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Tape strips and microneedle patches can read gene and protein activity in skin without a biopsy. What that means for choosing a psoriasis or eczema treatment, and what remains unproven.
Two patients can present with plaques that look nearly identical, receive the same biologic drug, and experience entirely different outcomes. One clears within a month. The other shows no meaningful improvement at three months and begins again with a different agent. The appearance of a plaque reveals surprisingly little about which inflammatory pathway is driving it. Transcriptomics and proteomics, the large-scale measurement of gene activity and protein output within a tissue sample, are now being studied as a way to close that gap, and a new generation of sampling tools makes those measurements possible without a scalpel.
Psoriasis and atopic dermatitis are both chronic immune-mediated inflammatory skin diseases, and both can now be treated with agents aimed at specific immune signals. Psoriasis is driven predominantly by the interleukin-23 and interleukin-17 axis. Atopic dermatitis is dominated by type 2 inflammation involving interleukin-4 and interleukin-13. The clinical descriptions found on the psoriasis and atopic dermatitis condition pages capture what the skin looks like and how it behaves over time, but they do not identify which cytokine is dominant in an individual patient.
Molecular profiling has shown that the distance between appearance and mechanism is substantial. A comparative transcriptomic analysis of lesional skin characterized atopic dermatitis as an interleukin-13-dominant disease carrying considerably greater molecular heterogeneity than psoriasis [1]. Patients grouped under a single diagnostic label therefore do not share a single molecular profile, and two patients with the same severity score may be biologically suited to different drug classes.
The cost of guessing. Because no routine test identifies the dominant pathway, drug selection proceeds sequentially. In a United States survey of community dermatologists, 82 percent reported switching biologics in 10 to 30 percent of their patients within the first year, and 93 percent reported waiting at least 12 weeks before concluding that a treatment had failed [2]. That survey was developed with industry involvement and reflects American formulary conditions rather than Canadian ones, but the pattern it describes is familiar in any clinic: each unsuccessful attempt costs a patient months of uncontrolled disease.
Transcriptomics measures messenger RNA, the transcribed copies of genes that a cell is actively using at the moment of sampling. RNA sequencing of a skin sample can quantify thousands of transcripts at once, producing a profile of which inflammatory programs are switched on, how strongly, and which barrier genes have been suppressed. Because transcription responds quickly to disease activity and to treatment, the same measurement can be repeated to assess whether a drug has engaged its intended target.
Proteomics measures the proteins themselves, which are the functional output of gene expression rather than the instructions for it. Platforms such as Olink and SOMAscan quantify panels of hundreds of proteins from very small amounts of tissue or blood. In one study of moderate-to-severe atopic dermatitis, the skin proteome showed significant upregulation of inflammatory and cardiovascular-associated proteins not only in lesional skin but also in clinically unaffected skin, and these changes were considerably more pronounced in skin than in blood [3]. Gene and protein measurements from the same individuals correlated moderately, which supports the use of either as a window on disease activity while confirming that the two are not interchangeable.
Most of what is known about the molecular biology of these diseases was learned from punch biopsies. A skin biopsy remains the reference standard for diagnosis, but it requires local anaesthetic, leaves a permanent scar, and cannot reasonably be repeated across multiple sites and multiple time points purely to monitor inflammation. That limitation is what drove the development of minimally invasive alternatives.
Tape stripping applies and removes adhesive discs from the skin surface, lifting away layers of stratum corneum together with the RNA and protein they contain. The technique leaves no scar and requires no anaesthetic. RNA sequencing of tape strips has identified a type 2-high endotype in atopic dermatitis [4] and has detected immune and barrier abnormalities in the skin of young children with early-onset atopic dermatitis, a population in whom biopsy is rarely justifiable [5].
The most informative result to date is a direct comparison of the two diseases. Tape strips taken from adults with moderate-to-severe atopic dermatitis, adults with psoriasis, and healthy controls yielded usable sequencing profiles in 96 of 100 samples. Atopic dermatitis lesions showed preferential type 2 skewing, with elevated interleukin-13, CCL17, and CCL18, whereas psoriasis lesions showed elevated interleukin-17A and interleukin-17F, interleukin-36, interferon gamma, CXCL9, and CXCL10 [6]. Both diseases shared reductions in terminal differentiation, tight junction, and lipid metabolism genes, consistent with barrier disruption in each.
