To understand why the target is unusual, it helps to look at the immunology of the disease. Psoriasis is a chronic autoimmune skin disorder affecting roughly two percent of the global population, and about thirty percent of those patients go on to develop psoriatic arthritis, a condition that combines joint inflammation, pain, and progressive structural damage. Both diseases are driven primarily by CD4-positive T cells, the immune cells whose fate is dictated by the cytokine environment they encounter. One of the most influential of these signals is TGF-beta, a molecule with a famously dual personality: it can push naive T cells toward Th17 cells, potent drivers of inflammation, or toward regulatory T cells, or Tregs, which restrain autoimmunity and protect tissue. In psoriasis and psoriatic arthritis, this balance tips sharply toward Th17 cells, while the protective regulatory arm underperforms.

Most existing therapies attack the downstream consequences of that imbalance rather than the balance itself. Tumor necrosis factor inhibitors and antibodies against the IL-17 axis have transformed treatment for many patients, but the study’s authors note that roughly thirty-five to forty percent of people with psoriatic arthritis fail to reach a minimum level of efficacy with these drugs, and resistance emerges over time in others. Blocking BAMBI offers a conceptually different approach. BAMBI is a pseudoreceptor, a membrane-bound protein that lacks an intracellular signaling domain and acts as a decoy that modulates signaling by the TGF-beta and related pathways. By inhibiting BAMBI with an antibody, the researchers aimed to enhance the signaling that favors regulatory T cell differentiation, thereby rebuilding the immune system’s own brakes instead of merely blocking its accelerators.

The antibody itself, hB101.37, is a humanized monoclonal antibody, meaning its protein framework has been engineered to resemble human antibodies closely enough to minimize the risk that a patient’s immune system will reject it as foreign. The team evaluated its therapeutic effect in three preclinical mouse models: an imiquimod-induced model of psoriasis, an IL-21-induced model of the skin disease, and a mannan-induced model of psoriatic arthritis. These models reproduce key features of the human conditions, from scaly skin inflammation to joint swelling, and are standard tools for testing whether a candidate biologic can plausibly work in patients before any clinical trial begins.

The results were striking on several fronts. Treatment with hB101.37 reduced disease in both the psoriasis and psoriatic arthritis models, confirming efficacy across the spectrum of the disease. Flow cytometry analyses of immune cells from treated animals showed that the antibody reduced the population of pro-inflammatory Th17 cells while promoting differentiation toward the regulatory T cell lineage, exactly the rebalancing effect the researchers had predicted from the mechanism. In molecular terms, the team traced the effect to activation of the Smad2/3 pathway, the canonical intracellular signaling route downstream of the TGF-beta receptor, which they assessed by western blot. In other words, blocking the decoy receptor BAMBI allowed the genuine TGF-beta signal to flow more freely into the Smad pathway, steering T cell fate toward tolerance.

Perhaps the most commercially and clinically significant comparison in the study is head-to-head with an established drug class. The researchers report that anti-BAMBI therapy showed potentially greater clinical efficacy in psoriasis than anti-IL-17A monoclonal antibodies, one of the most successful modern treatments for the disease. If that advantage translates to humans, it would represent a meaningful advance for the many patients whose disease is incompletely controlled by IL-17 blockade. Because the antibody works upstream of the IL-17 axis, reshaping the T cell populations that generate inflammatory cytokines in the first place, it could also, in principle, address multiple inflammatory pathways simultaneously rather than a single mediator.

Safety is where many promising immunomodulators stumble, and the Spanish team devoted considerable effort to characterizing the antibody’s preclinical safety profile. They performed histological and immunofluorescence analyses of murine tissues, measured inflammatory markers by ELISA and gene expression by quantitative PCR, and, notably, conducted transthoracic echocardiography after chronic administration of the antibody to assess cardiac function. Cardiac monitoring matters because TGF-beta family signaling is implicated in fibrosis and remodeling in multiple organs, so any therapy that perturbs this pathway must demonstrate that it does not provoke cardiovascular or structural toxicity. According to the authors, the preclinical phase confirmed the safety profile of the therapeutic antibody, an essential green light for moving toward clinical development.

The work also extended beyond mice. The researchers examined the effects of hB101.37 on human CD4-positive T cells in vitro, isolating the cells from buffy coat samples of anonymous healthy donors provided by the Blood and Tissue Bank of Cantabria under ethics committee approval. Demonstrating that the antibody can modulate T cell differentiation in human cells, not just in engineered mouse models, strengthens the translational case considerably, since species differences in cytokine biology frequently derail therapies that look spectacular in rodents. The animal studies were conducted under the approval of the University of Cantabria’s Institutional Laboratory Animal Care and Use Committee and in accordance with European directives on animal welfare.

