Keratinocyte
Keratinocytes are the architects of the epidermal barrier, moving through a differentiation programme driven by a precise calcium gradient. In clinical aesthetics, we leverage two critical levers: the COL17A1-mediated stem cell population governing renewal capacity, and the cytokine environment ( IL-4/ IL-13) that can suppress barrier outputs. Restoring the epidermis requires a strategic reset of the stem cell niche and the removal of inflammatory “brakes” to ensure a complete, functional barrier.
Keratinocytes comprise approximately 90% of epidermal cells and are the structural and functional foundation of the skin barrier. Their defining characteristic is not simply what they are but what they become: a keratinocyte begins as a proliferating cell in the basal layer of the epidermis and ends (approximately 40 to 56 days later) as a corneocyte at the skin surface, having passed through a precisely coordinated programme of structural transformation that constructs each layer of the epidermis on the way. That programme – its completeness, its speed, and the quality of cells it produces – is what determines whether the skin barrier functions well or poorly. Every other entity in the barrier biology cluster describes what keratinocytes make during that journey. Keratinocytes describe who is making it and what governs their capacity to do so.
The Differentiation Programme: From Basal Cell to Corneocyte
Keratinocyte differentiation is a one-way journey. Cells in the stratum basale divide asymmetrically: one daughter cell remains as a stem or progenitor cell, maintaining the basal population; the other commits to differentiation and begins migrating upward. As it moves through the stratum spinosum and stratum granulosum, it progressively withdraws from the cell cycle, activates epidermal differentiation complex (EDC) genes on chromosome 1q21, and shifts its protein production toward the structural components that will define each layer it passes through. [4]
The calcium gradient of the epidermis is the primary physical signal driving this progression. Calcium concentration is lowest in the stratum basale and rises progressively toward the stratum granulosum, with each increase triggering the next stage of differentiation. [2] Loricrin and involucrin (the cornified envelope proteins) are expressed in the upper layers as calcium concentrations rise, whilst filaggrin is produced in the stratum granulosum for keratin compaction. When the calcium gradient is disrupted by barrier damage, differentiation marker expression declines simultaneously. Loricrin, profilaggrin, and involucrin all fall, reflecting that the differentiation programme and the barrier state are coupled rather than sequential. Barrier disruption does not simply follow from poor differentiation. It can actively impair the differentiation of cells still in transit. [2]
Terminal differentiation at the stratum granulosum–stratum corneum transition involves the dismantling of the keratinocyte’s own nucleus and organelles in a caspase-dependent process that is distinct from apoptosis but uses elements of the same machinery. [1] The result is the anucleate, protein-dense corneocyte; not a cell death but a controlled structural conversion that the Corneocyte page describes in detail.
The Keratinocyte “Life Stages”
| Layer | Biological Activity | Clinical Significance | Key Biomarkers |
|---|---|---|---|
| Stratum Basale | Proliferation & Stem Cell Anchoring. | Determines skin thickness & renewal rate. | COL17A1, Keratin 5/14 |
| Stratum Spinosum | “The Spine” – Initial structural reinforcement. | Provides mechanical “bounce” and strength. | Involucrin, Desmogleins |
| Stratum Granulosum | Lipid synthesis & Filaggrin production. | The “Seal” – Where the barrier is made. | Filaggrin, Loricrin, Ceramides |
| Stratum Corneum | Corneocyte shedding (Desquamation). | Surface texture, “glow,” and hydration. | Corneodesmosomes, KLK enzymes |
The Stem Cell Population: COL17A1 and the Capacity to Renew
Not all basal keratinocytes have equal renewal capacity. The basal layer contains a stem cell population characterised by high expression of COL17A1 – the gene encoding type XVII collagen, a transmembrane structural component of hemidesmosomes that anchors basal keratinocytes to the basement membrane. COL17A1 does more than anchor cells. Research has demonstrated that it directly regulates keratinocyte stem cell motility by coordinating actin and keratin filament networks within the cell, coupling cell movement with self-renewal capacity. [5] The EGFR–COL17A1 axis is the mechanism through which EGF signalling drives not just proliferation but directed stem cell migration. This is the collective movement that enables re-epithelialisation after injury.
