Researchers measured baseline leukocyte counts in the Copenhagen General Population Study and UK Biobank, then used Cox regression to estimate their associations with subsequently diagnosed AMD. The results from the two cohorts were meta-analyzed. The investigators also used genetic instruments derived from genome-wide association studies to conduct one-sample Mendelian randomization and multivariable Mendelian randomization in the UK Biobank and Million Veteran Program.

These genetic analyses were designed to assess whether inherited variations associated with leukocyte counts supported a causal relationship with AMD rather than merely reproducing the observational association. Observationally, a one-standard-deviation increase in the total leukocyte count was associated with a 7% higher hazard of clinically diagnosed AMD, with a hazard ratio of 1.07 and a 95% confidence interval of 1.05 to 1.09. Neutrophil counts showed the same estimated increase: a hazard ratio of 1.07, also with a 95% confidence interval of 1.05 to 1.09.

A one-standard-deviation increase in monocyte, basophil and eosinophil counts was associated with hazard ratios of 1.05, 1.06 and 1.05, respectively, with respective 95% confidence intervals of 1.03 to 1.07, 1.04 to 1.08 and 1.03 to 1.06. All five observational associations had p-values below 0.0001. The genetic evidence pointed most specifically to eosinophil counts.

In the one-sample Mendelian randomization analysis, a one-standard-deviation increase in genetically determined eosinophil count was causally associated with a 7% increase in the odds of clinically diagnosed AMD. The estimated odds ratio was 1.07, with a 95% confidence interval of 1.00 to 1.15 and p = 0.038. Multivariable Mendelian randomization produced an odds ratio of 1.12, with a 95% confidence interval of 1.03 to 1.21 and p = 0.006.

Estimates from the genetic analyses were then meta-analyzed, leading the authors to conclude that elevated eosinophil counts are causally linked to the risk of clinically diagnosed AMD and that systemic eosinophil-driven immune pathways may contribute to AMD pathogenesis. The study’s findings apply to the European-ancestry populations included in the three cohorts, and the reported endpoint was clinically diagnosed AMD. The results therefore do not quantify the risk faced by an individual with a particular eosinophil count, nor do they show that every person with elevated eosinophils will develop AMD.

The central distinction is between the prospective observations and the genetic evidence: higher counts of several leukocyte subtypes were associated with subsequent AMD diagnoses, while the Mendelian randomization analyses specifically supported a causal association for genetically elevated eosinophil counts.

Subject of Research: Leukocyte counts and incident age-related macular degeneration in three prospective European-ancestry cohorts.

Article Title: Leukocytes and age-related macular degeneration

Article References: Sandau, N., Gorman, B. R., Luo, J., Peachey, N. S., Nordestgaard, B. G., Tybjaerg-Hansen, A., Thomassen, J. Q., Iyengar, S. K., & Frikke-Schmidt, R. (2026). Leukocytes and age-related macular degeneration. European Journal of Epidemiology. https://doi.org/10.1007/s10654-026-01471-6

Image Credits: AI Generated

DOI: 10.1007/s10654-026-01471-6

Keywords: age-related macular degeneration, eosinophils, leukocytes, Mendelian randomization, prospective cohorts, immune pathways, vision loss, UK Biobank, Copenhagen General Population Study, Million Veteran Program, age-related, macular

The research team, led by endocrinologists at Basaksehir Cam and Sakura City Hospital affiliated with the University of Health Sciences, analyzed records from 252 patients. The cohort comprised 132 patients with overt Cushing syndrome, subdivided into 75 with Cushing disease, where a pituitary tumor drives excess adrenocorticotropic hormone, and 57 with adrenal Cushing syndrome, where the adrenal gland itself overproduces cortisol. A further 68 patients had mild autonomous cortisol secretion, often abbreviated MACS, a subtle biochemical abnormality frequently detected in adrenal incidentalomas, and 52 patients had nonfunctioning adrenal tumors, or NFAT, which secrete no excess hormone. The investigators compared standard complete blood count parameters across these groups, including total white blood cell count and the individual counts of neutrophils, monocytes, lymphocytes, eosinophils, and basophils, together with two widely used derived indices, the neutrophil-to-lymphocyte ratio and the monocyte-to-lymphocyte ratio.

Cortisol is a potent immunomodulatory hormone, and its chronic excess has long been known to reshape circulating leukocyte populations. Glucocorticoids promote the release of mature neutrophils from the bone marrow, delay their apoptosis, and simultaneously drive the redistribution and death of lymphocytes, producing the classic picture of neutrophilia with relative lymphopenia seen in states of glucocorticoid excess. What has remained uncertain is whether the low-grade, often subclinical cortisol elevation of MACS produces hematological changes that are detectable and comparable to those of overt disease. Resolving this question matters clinically, because MACS is increasingly diagnosed as adrenal imaging becomes more common, yet its systemic consequences remain debated.