The research is the product of a collaboration that blends a small biotechnology company with academic immunology groups. Inhibitec Anticuerpos, based in Santander, developed the antibody, and several of its scientists are coauthors, while the University of Cantabria’s molecular biology and pharmacology departments and the CSIC-affiliated biomedicine institute contributed the disease models and mechanistic analyses. The work was funded by a constellation of Spanish public agencies, including the Centro para el Desarrollo Tecnológico Industrial, the Ministry of Science, Innovation and Universities, SODERCAN, and the Government of Cantabria, along with the United States National Psoriasis Foundation, reflecting the international interest in new psoriasis therapeutics. The authors note a conflict of interest: Ramón Merino is a cofounder and stockholder of Inhibitec, and several coauthors are company employees, with the company holding a license for a patent application covering monoclonal antibodies against BAMBI for inflammatory diseases.

Caveats remain. The findings are preclinical, generated in mouse models and human cells in culture, and the antibody has not yet been tested in patients, where questions of dosing, immunogenicity, long-term safety, and real-world efficacy will ultimately be decided. The published version of the paper was shared early as an accepted manuscript and remains subject to final editorial edits. Still, the study offers something the psoriasis field has lacked: a genuinely new point of intervention that does not simply block another inflammatory cytokine but instead reprograms the T cell balance itself, boosting the regulatory arm of immunity while shrinking the inflammatory one. For the large minority of patients with psoriatic arthritis who do not respond to TNF or IL-17 blockers, and for whom drug resistance looms over even successful treatments, a first-in-class antibody that teaches the immune system to regulate itself is a development worth watching closely as it advances toward the clinic.

Subject of Research: Development of a humanized anti-BAMBI monoclonal antibody for the treatment of psoriasis and psoriatic arthritis

Article Title: Humanized anti-BAMBI monoclonal antibody as a novel therapeutic strategy for psoriatic arthritis

Article References: Perez-Adrian, P., Romero, D., Cappitelli, V., Gallego, F., Ruso-Julve, F., Calvo, M., Garcia, R., Puyalto, A., Gomez, I., Merino, D., Gil-de-Gomez, L., Merino, R., & Casado-Medrano, V. (2026). Humanized anti-BAMBI monoclonal antibody as a novel therapeutic strategy for psoriatic arthritis. Journal of Translational Medicine. https://doi.org/10.1186/s12967-026-09038-5

Image Credits: AI Generated

DOI: 10.1186/s12967-026-09038-5

Keywords: psoriasis, psoriatic arthritis, BAMBI, monoclonal antibody, Th17 cells, regulatory T cells, TGF-beta, immunotherapy, biologics, Smad2/3 pathway, preclinical models, autoimmune disease

The research team, led by Krisztina Szalkay and Kinga Farkas of Semmelweis University in Budapest, set out to answer a question that has long hovered at the edge of autism research: could the way autistic children eat, and the way they sense the world, form a recognizable early behavioral pattern that clinicians could use to spot children who need closer developmental follow-up? With autism now affecting roughly 2.8 percent of children, or about 1 in 36 eight-year-olds in the United States, and with diagnosis often arriving years after symptoms first appear, the search for early, non-social behavioral correlates has taken on real urgency. Widely used screening instruments such as the M-CHAT-R/F focus almost exclusively on social communication and repetitive behaviors, leaving sensory and feeding signs largely invisible to routine surveillance.

That blind spot matters because feeding problems are extraordinarily common in autism. Previous estimates cited in the review suggest they affect between 46 and 89 percent of autistic children, compared with just 1 to 2 percent of typically developing peers. These difficulties frequently emerge between 15 and 36 months of age, a developmental window that precedes or coincides with the onset of core autism symptoms, and they can cascade into malnutrition, growth faltering, poorer academic performance, and impaired social functioning. Atypical sensory processing, formally recognized in the DSM-5 as part of the restricted and repetitive behavior domain, affects more than 70 percent of autistic children and may appear as early as six months of age, potentially before social-communication differences such as impaired joint attention become apparent.

