flexural involvement, history of dry skin, personal history of other atopic disease, and visible flexural dermatitis.
Sensitive skin, by contrast, is not a medical diagnosis. It is a descriptive term for subjective discomfort — stinging, burning, reactivity — in response to products, environmental triggers (wind, heat, cold), or irritants. Skin associated with AD is sensitive, but not all sensitive skin is atopic dermatitis. Sensitive skin can be a manifestation of barrier impairment from any cause, or it can be a constitutional response threshold that exists independent of measurable barrier dysfunction.
The distinction is clinically important because sensitive skin responds well to barrier support and product avoidance, while AD requires this plus medical management of inflammation and immune dysregulation. A person with sensitive skin from over-use of harsh skincare may recover with barrier repair alone. A person with FLG-mutation-driven AD will improve with barrier repair but will likely require additional medical therapy for sustained disease control.
The term "eczema" is often used interchangeably with "atopic dermatitis" in consumer contexts, but dermatologically they are distinct: "eczema" is a broad category including atopic dermatitis, contact dermatitis, irritant dermatitis, seborrheic dermatitis, and others. Proper AD diagnosis requires evaluation by a healthcare provider using accepted diagnostic criteria.
Filaggrin: The Protein That Holds Moisture in Skin
Filaggrin is a large, histidine-rich structural protein synthesized in the keratinocytes of the stratum granulosum — the layer just above the stratum corneum. It is produced initially as a giant precursor called pro-filaggrin, which is then progressively cleaved by caspase-14 protease (and other proteases) into filaggrin monomers.
The filaggrin cleavage cascade:
- Pro-filaggrin (12 filaggrin repeats linked together) is produced in the stratum granulosum
- Caspase-14 cleaves pro-filaggrin into individual filaggrin monomers during terminal keratinocyte differentiation
- Filaggrin monomers are further broken down by exopeptidases and other proteases into amino acids and small molecular weight compounds
- Final degradation products form the natural moisturising factor (NMF): free amino acids, urea, pyrrolidone carboxylic acid (PCA), lactate, citrate, and other hygroscopic molecules
It is this final degradation step — the conversion of filaggrin into free amino acids and small molecules — that is functionally critical. These degradation products are hygroscopic: they attract and bind water, maintaining stratum corneum hydration even in dry environments. Without adequate NMF, the stratum corneum loses its ability to retain water, and transepidermal water loss (TEWL) increases dramatically.
Quantitatively, filaggrin degradation products constitute approximately 40-50% of the dry weight of the stratum corneum's natural moisturising factor. This makes filaggrin deficiency a direct, measurable cause of NMF depletion and stratum corneum desiccation in atopic dermatitis.
Stratum Granulosum Keratinocytes: Pro-filaggrin is synthesized from the FLG gene mRNA
↓ Caspase-14 + proteases
Filaggrin Monomers: Linked filaggrin repeats are cleaved into individual monomers; anchored to keratinocyte cytoskeleton and corneodesmosomes
↓ Exopeptidases + post-mortem proteolysis
Amino Acids + Small Molecules (NMF): Filaggrin is completely degraded into free amino acids (histidine, alanine, valine, glycine, tyrosine), urea, pyrrolidone carboxylic acid, lactate, glucose, citrate — all hygroscopic molecules that bind water
↓ Hygroscopic binding
Stratum Corneum Hydration: NMF maintains 20-40% water content in stratum corneum, necessary for barrier resilience and normal skin function
FLG Mutations and the Genetic Basis of AD
The filaggrin gene (FLG) is located on chromosome 1q21.3. It contains a region encoding tandem repeats of filaggrin protein — multiple copies of the same DNA sequence that code for identical filaggrin monomers. This repetitive structure makes the FLG gene particularly susceptible to mutations during DNA replication and recombination.
Types of FLG mutations:
| Mutation Type | Common Examples | Frequency (European) | Effect |
|---|---|---|---|
| Null mutations (cause protein truncation) | R501X, 2282del4, R2447X, S3181X | 5-10% carry at least one | Produce non-functional truncated filaggrin or no protein — complete loss of function |
| Missense mutations (alter protein structure) | R501H | Variable | Produce altered filaggrin with reduced function or altered cleavage efficiency |
| Frameshift mutations | Insertions/deletions in tandem repeats | Less common | Disrupt filaggrin sequence, typically producing non-functional protein |
The two most common null mutations are R501X and 2282del4, accounting for the majority of FLG mutation-associated AD in European populations. The prevalence of FLG mutations varies by ethnicity: approximately 10% of Europeans carry at least one FLG null mutation, compared to 3-5% of East Asian and African populations.