The results were clear-cut at the extremes. Total white blood cell count, neutrophil count, monocyte count, and the monocyte-to-lymphocyte ratio were all significantly higher in patients with overt Cushing syndrome than in either the MACS group or the NFAT group, with p values at or below 0.002. The neutrophil-to-lymphocyte ratio, a marker frequently studied in inflammatory and endocrine disease, was significantly elevated in overt Cushing syndrome only in comparison with MACS once the analysis was corrected for multiple comparisons using the Bonferroni method. This pattern indicates that the myeloid expansion characteristic of glucocorticoid excess, with more neutrophils and monocytes relative to lymphocytes, is a feature of overt disease rather than of the milder biochemical state.

In striking contrast, no significant differences emerged between the MACS and NFAT groups on any individual parameter, with all p values exceeding 0.05. The effect sizes separating these two groups were uniformly small, with Cohen’s d values ranging from 0.02 to 0.17, a range conventionally interpreted as negligible. The authors note that any true difference between mild autonomous cortisol secretion and nonfunctioning tumors is likely to be small, although they caution that subtle effects cannot be entirely excluded by a study of this size. In practical terms, a routine blood count cannot currently distinguish a patient with mild cortisol autonomy from one with a hormone-silent adrenal mass.

Beyond group comparisons, the study examined how leukocyte parameters track with biochemical measures of cortisol burden. Neutrophil count, monocyte count, the neutrophil-to-lymphocyte ratio, and the monocyte-to-lymphocyte ratio each correlated positively with multiple cortisol markers, which in this clinical context typically include urinary free cortisol, late-night salivary cortisol, and the dexamethasone suppression test. This dose-response relationship strengthens the biological plausibility of the findings: the more cortisol circulating, the more pronounced the shift toward myeloid cells in the peripheral blood. It also suggests that these inexpensive, routinely measured indices could serve as accessible proxies for the immunological impact of cortisol excess.

To move beyond univariate comparisons, the researchers performed an exploratory linear discriminant analysis, a multivariate statistical technique that seeks linear combinations of variables best separating predefined groups. The analysis aimed to characterize the overall leukocyte profiles of Cushing disease, adrenal Cushing syndrome, MACS, and NFAT. On the primary discriminant axis, basophil count emerged as the parameter with the highest normalized loading. However, the authors themselves flag an important statistical caveat: because basophil counts are small in absolute magnitude, their loadings can be inflated by scale-related artifacts rather than reflecting a genuine biological signal. This transparency is a notable feature of the paper, which consistently frames its multivariate results as exploratory.

Indeed, the authors are explicit that the classification performance of the discriminant model was modest and not validated in an independent cohort. They emphasize that these findings are hypothesis-generating and should not be interpreted as evidence of a validated diagnostic tool or of a pathophysiological continuum linking mild and overt cortisol excess. This restraint matters in a field where machine-learning-style analyses of routine laboratory data are increasingly promoted as diagnostic shortcuts. The study instead delivers a more measured message: overt hypercortisolism leaves a clear myeloid signature in the blood, but mild autonomous cortisol secretion, at least as captured by standard hematological parameters, does not.

The clinical implications cut in two directions. For patients with overt Cushing syndrome, the correlation between myeloid indices and cortisol burden adds to the evidence that chronic glucocorticoid excess produces measurable systemic inflammation-like changes, which may be relevant to the elevated cardiovascular and infectious risk seen in these patients. For the growing population of patients found to have adrenal incidentalomas, the absence of hematological differences between MACS and NFAT suggests that routine blood counts offer no added diagnostic value in characterizing the functional status of such tumors, and that established endocrine testing remains essential.

As a single-center retrospective cross-sectional study, the work has inherent limitations, including the possibility of selection bias and the inability to establish causality or track changes over time within individual patients. Nevertheless, by systematically comparing four clinically distinct adrenal and pituitary states within a single cohort, the study provides one of the clearest pictures to date of where, on the spectrum of cortisol excess, the immune system begins to visibly shift. The answer, apparently, is not at the mild end. Future prospective studies with larger MACS cohorts and longitudinal sampling will be needed to determine whether subtle immune changes emerge over time, and whether any leukocyte signature could eventually complement, rather than replace, the biochemical tests that currently define this enigmatic condition.