With age, EGFR signalling declines. This leads directly to COL17A1 proteolysis – the protein is degraded rather than maintained – and stem cells with reduced COL17A1 expression show measurably impaired motility and reduced regenerative capacity. [7] UV irradiation independently downregulates COL17A1 expression in keratinocytes, creating a photodamage-specific route to the same stem cell depletion. Reduced COL17A1 correlates positively with impaired keratinocyte regeneration, thinning epidermis, and reduced DEJ integrity in aged skin. This is not simply about having fewer stem cells. It is about the remaining stem cells losing the structural protein that governs their ability to move, self-renew, and maintain the epidermal population. [7]
Keratinocytes as Immune Sensors: The Inflammatory Interface
Keratinocytes are not passive structural cells. They express pattern recognition receptors and cytokine receptors, making them active participants in the skin’s immune environment and active targets of the inflammatory signals that compromise barrier function.
IL-4 and IL-13, the type 2 inflammatory cytokines characteristic of atopic conditions and chronic skin sensitivity, suppress keratinocyte differentiation through multiple concurrent routes. They directly reduce FLG gene expression – the filaggrin suppression described in the Filaggrin page – and simultaneously disrupt tight junction protein expression and localisation. Research has confirmed that IL-4 reduces transepithelial resistance in keratinocyte models and causes mislocalisation of claudin-4 from cell junctions into cytoplasmic vesicles, impairing the second-barrier function of the stratum granulosum tight junction belt. [3] IL-4 and IL-13 also suppress loricrin and involucrin alongside filaggrin – three cornified envelope proteins simultaneously impaired – meaning the acquired differentiation deficit from type 2 inflammation is considerably broader than filaggrin deficiency alone.
This is not incidental to how keratinocytes behave in inflamed skin. It establishes that the inflammatory environment does not merely damage a completed barrier, it actively impairs the production of the cells that would rebuild it. The differentiation programme is running in a cytokine environment that is simultaneously suppressing its key outputs. Addressing barrier dysfunction without addressing that environment is like repairing a wall whilst the materials keep being removed.
Keratinocyte Renewal and Hormonal Decline
Oestrogen has direct effects on keratinocyte proliferation through epidermal oestrogen receptors. Post-menopause, declining oestrogen reduces the proliferative rate of basal keratinocytes, contributing to the 1.13% per year reduction in skin thickness documented post-menopause. [6] Administration of topical oestrogen increases keratinocyte proliferation and epidermal thickness, confirming the direct receptor-mediated effect rather than an indirect systemic one.
Beyond proliferation, oestrogen has a specific role in keratinocyte ceramide metabolism (the Corneocyte page covers this in detail) meaning that declining oestrogen simultaneously reduces how many new keratinocytes enter the differentiation programme and the quality of barrier lipids those keratinocytes produce as they differentiate. Two independent mechanisms of epidermal deterioration converge at the same hormonal transition. [8] The result in post-menopausal skin is a thinner epidermis populated by cells that arrived in a less favourable lipid synthesis environment and that stay at the surface longer before being shed, because the renewal rate has also slowed.
The Inflammatory “Brake” vs. The Stimulus “Gas”
| Scenario | Impact on Keratinocytes | Resulting Barrier Status | Strategy |
|---|---|---|---|
| Type 2 Inflammation (IL-4/13) | Suppresses Filaggrin & Loricrin genes. | “Leaky” barrier; “Melted” tight junctions. | CAP to “quiet” the signal. |
| Hormonal Decline (Estrogen) | Slows proliferation; reduces ceramides. | Thinned epidermis; chronically dry skin. | Retinoids / Niacinamide to boost signals. |
| UV Damage (COL17A1 loss) | Stem cell motility failure. | Fragile skin; poor wound healing. | Thulium for population reset. |
Clinical Application
The keratinocyte description frames treatments differently from fibroblast or collagen pages. Fibroblasts and collagen describe a production and degradation balance – treatments work by shifting that balance. Keratinocytes describe a population and programme quality – treatments work by improving the health of the stem cell population feeding the programme, the completeness of the differentiation programme itself, or the inflammatory environment in which both are operating. Those are distinct targets, and they warrant distinct treatment logic.