However, not all FLG mutation carriers develop atopic dermatitis. Penetrance — the proportion of mutation carriers who show the phenotype — is approximately 50-80% for homozygous null mutations and lower for heterozygous carriers. This means FLG mutations increase AD risk substantially, but additional factors (environmental triggers, other genetic variants, immune status) determine whether disease actually manifests.
Homozygous carriers (inheriting null mutations from both parents) have a filaggrin level reduced to approximately 0-20% of normal — severe barrier dysfunction and high AD penetrance (~70-80%). Heterozygous carriers (inheriting one mutant allele) have approximately 50% of normal filaggrin levels — moderate barrier impairment and lower AD penetrance. Compound heterozygotes (inheriting different mutations from each parent) show intermediate risk depending on the mutations.
The Barrier Dysfunction Hypothesis of Atopic Dermatitis
The barrier dysfunction hypothesis proposes that filaggrin deficiency is the primary defect in AD, and immune dysregulation is secondary to barrier breakdown. The evidence for this model is substantial:
Evidence supporting barrier-first model:
- FLG null mutations are the strongest genetic risk factor for AD, present in 20-30% of cases
- Filaggrin-deficient skin has measurably elevated TEWL even before clinical inflammation appears
- TEWL elevation precedes visible skin inflammation in flare development in some AD patients
- Barrier-repair interventions reduce flares and disease severity in FLG-mutation-positive and negative AD alike
- Conversely, treatments targeting only immune dysregulation (without barrier support) are less effective
The proposed cascade is:
Filaggrin deficiency → Reduced NMF → Stratum corneum desiccation → Increased TEWL → Increased permeability to irritants & allergens → Irritant/allergen ingress → Pattern recognition receptors activated → Innate immune response → Th2 skewing → Chronic inflammation → AD phenotype
Importantly, this is not a unidirectional model. Once inflammation is established in AD, it can itself downregulate filaggrin expression — creating a self-perpetuating cycle where barrier dysfunction drives inflammation, and inflammation drives further filaggrin downregulation. Breaking this cycle requires intervention at both levels: barrier repair (to reduce irritant ingress) AND appropriate immune management (to reduce ongoing inflammation).
Natural Moisturising Factors (NMF) and Why They Matter
Natural moisturising factors are the small molecular weight hygroscopic compounds that constitute approximately 8-12% of the stratum corneum dry weight. They exist in equilibrium between the hydrophilic environment of the intracellular space and the hydrophobic intercellular lipid matrix.
The primary components of NMF are:
| NMF Component | Source | % of NMF | Hygroscopic Function |
|---|---|---|---|
| Free amino acids (histidine, serine, alanine, valine, glycine) | Filaggrin degradation | ~40% | Zwitterionic — bind water strongly across range of humidities |
| Pyrrolidone carboxylic acid (PCA) | Glutamic acid cyclisation | ~12% | Highly hygroscopic; maintains hydration in dry conditions |
| Lactate | Lactate oxidase pathway | ~5% | Weak hygroscopic; also maintains skin pH |
| Urea | Protein catabolism | ~7% | Hygroscopic; also acts as natural humectant and keratolytic |
| Sugars & polyols (glucose, fructose, sorbitol) | Glycolysis / polyol metabolism | ~8% | Hygroscopic; bind water effectively |
| Citrate & other anions | Tricarboxylic acid cycle | ~5% | Weaker hygroscopic function; contribute to ionic balance |
The functional importance of NMF is its hygroscopic capacity: the ability to attract and bind water across the range of environmental humidities encountered daily. This maintains stratum corneum water content at 20-40% — the optimal range for barrier function and normal skin feel. Below this range, skin becomes brittle and permeable; the stratum corneum becomes more permeable to irritants and allergens; barrier dysfunction manifests as dryness, itching, and flaking.
