Why Disease Comes Back in the Same Spot
In this special conference coverage from the 2026 Elevate-Derm RAPIDS Conference, guest host Victoria Garcia Albea, a dermatology NP, opens with what Dr. Jason Hawkes calls his favorite 'nerdy stuff': resident memory T cells. Hawkes explains that these are long-acting cells that stay in tissue for years, distinct from the T cells clinicians typically discuss in psoriasis or atopic dermatitis. Even after shutting off an immune response, these cells can linger and drive disease locally many years later.
That biology, Hawkes says, explains clinical patterns APPs see every day — why psoriasis patients keep getting plaques on the same knees and elbows, and why fixed drug reactions recur at the identical spot. The practical implication: getting closer to true remission or long-term control probably means hitting these long-acting tissue cells, not just the immune signaling that starts in the lymph nodes.
Hawkes frames these cells as originally protective. The skin is a first line of defense, so having primed T cells there made evolutionary sense — psoriasis, for instance, ramps up antimicrobial peptides. Many of these diseases, he notes, represent something once protective that became pathologic once the original selection pressures fell away.
Oral 'Peptibodies': Icotrokinra and Closing the Gap
The conversation turns to the shift toward oral therapy, and specifically icotrokinra (icotide). Hawkes breaks down why the biologic-versus-small-molecule debate is so polarizing and why neither is inherently 'better.' Biologics are big molecules — expensive, injectable or IV, refrigerated — but they act like snipers with consistent drug levels and infrequent dosing. Small molecules go through tissue and the liver easily, but carry drug-drug interactions and don't stay on target well, which is why they tend to be less effective unless broadly acting like JAK inhibitors.
Icotrokinra, Hawkes explains, is a small peptide roughly ten times the size of a small molecule — enough surface area to bind its target more like a biologic while still small enough to get inside cells. It blocks IL-23, and Hawkes notes it has a head-to-head against ustekinumab that he thinks it has a good chance of winning. The upshot he offers APPs: an oral pill approaching biologic-level efficacy with an IL-23-class safety profile — no liver metabolism, no drug-drug interactions in the label.
On monitoring, Hawkes says he has essentially no special concerns, citing the familiarity of the IL-23 class. He and Garcia Albea both point to updated NPF/AAD guidance suggesting tuberculosis testing isn't really needed for IL-17 and IL-23 blockade. His practical stance: a baseline QuantiFERON if you're starting a biologic and have concern, but no basis for annual rechecking absent risk factors or a payer requirement. Garcia-Albea highlights a unique practical perk — icotide can be dissolved in about four ounces of water (wait until it clears, add more, then take) and is available down to age 12, useful for adolescents who can't swallow pills.
GLP-1s and the Psoriasis–Obesity Link
Hawkes and Garcia Albea discuss incorporating GLP-1s into inflammatory skin disease. Hawkes references the VIP trials (Gelfand, Mehta and others), which showed that good psoriasis control didn’t reliably improve comorbidities—evidence of a complex relationship. He cites an ixekizumab-versus-tirzepatide trial suggesting an obesity-targeted drug can help both skin and how patients feel, and notes psoriasis carries increased mortality, likely on the order of five to seven years.
On prescribing, Hawkes is pragmatic. Many patients are already on these agents or asking about them. He personally feels comfortable prescribing GLP-1s and considers them no harder to manage than cyclosporine, methotrexate, or acitretin — but he stresses it doesn't have to fall to dermatology. What matters is having the conversation and monitoring comorbidities. He flags the clinical-trial detail that patients also met with dietitians to address muscle wasting through protein intake and exercise.
For non-obese psoriatic patients, Hawkes cautions against over-reading the GLP-1 receptor expression seen in psoriatic plaques — it signals an immunology-obesity link but isn't a core disease driver. In patients with psoriatic arthritis and no metabolic risk factors, he sees little rationale to start therapy, but recommends counseling about future risk and keeping a low threshold to act if metabolic disease develops.
Long Half-Life Biologics: A Real Trade-Off
On extended-half-life biologics, Hawkes acknowledges the patient appeal — a once-a-year shot 'like your flu shot' — but lays out the trade-offs. If a side effect appears, you can't 'suck the medication out.' He's reassured that the IL-23 pathway is very safe even at high doses (the breakout study dosed up to four times risankizumab with no safety signals), but worries more about IL-17A/F, where candidiasis events could theoretically persist longer with an extended half-life.
He also warns that longer isn't always better: spacing doses too far apart caused rebound between injections, as seen historically when ustekinumab moved from 12-week to 8-week dosing. Extending duration requires hitting the target harder — he points to higher-dose, extended designs patterned after risankizumab. And psychologically, some patients prefer 'fast on, fast off' agents (like the JAK inhibitors or remibrutinib for CSU) that they can stop before surgery. A final practical wrinkle: 75-day half-lives can lock patients out of clinical trial enrollment for extended washout periods.