Restoring the Stem Cell Population: COL17A1 and EGFR Signalling
For clients where the primary keratinocyte problem is a depleted or photodamaged stem cell population – the presentation common in mature or significantly UV-exposed skin where epidermal thinning, surface dullness, and impaired renewal are the dominant features – the treatment priority is restoring the COL17A1-expressing basal population rather than stimulating an already-compromised one harder.
Thulium 1927nm fractional laser is uniquely positioned here. The MTZ injury drives re-epithelialisation specifically from hair follicle keratinocyte stem cells that retain higher COL17A1 expression than the photodamaged surface population they replace. [5] The cells migrating inward to repopulate treated zones bring a younger stem cell signature with them, restoring the renewable population rather than simply triggering turnover of an existing depleted one. For clients where years of UV exposure have progressively eroded the basal COL17A1+ population, this is qualitatively different from any treatment that stimulates existing basal cells.
iPRF contributes through the EGF and PDGF growth factors in its preparation. EGF directly supports the EGFR–COL17A1 axis whose age-related decline drives stem cell motility impairment. [5] It does not restore COL17A1 expression directly, but it provides the growth factor signal whose absence allows COL17A1 proteolysis to proceed. For clients in earlier stages of stem cell decline – where the EGFR signal has weakened but COL17A1 expression is not yet severely depleted – iPRF can slow the progression of that deterioration whilst the keratinocyte population remains sufficiently responsive.
Restoring the Differentiation Programme: Activating What’s Already There
Where the stem cell population is reasonably intact but the differentiation programme is running below capacity – common in younger reactive or sensitised skin, or in clients where post-inflammatory barrier disruption has impaired the calcium gradient – treatments that trigger the wound-healing and differentiation cascade produce the most direct benefit.
Microneedling activates the keratinocyte differentiation gene programme through the wound-healing response, with gene expression analysis documenting upregulation across cornification, keratinocyte differentiation, and epidermis development pathways alongside SPTLC3 ceramide synthesis. The differentiation programme and lipid production machinery are activated together, not sequentially. For clients where the barrier is structurally impaired but the keratinocyte population is not severely depleted, microneedling activates more complete differentiation in the cells already present.
Microneedling with topical exosome delivery extends this by restoring SPTLC1 expression, PPAR-α, filaggrin, and involucrin in treated keratinocytes, addressing the completeness of the differentiation programme and the lipid synthesis capacity of newly differentiating cells simultaneously. Where microneedling activates the programme, exosomes help ensure it completes more fully.
Resolving Inflammatory Suppression of the Differentiation Programme
For clients where type 2 inflammatory signalling is the active constraint – reactive, atopic-tendency, or chronically sensitised skin – stimulating the differentiation programme through injury-based treatments into a still-suppressed inflammatory environment produces incomplete results. The programme is being activated at one end whilst IL-4 and IL-13 are suppressing its key outputs (filaggrin, loricrin, involucrin, and tight junction proteins) at the other.
CAP is the professional treatment most directly positioned at this mechanism for keratinocytes. Its RONS-mediated NF-κB modulation reduces the IL-4 and IL-13 burden in sensitised superficial tissue, lifting the cytokine suppression of the differentiation programme rather than pushing harder against it. For clients with persistent reactive skin where previous barrier support has produced only temporary improvement, CAP addresses the reason topical support alone is insufficient; it cannot restore differentiation programme outputs whilst the signals suppressing those outputs remain active.
Polynucleotides complement this through their A2AR-mediated anti-inflammatory pathway, calming the tissue environment in which keratinocyte differentiation is occurring. Where the inflammatory suppression involves both epidermal and dermal compartments simultaneously (as it frequently does in chronically reactive perimenopausal skin) combining CAP and polynucleotides addresses the environment from both the surface and tissue-depth perspective.
The Homecare Layer for Keratinocyte Quality
Niacinamide supports keratinocyte differentiation through its upregulation of SPTLC2 and broader EDC gene activity, making it the topical active with the most direct and evidenced effect on differentiation programme quality from the homecare category. It addresses ceramide synthesis and keratinocyte differentiation within the same mechanism rather than two separate steps.
Retinoids accelerate keratinocyte turnover and improve differentiation programme completeness over time through TGF-β upregulation. This is relevant both for clients wanting to improve renewal rate and for those managing photodamage where the basal population quality has declined.