In filaggrin-deficient skin, NMF is depleted to approximately 20-30% of normal levels. This translates directly to reduced stratum corneum water content and increased TEWL — measurable in clinical studies as TEWL values 2-5x higher in AD skin compared to healthy controls.
The Immune Component of AD — Beyond Barrier Defects
While filaggrin deficiency is the primary driver in genetically-determined AD, the disease phenotype also involves immune dysregulation that goes beyond simply responding to increased irritant ingress.
Th2 skewing: AD is characterised by elevated Th2 responses (IL-4, IL-5, IL-13 production) and reduced Th1/regulatory responses. This skewing exists independently of barrier dysfunction — it reflects a constitutional predisposition to heightened allergic-type immune responses. The result is amplified inflammatory response to irritants and allergens, and increased IgE production against environmental antigens.
Reduced antimicrobial peptides: Healthy skin produces antimicrobial peptides (cathelicidins, defensins) that control bacterial colonisation and trigger antimicrobial immunity. AD skin produces lower levels of these peptides, particularly Staphylococcus aureus-targeting peptides. This creates a permissive environment for S. aureus overgrowth — present in 70-90% of AD lesions. S. aureus colonisation both worsens inflammation and triggers secondary immune activation, creating a vicious cycle.
Increased IgE: Approximately 80% of AD patients have elevated total serum IgE, and 50-80% show IgE responses to common environmental allergens (dust mite, pollen, dander). IgE-mediated responses amplify inflammatory mediator release and drive acute flares.
The implication: barrier repair alone, while necessary, is often insufficient for severe AD. Immune management (topical or systemic corticosteroids, calcineurin inhibitors, newer biologics targeting IL-4/IL-13 or IL-31) is typically required alongside barrier-supportive skincare.
AD Flare Triggers and How to Manage Them
AD flares are episodes of heightened inflammation and visible symptoms (redness, itch, oozing, scaling). They are triggered by identifiable factors that either increase barrier stress or amplify immune reactivity.
| Trigger Category | Specific Triggers | Mechanism | Management |
|---|---|---|---|
| Irritant contact | Harsh soaps · Hot water · Prolonged bathing · Friction · Wool textiles | Increase TEWL · Disrupt intercellular lipid matrix · Increase skin pH | Use gentle, non-ionic cleansers · Lukewarm water · Brief bathing · Cotton clothing · Emollients immediately post-bathing |
| Allergen contact | Dust mite allergen · Pollen · Animal dander · Food allergens (contact urticaria) | IgE-mediated mast cell activation in sensitized individuals | Identify specific allergens via testing if recurrent · Environmental control · Allergen avoidance where possible |
| Infection | Staphylococcus aureus colonisation / infection · Viral infections (HSV, VZV) · Other bacterial colonisation | Bacterial toxins amplify inflammation · Viral replication triggers immune response | Rapid treatment of infection · Antimicrobial wound care · Avoid scratching (entry point for infection) |
| Environmental stress | Low humidity · Cold weather · Dry climate · Air conditioning / heating | Increase evaporative water loss from skin surface | Humidifiers in dry conditions · Frequent emollient application · Barrier support in seasonal patterns |
| Emotional / stress | Psychological stress · Anxiety · Sleep deprivation | HPA-axis activation · Decreased antimicrobial peptide production · Increased inflammatory mediator release | Stress management · Sleep prioritization · Counseling if persistent psychological stressors |
| Product ingredients | Fragrances · Essential oils · Preservatives · Alcohol · Surfactants in cleansers | Direct irritation · Contact sensitisation · Barrier disruption | Fragrance-free skincare · Minimal ingredient formulations · Avoid astringent or harsh products |
Triggers cause barrier stress or allergen/irritant ingress → inflammatory mediator release → itching intensifies → scratching damages skin and increases barrier permeability further → more irritant ingress → inflammation amplifies → visible flare develops. Breaking this cycle requires early intervention: manage triggers to prevent the flare, and interrupt scratching (via itch management) to prevent self-perpetuation of inflammation through skin damage.
Clinical Diagnosis and Severity Assessment
AD diagnosis is clinical, based on history and physical examination using established criteria. Skin testing and IgE measurements are supportive but not diagnostic.