Tape strips sample the surface. A second approach reaches deeper and corresponds to the products patients encounter described loosely as nano patches or microneedle strips. One published platform consists of a patch approximately 2 centimetres across carrying an array of 100 pyramidal microneedles, each 750 micrometres long, chemically modified with single-stranded DNA probes that bind messenger RNA. Applied with a spring-loaded applicator for five minutes, the needles penetrated to roughly 350 to 400 micrometres, deep enough to reach the upper dermis without contacting the nerve endings and vessels of the deeper dermis [7].
In that first evaluation, patches were applied to healthy skin and to psoriatic lesions in seven subjects across 33 samples, and the recovered transcriptome reproduced the molecular information obtained from matched punch biopsies in the same patients [7]. Seven subjects is a feasibility cohort rather than a validation study, but the principle was demonstrated: a biopsy-grade molecular read can be obtained from a device that leaves no scar.
A third method collects superficial skin by scraping rather than by adhesion. A 2024 review compared the two commercial platforms furthest advanced in this field, one built on a dermal diagnostic patch and one on superficial skin scrapings, and concluded that both show promise for predicting response to biologics while facing practical obstacles in insurance coverage and patient acceptance [8].
Measuring a profile is not the same as using it to choose a drug. Work on prediction began with small multi-omic pilots. A framework study within the Psoriasis Stratification to Optimise Relevant Therapy consortium sequenced RNA from blood, lesional skin, and non-lesional skin and analysed the serum proteome across three time points in 10 patients with severe psoriasis treated with etanercept, identifying candidate response signals in tumour necrosis factor signalling pathways [9]. Ten patients cannot establish clinical utility, but the study set out how such data can be integrated.
The largest prospective result so far comes from the MATCH study, a randomized trial of a machine-learning test that predicts response to biologic drug classes using a dermal biomarker patch applied to lesional skin. Of 210 patients enrolled, prescribing behaviour was assessed in 205. Physicians given the test result selected a biologic concordant with that result in 92.3 percent of cases, against 62.9 percent when the result was withheld. Patients whose physicians followed the result were more likely to reach a 75 percent reduction in the Psoriasis Area and Severity Index at 12 weeks, and more reached that threshold by week 4 [10].
The caveats matter. That study was funded and conducted by the test manufacturer, and several authors are employees of or hold equity in the company. Part of the comparison relied on a previously collected dataset rather than a concurrently randomized control arm. The headline finding concerns prescribing behaviour, which measures how physicians act on a test result rather than proving directly that the underlying biology was read correctly. Independent replication has not been published.
For atopic dermatitis the position is more conservative still. A review published on behalf of the International Eczema Council surveyed candidate biomarkers across blood, skin, and minimally invasive sampling and concluded that none has been validated to the standard required for routine clinical decisions [11]. Biomarkers are used extensively in atopic dermatitis research. They do not yet direct treatment at the bedside.
Supported: psoriasis and atopic dermatitis are molecularly distinct from one another and internally heterogeneous, and tape strips, microneedle patches, and superficial scrapings can all recover interpretable transcriptomic and proteomic data without a biopsy.
Promising but unproven: using that data prospectively to select among biologic classes. One manufacturer-led randomized study supports the approach in psoriasis. Independent validation, replication in atopic dermatitis, and comparison against careful clinical judgement are all outstanding.
Not yet routine in Canada: these tests are marketed in the United States and are not part of standard dermatology practice or public funding in Canada. A patient cannot currently request one as part of an insured assessment here.
In the meantime, biologic and advanced small molecule therapy is selected on the basis of disease phenotype and severity, the sites involved, comorbidities such as psoriatic arthritis, the response to and tolerability of previous treatments, pregnancy planning, infection and malignancy history, and provincial funding criteria. These factors remain a reasonable basis for a first choice, and formal reassessment at a defined interval remains part of the plan rather than an admission of failure.
Getting the first choice right nonetheless matters more than it once did. Both diseases are increasingly understood through the lens of disease modification and an early window of opportunity, as discussed for psoriasis and for eczema. If early effective control genuinely alters the long-term trajectory of disease, then months spent on an ineffective agent carry a cost beyond the inconvenience of switching. That is the argument that makes molecular profiling worth following closely even while it remains a research tool.
Skin that looks the same does not necessarily behave the same, and the technology to read the difference now exists. What has not been demonstrated is that reading it produces better decisions than an experienced clinician reaches without it. Patients whose psoriasis or eczema has not responded to successive treatments are encouraged to review the full range of current options at a dermatology consultation.
This article is intended for educational purposes and does not replace professional medical advice. Please consult your dermatologist for personalized recommendations.
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