For the post-menopausal client group, the homecare layer needs to address both dimensions of the oestrogen-withdrawal problem: the reduced proliferation rate and the ceramide production deficit. Niacinamide and vitamin C together address the lipid synthesis and hydroxylation steps; retinoids address the differentiation environment. None of these replaces the proliferative signal that oestrogen was providing, but together they support the programme capacity of whatever population is renewing.
Keratinocyte Intervention Matrix
| Goal | Treatment Mechanism | Best For… |
|---|---|---|
| Population Reset | Recruiting “fresh” stem cells via MTZs. | Thulium 1927nm (Mature/Photoaged skin) |
| Programme Speed | Growth factors triggering the EGFR-axis. | iPRF (Early aging/Slower renewal) |
| Lipid & Protein Quality | Restoring SPTLC1 & FLG expression. | Exosomes + Microneedling (Barrier repair) |
| Lifting Suppression | RONS-mediated NF-κB modulation. | CAP (Reactive/Atopic skin) |
Treatment Sequencing for Keratinocyte Quality
For reactive or inflamed presentations: CAP (and polynucleotides where dermal involvement is present) resolves inflammatory suppression before differentiation-stimulating treatments are introduced. This is the same Phase 1 logic established in the Corneocyte clinical context: stimulating a programme that is being actively suppressed at its key outputs produces attenuated results.
For photodamaged or post-menopausal presentations with depleted stem cell populations: thulium for population reset, then microneedling with exosomes to activate the differentiation programme and lipid synthesis machinery in the reconstituted population. iPRF provides EGF-driven support for the EGFR–COL17A1 axis throughout.
For age-related renewal decline without active inflammation: microneedling with exosomes, iPRF for stem cell support, and niacinamide-retinoid homecare form a coherent programme addressing the differentiation cycle, the lipid synthesis machinery, and the basal cell environment between sessions.
The unifying principle is that keratinocyte quality depends on both the population producing them and the environment in which production occurs. A healthy stem cell population running a differentiation programme in a cytokine-suppressed or lipid-depleted environment produces a barrier that underperforms relative to what its cell numbers suggest. Restoring both the population and the programme environment is what produces durable improvement rather than temporary surface change. [4]
References
Allombert-Blaise C, Tamiji S, Mortier L, et al. (2003). Terminal differentiation of human epidermal keratinocytes involves mitochondria- and caspase-dependent cell death pathway. Cell Death Differ, 10(7), 850-2 . doi.org/10.1038/sj.cdd.4401245
Bikle DD, Xie Z, Tu CL (2012). Calcium regulation of keratinocyte differentiation. Expert Rev Endocrinol Metab, 7(4), 461-472 . doi.org/10.1586/eem.12.34
Brewer MG, Yoshida T, Kuo FI, et al. (2019). Antagonistic Effects of IL-4 on IL-17A-Mediated Enhancement of Epidermal Tight Junction Function. Int J Mol Sci, 20(17) . doi.org/10.3390/ijms20174070
Moltrasio C, Romagnuolo M, Marzano AV (2022). Epigenetic Mechanisms of Epidermal Differentiation. Int J Mol Sci, 23(9) . doi.org/10.3390/ijms23094874
Nanba D, Toki F, Asakawa K, et al. (2021). EGFR-mediated epidermal stem cell motility drives skin regeneration through COL17A1 proteolysis. J Cell Biol, 220(11) . doi.org/10.1083/jcb.202012073
Thornton MJ (2013). Estrogens and aging skin. Dermatoendocrinol, 5(2), 264-70 . doi.org/10.4161/derm.23872
Xiang Y, Liu Y, Yang Y, et al. (2022). Reduced expression of Collagen 17A1 in naturally aged, photoaged, and UV-irradiated human skin in vivo: Potential links to epidermal aging. J Cell Commun Signal, 16(3), 421-432 . doi.org/10.1007/s12079-021-00654-y
Unknown Author. PMC: PMC9755298. PMC9755298
Also Known As
- keratinocytes
Anatomical Relationships
Structural Connections
- Produces Ceramides Evidence: Upregulation across cornification, keratinocyte differentiation… alongside SPTLC3 ceramide synthesis
- Produces Claudin-1 Evidence: IL-4 disrupts tight junction protein expression and localisation
- Produces Filaggrin
- Produces Interleukin-33 Evidence: Keratinocytes are the primary source of IL-33 alarmin in skin releasing it upon damage to activate innate immune cells and amplify type 2 inflammation. Cevikbas & Steinhoff JID 2012 doi:10.1038/jid.2012.66
- Produces Keratin Evidence: Keratinocytes produce keratin intermediate filaments (K5/K14 basal K1/K10 suprabasal) as primary structural scaffold throughout differentiation. Standard keratinocyte biology.