To build their synthesis, the Hungarian team searched PubMed, Embase, Scopus, and the Cochrane Central Register through November 15, 2023, following PRISMA 2020 guidelines and registering the protocol in PROSPERO. From 11,202 articles identified by the search key, plus 1,067 more found through citation chasing, 46 studies survived screening. Most were cross-sectional, spanning participants aged 2 to 19 years, and the majority relied on parent-report questionnaires such as the BAMBI, the Child Eating Behavior Questionnaire, and the Sensory Profile family of instruments. Risk of bias was assessed with the QUIPS tool; ten studies were rated low risk, six moderate, and one high. Statistical pooling used random-effects models with restricted maximum likelihood estimation and Hartung-Knapp adjustment, and correlations were Fisher z-transformed before aggregation.

The meta-analytic numbers are striking. Beyond the large overall difference in mealtime behavior, the Limited Variety subscale, reflecting restricted food repertoires, showed a standardized mean difference of 1.18 across seven studies involving more than 700 children. Disruptive mealtime behaviors differed by 0.86, and food refusal showed a moderate effect of 0.70 with a clear trend toward higher refusal in autistic children, a pattern the authors suggest may reflect communication difficulties around food. On the sensory side, autistic children scored dramatically lower on the Short Sensory Profile total, with a mean difference of minus 26.03 points, indicating far more atypical behavioral and emotional responses to everyday sensory input.

When the team standardized scores across different sensory assessment tools to allow direct comparison, one modality stood out above all others: touch. Tactile sensitivity showed the largest group difference of any domain, with a standardized mean difference of minus 1.80, followed by auditory filtering at minus 1.35, sensation seeking at minus 1.23, and taste-smell sensitivity at minus 1.05. For a child who experiences the texture of a lumpy sauce or the seam of a sock as genuinely aversive, the dinner table becomes a sensory minefield, and the data suggest that this is not fussiness but a measurable neurodevelopmental profile.

Perhaps the most clinically consequential finding is the correlation itself. Across studies, the pooled association between the severity of sensory processing differences and the severity of feeding difficulties was moderate, with an absolute correlation coefficient of 0.47 and, notably, near-zero heterogeneity, suggesting the relationship is remarkably stable across study contexts. The link between taste-smell sensitivity and limited food variety was even stronger, at 0.58. Individual studies reported correlations as high as 0.63 to 0.74 between overall sensory and feeding scores, and strong associations between oral and taste-smell processing and restricted eating even when different instruments and patient selection criteria were used. Tactile processing correlated with feeding problems in the 0.29 to 0.53 range, while visual sensitivity, auditory sensitivity, and auditory filtering were also linked to overall eating difficulties.

From these data, the authors distilled five recurrent dimensions of autism-associated feeding difficulty: limited food variety, food refusal, disruptive mealtime behaviors, sensory-based eating problems such as food touch aversion and temperature sensitivity, and oral-motor challenges. They mapped these dimensions onto existing diagnostic frameworks, including the DC:0-3R and DC:0-5 developmental classification systems and the ARFID-related constructs of DSM-5 and ICD-11, offering clinicians a structured way to think about feeding presentations without inventing new diagnostic categories. The framework is explicitly descriptive and hypothesis-generating, and the authors stress it requires empirical validation in longitudinal and comparative studies before it could inform formal practice.

Caution is warranted on several fronts, and the authors are candid about the limitations. Nearly all the evidence is cross-sectional, meaning the sensory-feeding profiles are best understood as early-emerging correlates of autism rather than established predictive markers. Most samples were assessed after diagnosis, in the preschool and early school-age years, with very little data from infancy and toddlerhood. The instruments were largely developed and normed in Western populations, and most studies came from North America, Europe, or Australia, raising questions about cross-cultural generalizability. Caregiver factors such as feeding-related stress and parent-child mealtime dynamics were rarely reported, comparator groups were transdiagnostically heterogeneous, and publication bias could not be formally assessed because fewer than ten studies contributed to each meta-analysis. Substantial heterogeneity in the between-group analyses further means the pooled effect sizes should be read as distributions of study-specific effects rather than single universal values.