Hanifin-Rajka Criteria (require pruritis + ≥3 of the following):
- Early age of onset (usually before age 5)
- History of atopic disease (asthma, allergic rhinitis, or atopic dermatitis in first-degree relatives)
- Dry skin
- Visible inflammation on examination (erythema, scaling, erosions, lichenification)
- Tendency toward non-infectious dermatitis
- Elevated serum IgE OR two skin prick test reactions (positive reactions to common allergens)
Severity assessment scales:
EASI (Eczema Area and Severity Index): Objective measure combining affected body surface area (0-72 points) with severity scoring for erythema, edema/papulation, excoriation, and lichenification (0-4 each) in four body regions. Total score 0-72; higher = more severe.
SCORAD (Scoring Atopic Dermatitis): Combines extent (0-100% of body surface), intensity (6 parameters: erythema, edema, oozing, excoriation, lichenification, dryness, each 0-3), and subjective symptoms (itching and sleep loss, each 0-10). Total score 0-103.
POEM (Patient-Oriented Eczema Measure): Seven-item self-reported measure of itch, sleep disturbance, and skin damage; 0-28 scale.
These scores are used both clinically to track disease severity and in research to evaluate treatment efficacy.
Skincare Protocols for AD Barrier Management
Evidence-based skincare for AD is built on three pillars: (1) gentle cleansing that preserves baseline barrier lipids, (2) immediate post-bathing moisturiser application to trap water and deliver barrier lipids, and (3) flare prevention through trigger management.
The Basic Protocol:
- Cleanse with lukewarm water and a gentle, non-ionic cleanser. Avoid harsh anionic surfactants (sodium lauryl sulfate), hot water, and prolonged scrubbing. Cleanse for 5-10 minutes maximum. Frequency: 1-2 times daily, depending on skin condition.
- Pat (do not rub) skin gently dry — leaving skin slightly damp. Do not over-dry; residual moisture helps subsequent moisturiser application.
- Apply emollient to damp skin within 3 minutes of bathing. This "traps" residual moisture in the stratum corneum. The formulation should be rich — preferably combining NMF-replacement ingredients (urea, amino acids, glycerol) with ceramides, cholesterol, and fatty acids.
- Reapply emollient as needed throughout the day. In acute flares or severe xerosis, multiple daily applications are indicated.
- Identify and avoid triggers. Common triggers: harsh products, hot water, wool, stress, infections, dry environments.
Advanced Protocol (for refractory cases): Layer complementary products to deliver multiple mechanisms simultaneously:
- Gentle cleanser → lukewarm water
- Hydrating serum (containing glycerol, sodium hyaluronate) → applied to damp skin to increase overall hydration
- Barrier repair emollient (ceramides, cholesterol, fatty acids) → seals hydration and delivers lipids
- Optional: targeted actives if tolerated (e.g., colloidal oatmeal for mild anti-inflammatory effect, licorice extract for inflammatory support) — only if flare is controlled
- SPF during day (some UV exposure can worsen itching and inflammation in AD; SPF protects)
Studies support this stepped approach: simple barrier repair reduces disease burden; more complex multi-active formulations provide incremental benefit in refractory cases.
Key Ingredients for AD — NMF Replacement and Lipid Restoration
| Ingredient | Mechanism | Evidence Level | Typical Use |
|---|---|---|---|
| Urea | Replacement NMF component · Direct hydration · Mild keratolytic | Strong — multiple RCTs in AD | 5-10% in moisturisers for xerosis |
| Free amino acids (histidine, alanine, glycine, valine) | Replace filaggrin degradation products · Direct NMF replacement | Strong — documented in AD protocols | 1-5% in formulations; multiples acids provide broader coverage |
| Glycerol | Hygroscopic humectant · Increases stratum corneum hydration | Strong — evidence-supported across skin conditions | 3-10% in moisturisers |
| Ceramides (NP, EOP, AP, NS) | Replace intercellular lipid matrix · Reduce TEWL · Fundamental barrier repair | Strong — extensive clinical evidence | With cholesterol & fatty acids in 3-component systems |
| Cholesterol | Intercellular lipid component · Essential for lamellar organisation | Strong — part of physiological lipid ratio | In formulations with ceramides & fatty acids (equimolar ratio) |
| Free fatty acids (linoleic, palmitic, stearic) | Intercellular lipid component · Linoleic acid specifically supports lamellar architecture | Strong — foundational barrier science | With ceramides & cholesterol |
| Panthenol (Provitamin B5) | Supports ceramide synthesis via Coenzyme A pathway · Absorbs water · Skin conditioning | Moderate — supportive but not primary | 2-5% in moisturisers; synergistic with ceramides |
| Colloidal oatmeal | Mild anti-inflammatory · Hydrating · Soothing · Contains avenanthramides | Moderate — traditional agent with emerging evidence | In bathing products or wash-offs; gentle anti-inflammatory for mild flares |
The most clinically supported formulation for AD barrier repair combines ceramides (ideally 3+ subclasses), cholesterol, and free fatty acids in approximately equimolar ratios (roughly 1:1:1 by molar concentration, though weight-based ratios vary). Published research consistently demonstrates superior barrier recovery with this three-component system compared to ceramides alone or single-component alternatives. This mimics the natural stratum corneum lipid composition and provides both barrier volume (ceramides) and architectural precision (cholesterol, linoleic acid).