- Produces Loricrin Evidence: Loricrin (>70% of cornified envelope) is produced by keratinocytes in stratum granulosum during terminal differentiation. Jeddy et al. J Oral Maxillofac Pathol 2015 doi:10.4103/0973-029X.157204
- Located in Epidermis Evidence: Keratinocytes comprise approximately 90% of epidermal cells and are the structural and functional foundation of the skin barrier
- Located in Stratum granulosum Evidence: Differentiating keratinocytes occupy stratum granulosum producing lamellar body ceramide precursors and profilaggrin before terminal differentiation. Tu et al. Expert Rev Dermatol 2012 doi:10.1586/eem.12.34
- Affects Fibroblast Evidence: Keratinocytes signal to fibroblasts via integrin-mediated and paracrine routes regulating fibroblast collagen and proteoglycan synthesis through bidirectional DEJ crosstalk. Costello et al. J Cell Physiol 2024 doi:10.1002/jcp.31463
- Requires Vitamin A Evidence: Retinoids (Vitamin A derivatives) regulate keratinocyte differentiation via RAR nuclear receptors; retinoic acid upregulates loricrin and involucrin and modulates keratin expression. Rorke & Eckert Environ Health Perspect 1989 doi:10.1289/EHP.8980109
- Requires Vitamin D Evidence: Vitamin D (1,25-dihydroxyvitamin D3) regulates keratinocyte differentiation via VDR-coactivator complexes driving loricrin filaggrin and barrier lipid synthesis. Teichert et al. J Steroid Biochem 2010 doi:10.1016/j.jsbmb.2010.03.027
- Precedes Corneocyte
- Precedes Stratum granulosum Evidence: Keratinocytes differentiating from stratum spinosum become the filaggrin-producing lipid-synthesising cells of stratum granulosum before cornification. PMC9102508
- Has sub-structure Mitochondria Evidence: Keratinocytes in the basal layer are particularly mitochondria-rich; mitochondrial ROS are required signals for keratinocyte differentiation programme (PMC3891634).
- Dermatitis Evidence: Keratinocytes are primary target of IL-4/IL-13 suppression in atopic dermatitis; produce IL-33 and TSLP amplifying type 2 inflammation. Fujii Biol Pharm Bull 2020 doi:10.1248/bpb.b19-00088
- Perimenopausal skin changes Evidence: Declining oestrogen reduces the proliferative rate of basal keratinocytes, contributing to the 1.13% per year reduction in skin thickness documented post-menopause
- Psoriasis Evidence: Keratinocytes are central effectors in psoriasis: hyperproliferate in response to TNF-α IL-17 IL-22 and produce antimicrobial peptides amplifying the inflammatory loop. Kamata & Tada Front Immunol 2023 doi:10.3389/fimmu.2023.1286344
- Skin barrier dysfunction Evidence: What keratinocytes make during that journey… determines whether the skin barrier functions well or poorly
- Topical steroid withdrawal Evidence: Topical steroid use suppresses keratinocyte barrier gene expression (filaggrin loricrin); withdrawal causes rebound inflammation in keratinocyte-rich epidermis. Standard clinical dermatology.