Feeding difficulties, moreover, are not unique to autism. Comparable sensory and feeding features appear in children with ADHD, obsessive-compulsive symptoms, Tourette syndrome, and avoidant/restrictive food intake disorder, and a recent prevalence-based meta-analysis documented substantial co-occurrence between autism and ARFID, recommending bidirectional screening in clinical settings. The authors therefore argue that feeding inventories and sensory questionnaires should function as structured prompts within routine pediatric and developmental assessments, flagging children who warrant closer neurodevelopmental evaluation, rather than as stand-alone autism screening tools. They complement, rather than replace, existing evidence-based screening recommendations. What the review delivers is a quantified, multi-modal portrait of a behavioral pattern that emerges early, persists over time, and is measurable with brief parent-report instruments already in clinical use. Confirming whether that pattern can genuinely predict autism, and whether intervening on sensory-driven feeding problems during periods of heightened neuroplasticity improves nutritional status, daily functioning, and family quality of life, will require the prospective longitudinal cohorts the authors call for, following children from infancy through childhood with both high-risk samples and community controls. Until then, the dinner table, long a site of quiet struggle, has gained new scientific significance as a window onto the developing autistic brain.

Subject of Research: The association between early-life feeding behavior and sensory processing differences in children with autism spectrum disorder

Article Title: Early-Life Feeding Behavior and Sensory Processing in Autism Spectrum Disorder: A Systematic Review and Meta-Analysis

Article References: Szalkay, K., Gergő, D., Kói, T., Kenesei, D., Ocskay, K., Garami, M., Hegyi, P., Nagy, R., & Farkas, K. (2026). Early-Life Feeding Behavior and Sensory Processing in Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. Journal of Autism and Developmental Disorders. https://doi.org/10.1007/s10803-026-07543-6

Image Credits: AI Generated

DOI: 10.1007/s10803-026-07543-6

Keywords: autism spectrum disorder, feeding difficulties, sensory processing, food selectivity, meta-analysis, systematic review, tactile sensitivity, taste-smell sensitivity, early detection, BAMBI, Sensory Profile, child development

The research team, led by Gül Eda Kılınç Tulum together with Yasemin Açar Kuru and Aliye Özenoğlu, set out with three linked goals: to characterize the feeding-related behaviors of children and adolescents with autism, to identify feeding-related factors from the perspective of caregivers, and to examine how nutritional status, quality of life, and behavioral problems relate to one another. Rather than relying on a single measure, the investigators assembled a battery of validated instruments, each targeting a different layer of the mealtime experience. The Brief Autism Mealtime Behavior Inventory, known as BAMBI, captured child mealtime behaviors; the Screening Tool of Feeding Problems, or STEP, flagged feeding difficulties; the Feeding Strategies Questionnaire documented parental approaches; the Quality of Life in Autism questionnaire, QoLA, assessed caregiver well-being; and a food frequency questionnaire charted dietary intake patterns.

The sample itself reflects the demographic profile often seen in pediatric autism research. The children and adolescents had a mean age of 8.98 years, with a standard deviation of 3.86, and three-quarters of them, 75.0 percent, were male. Perhaps more striking was the anthropometric finding: 33.3 percent of the participants were classified as overweight or obese according to World Health Organization growth references. This figure echoes a growing body of meta-analytic evidence showing that children with autism face elevated risks of excess weight gain, a pattern that may seem paradoxical in a population famous for picky eating but is consistent with diets dominated by energy-dense, highly processed, and palatable foods that survive even the strictest food selection filters.

On the BAMBI, the mean total score was 40.25 with a standard deviation of 8.24, and the sub-dimension analysis revealed where the trouble concentrates. The limited variety subscale scored highest at 20.6, with a standard deviation of 5.87, indicating that restricted food variety was the single most prominent feeding concern in this cohort. Food selectivity in autism is well documented in the broader literature; systematic reviews and large clinical cohorts have repeatedly found that children with autism accept fewer foods, reject entire food groups, and demand ritualized presentation far more often than their neurotypical peers. What the new study adds is a quantified hierarchy: within this sample, the narrowness of the accepted diet outweighed other mealtime behaviors such as food refusal or disruptive conduct at the table.

The STEP results told a complementary story. Among its sub-dimensions, nutrition-related behavioral problems achieved the highest mean score, 3.27 with a standard deviation of 3.12. This category encompasses difficulties that directly interfere with adequate nourishment, from refusing entire texture classes to vomiting or distress around specific nutrients and food types. Meanwhile, the Feeding Strategies Questionnaire revealed that the highest-scoring parental approach fell under child control of intake, with a mean of 19.33 and a standard deviation of 6.14. In practical terms, parents reported ceding substantial authority over what and how much their children eat. Clinicians will recognize this dynamic: when every meal risks a meltdown, allowing the child to dictate the menu can feel like the only sustainable path, even as it narrows the diet further and shifts the household’s nutritional baseline.