Cleansing and Bathing Strategies for AD
Cleansing is essential for hygiene and removal of irritants and allergens, but it is also one of the most significant barrier stress events in daily life. Every cleansing removes some of the skin's natural oils and can increase TEWL by 50-100% if inappropriate products or techniques are used.
Critical cleansing principles for AD:
- Use non-ionic or amphoteric surfactants, not anionic surfactants. Anionic surfactants (sodium lauryl sulfate, sodium laureth sulfate) are highly effective at removing oils but also denature filaggrin and disrupt the intercellular lipid matrix. Non-ionic surfactants (polysorbates, cetyl alcohol derivatives) are gentler. Amphoteric surfactants (cocamidopropyl betaine) are moderate in intensity.
- Use lukewarm water, not hot. Hot water increases skin temperature, accelerates TEWL, and can denature barrier lipids and proteins. Lukewarm (30-34°C / 86-93°F) is optimal.
- Keep bathing/showering to 5-10 minutes maximum. Prolonged water exposure (beyond ~15 minutes) causes stratum corneum swelling and dehydration upon drying, increasing irritation susceptibility.
- Pat skin dry gently; do not rub. Rubbing with a towel creates friction that can trigger itch and further damage skin.
- Apply moisturiser within 3 minutes of drying. The "occlusion window" — the period during which the skin surface is still slightly damp and moisture can be effectively trapped — is approximately 3-5 minutes post-bathing. Beyond this window, stratum corneum rehydrates less effectively.
Cleanser selection: Look for labels indicating "fragrance-free" (not just "unscented"), "non-soap", "gentle cleanser", or "non-foaming" formulations. pH should be close to neutral or slightly acidic (pH 5.5-7.0 is better tolerated than alkaline cleansers). Avoid drying actives like salicylic acid or glycolic acid during active flares.
Frequently Asked Questions
- Palmer, C.N., et al. (2006). Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. Nature Genetics, 38(4), 441–446.
- Irvine, A.D., et al. (2011). Filaggrin dysfunction and the pathogenesis of atopic dermatitis. Journal of Allergy and Clinical Immunology, 127(2), 267–273.
- Elias, P.M., & Steinhoff, M. (2008). "Outside-to-inside" (and now back to "outside") pathogenic mechanisms in atopic dermatitis. Journal of Investigative Dermatology, 128(5), 1067–1070.
- Loden, M. (2003). Role of topical emollients and moisturizers in the treatment of dry skin barrier disorders. American Journal of Clinical Dermatology, 4(12), 771–788.
- Proksch, E., et al. (2006). The skin barrier function in atopic dermatitis. Clinics in Dermatology, 24(1), 52–61.
- Kezic, S., et al. (2019). Filaggrin deficiency — the road to atopic dermatitis? Advances in Dermatology, 35, 21–35.
- Brown, S.J., & McLean, W.H. (2012). One remarkable molecule: filaggrin. Journal of Investigative Dermatology, 132(3), 751–762.
- Hanifin, J.M., & Rajka, G. (1980). Diagnostic features of atopic dermatitis. Acta Dermato-Venereologica, 92(S), 44–47.
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