- Cold Atmospheric Plasma therapy Evidence: CAP is the professional treatment most directly positioned at this mechanism for keratinocytes. Its RONS-mediated NF-κB modulation reduces the IL-4 and IL-13 burden
- Injectable Platelet-Rich Fibrin Evidence: iPRF EGF and PDGF support the EGFR-COL17A1 axis in keratinocyte stem cells slowing COL17A1 proteolysis and maintaining stem cell motility. PMC8563287
- Microneedling Evidence: Microneedling activates the keratinocyte differentiation gene programme through the wound-healing response, with gene expression analysis documenting upregulation across cornification
- Polynucleotides Evidence: Polynucleotides complement this through their A2AR-mediated anti-inflammatory pathway, calming the tissue environment in which keratinocyte differentiation is occurring
- Thulium Fractional Laser Evidence: MTZ injury drives re-epithelialisation from hair follicle keratinocyte stem cells that retain higher COL17A1 expression than the photodamaged surface population
Referenced in Conditions & Treatments
- this Stimulated by Epidermal growth factor Evidence: The EGFR–COL17A1 axis is the mechanism through which EGF signalling drives not just proliferation but directed stem cell migration
- this Stimulated by Fibroblast growth factor
- this Stimulated by Injectable Platelet-Rich Fibrin Evidence: iPRF contributes through EGF and PDGF growth factors… EGF directly supports the EGFR–COL17A1 axis whose age-related decline drives stem cell motility impairment
- this Stimulated by Interleukin-33 Evidence: IL-33 acts on keratinocyte ST2 receptors in autocrine manner amplifying type 2 cytokine production and inflammatory signalling. Cevikbas & Steinhoff JID 2012 doi:10.1038/jid.2012.66
- this Stimulated by Oestrogen Evidence: Oestrogen has direct effects on keratinocyte proliferation through epidermal oestrogen receptors
- this Stimulated by Tumour necrosis factor Evidence: TNF-α activates NF-κB in keratinocytes driving IL-6 IL-8 CXCL1 production; TNF receptor signalling triggers IL-24-dependent psoriasis-like inflammation. Kumari et al. Immunity 2013 doi:10.1016/j.immuni.2013.10.009
- this Inhibited by Cortisol Evidence: Text: Cortisol impairs keratinocyte migration and differentiation; pmc.ncbi.nlm.nih.gov/articles/PMC3623592/
- this Inhibited by Interleukin-13 Evidence: IL-4 and IL-13 also suppress loricrin and involucrin alongside filaggrin – three cornified envelope proteins simultaneously impaired
- this Inhibited by Interleukin-4 Evidence: IL-4 and IL-13… suppress keratinocyte differentiation; directly reduce FLG gene expression and disrupt tight junction protein expression
- this Affected by Fibroblast Evidence: Papillary fibroblasts signal to keratinocytes via KGF/FGF7 TGF-β; fibroblast senescence impairs epidermal differentiation through breakdown of DEJ crosstalk. Costello et al. J Cell Physiol 2024 doi:10.1002/jcp.31463
- this Affected by Polynucleotides Evidence: PN-HA combination enhanced HaCaT keratinocyte migration, proliferation, and VEGF/MMP gene expression in vitro; PN affects keratinocyte function. PMID 40009152, 2025.
- this Affected by Psoriasis Evidence: IL-17A, IL-22, and TNF-alpha from Th17 cells drive keratinocyte hyperproliferation, reducing turnover from 28 days to 3-4 days; cytokine signalling drives abnormal keratinocyte behaviour (PMC8657643).
- this Affected by Retinoid Evidence: Text: Retinoids regulate keratinocyte proliferation and differentiation via RAR; academic.oup.com/bjd/article/139/s52/3/6683761
- this Affected by Transforming growth factor beta Evidence: Platelet-derived TGF-beta1 promotes keratinocyte proliferation in cutaneous wound healing during re-epithelialisation; TGF-beta signalling in keratinocytes modulates wound chronification (PMC7216944; PMC3857353).
- this Required by Tissue regeneration Evidence: Keratinocyte re-epithelialisation from hair follicle and interfollicular stem cell reservoirs is the primary process restoring the epidermal barrier; keratinocyte migration/proliferation is a defining feature of regenerative healing (PMC3663196).
- this Part of Epidermis Evidence: Keratinocytes comprise >90% of epidermal cells and are the structural unit of the epidermal barrier. Entity text: keratinocyte differentiation programme defines epidermal function.
Learn More
This topic is discussed in 6 articles:
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The predominant cell type of the epidermis, produced in the basal layer and progressively differentiating through epidermal strata to become the corneocytes that form the stratum corneum barrier.
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The predominant cell type of the epidermis, produced in the basal layer and progressively differentiating through epidermal strata to become the corneocytes that form the stratum corneum barrier.
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The predominant cell type of the epidermis, produced in the basal layer and progressively differentiating through epidermal strata to become the corneocytes that form the stratum corneum barrier.