The statistical heart of the paper lies in its correlation analyses, which connect the child’s feeding profile to the parent’s lived experience. The BAMBI and STEP total scores were significantly and positively correlated, with a p-value of 0.009, meaning that children rated as showing more problematic mealtime behaviors were also flagged for more feeding problems on an independent instrument, a convergence that strengthens confidence in the measurement. More consequential for family well-being, the BAMBI total score was negatively correlated with the QoLA Part A score, which reflects the parent’s perception of the child’s quality of life, at p = 0.039. In other words, the more severe the mealtime behavior problems, the poorer parents rated their child’s overall quality of life, positioning feeding not as an isolated domain but as a lens through which families judge broader functioning.

The second key association ran in the opposite emotional direction. The STEP total score was positively associated with the QoLA Part B score, which measures parental quality of life and the burden parents experience, at p = 0.004. Because higher Part B scores on the QoLA correspond to greater difficulty and lower parental well-being, this finding indicates that more severe feeding problems were linked to worse caregiver quality of life. The mean QoLA scores in the sample, 91.0 with a standard deviation of 16.53 for Part A and 59.88 with a standard deviation of 19.27 for Part B, provide context for where these families sit on both dimensions. Together, the two correlations sketch a bidirectional picture: feeding problems color how parents see their child’s life, and they also erode the parents’ own well-being, a pattern consistent with prior research showing that mealtime stress is a significant contributor to caregiver strain in autism households.

The nutritional implications of such restricted eating are not trivial. The wider literature cited by the authors, including meta-analyses comparing dietary intake between children with autism and typically developing peers, documents inadequate intakes of several micronutrients, and scoping reviews have catalogued deficiencies in vitamins and minerals among selectively eating autistic children. In severe cases, case reports and case series have described nutritional deficiency diseases arising from avoidant and restrictive eating patterns associated with autism. The one-third of this sample classified as overweight or obese adds a second, seemingly contradictory risk layer, since energy-dense selective diets can simultaneously deliver excess calories and insufficient micronutrients. This double burden, overenergy alongside undernutrition, is increasingly recognized as a signature nutritional challenge in pediatric autism and underscores why routine growth monitoring and dietary assessment belong in standard care pathways.

The authors conclude that food selectivity and feeding problems are common in children and adolescents with autism spectrum disorder and are associated with lower parental quality of life for both the affected individuals and their caregivers, a conclusion they argue highlights the need for early, family-centered, multidisciplinary nutritional interventions. The emphasis on family-centered care is significant. Because the study found parents deferring to child control of intake, interventions that target the child alone may miss the relational dynamics that sustain restrictive eating. Multidisciplinary teams that combine dietitians, behavioral therapists, occupational therapists addressing sensory sensitivities, and clinicians monitoring gastrointestinal health are better positioned to broaden diets gradually while reducing the mealtime conflict that wears parents down.

As with all cross-sectional designs, the study captures associations rather than causal pathways, and its modest sample of 48 children means the findings are best read as a carefully measured snapshot rather than a definitive epidemiological estimate. Even so, the convergence of independent instruments, the alignment with international meta-analytic evidence on obesity and food selectivity in autism, and the explicit linkage between child feeding severity and caregiver quality of life give the results practical weight. For clinicians, the message is to screen for feeding problems early and treat them as a legitimate clinical target rather than a behavioral footnote. For parents exhausted by the nightly standoff over a single accepted brand of pasta, the study offers validation: the struggle at the table is real, measurable, and, importantly, treatable with the right support.

Subject of Research: Feeding problems, nutritional status, and parental quality of life in children and adolescents with autism spectrum disorder

Article Title: Beyond Food Selectivity: Feeding Problems, Nutritional Status, and Parental Quality of Life in Autism Spectrum Disorder

Article References: Kılınç Tulum, G. E., Açar Kuru, Y., & Özenoğlu, A. (2026). Beyond Food Selectivity: Feeding Problems, Nutritional Status, and Parental Quality of Life in Autism Spectrum Disorder. Journal of Autism and Developmental Disorders. https://doi.org/10.1007/s10803-026-07558-z

Image Credits: AI Generated

DOI: 10.1007/s10803-026-07558-z

Keywords: autism spectrum disorder, food selectivity, feeding problems, nutritional status, parental quality of life, mealtime behavior, pediatric nutrition, overweight and obesity, BAMBI, STEP, QoLA, family-centered intervention