Subject of Research: Peripheral leukocyte profiles across clinical forms of hypercortisolism and nonfunctioning adrenal tumors

Article Title: Peripheral leukocyte profiles in different clinical forms of hypercortisolism and nonfunctioning adrenal tumors: a retrospective cross-sectional study

Article References: Burhan, S., Ozkahraman, A. U., Korkmaz Yilmaz, M., Akbulut, S., Cicek, M. Z., Niyazoglu, M., & Hatipoglu, E. (2026). Peripheral leukocyte profiles in different clinical forms of hypercortisolism and nonfunctioning adrenal tumors: a retrospective cross-sectional study. BMC Endocrine Disorders. https://doi.org/10.1186/s12902-026-02668-2

Image Credits: AI Generated

DOI: 10.1186/s12902-026-02668-2

Keywords: Cushing syndrome, mild autonomous cortisol secretion, adrenal incidentaloma, leukocytes, neutrophil-to-lymphocyte ratio, monocyte-to-lymphocyte ratio, cortisol, endocrinology, hematology, linear discriminant analysis, biomarkers, nonfunctioning adrenal tumor

The research team, led by M. J. Dunnet and Tim Hore of the University of Otago in New Zealand, set out to find genomic regions that could cleanly separate leukocytes, the white blood cells that drive inflammation, from every other tissue in the body. Their starting point was a comprehensive human methylation atlas containing data for more than 423,000 CpG sites across blood cell preparations and nine other tissue types that were believed to be free of immune and vascular contamination. For each CpG site, the team calculated the difference between the average methylation level in leukocytes and the average across all non-leukocyte tissues. Sites with a difference of 0.8 or more on a scale from 0 to 1 were classified as leukocyte-specific differentially methylated positions, or ls-DMPs. The screen yielded 77 such sites, of which 19 were highly methylated in blood cells and 58 were essentially unmethylated.

From this list, the researchers focused on the only two CpG islands containing multiple leukocyte-specific sites. The first sits within the HOXA3 locus on chromosome 7, and the second lies within exon 26 of the MAP4K1 gene on chromosome 19. At both loci, the top CpG sites showed very high methylation in leukocytes, moderately low methylation in adipocytes, lung epithelial cells and vascular endothelial cells, and virtually no methylation in colonic epithelium, cortical neurons, hepatocytes and pancreatic cell types. When the team examined methylation across ten different immune cell populations, all mature leukocyte subpopulations were highly methylated at both markers. Intriguingly, the pattern appears to be laid down early in development: foetal liver CD34-positive haematopoietic stem cells showed significant demethylation compared with their adult counterparts, suggesting that methylation accumulates specifically in the foetal stem cells of the blood-forming lineage and is then maintained through every subsequent stage of differentiation and ageing.

Array-based methylation platforms, which measure thousands of CpG sites simultaneously, are powerful discovery tools but are expensive per sample and rely on single probes that risk under-sampling each region. To turn their discovery into something closer to a diagnostic test, the researchers adapted a rapid, cost-effective amplicon bisulphite sequencing assay. Bisulphite treatment converts unmethylated cytosines into uracils while leaving methylated cytosines untouched, so sequencing the treated DNA reveals the methylation state of every CpG within the amplified fragment. Because neighbouring CpGs in a CpG island tend to share the same methylation state, reading multiple sites per DNA molecule dramatically increases the discriminatory power of the test. The team amplified the HOXA3 and MAP4K1 regions using a dual-index, four-primer PCR strategy and sequenced the products on a benchtop instrument.

The validation strategy was elegantly simple. The researchers purified DNA from peripheral blood mononuclear cells, which represent the nucleated fraction of blood, and from cultured intestinal organoids, three-dimensional structures grown from rectal crypt stem cells that contain no blood or vascular contamination. Pure organoid DNA showed mean methylation of just 0.83 percent at HOXA3 and 1.02 percent at MAP4K1, while pure blood cell DNA showed 94.0 percent and 93.1 percent respectively. When the two DNA sources were mixed at seven precisely defined ratios and subjected to the assay, individual sequencing reads fell into two clean clusters with almost no intermediate methylation. A classification system that assigned reads as blood-derived or organoid-derived based on the number of methylated CpGs per fragment produced correlations with the input DNA ratios of R-squared 0.999 for HOXA3 and 0.9985 for MAP4K1, demonstrating near-perfect quantitative accuracy.

The team then moved to a genuinely heterogeneous, uncultured human sample: saliva. Saliva is attractive for epigenetic epidemiology because collection is non-invasive, but it contains an unpredictable mixture of leukocytes secreted from the oral gingiva and buccal epithelial cells sloughed from the cheek. Using flow cytometry and cellular filtration, the researchers purified buccal cells and salivary leukocytes to purities of 97.1 percent and 99.4 percent respectively, and confirmed that the two populations carried the expected opposite methylation patterns. In a mixed saliva sample that microscopic cell counting showed to be 38 percent leukocytes, the methylation-based test predicted leukocyte proportions of 38.1 percent using HOXA3 and 39.3 percent using MAP4K1, with linear regression R-squared values of 0.998 and 0.997. For researchers who use saliva in large epidemiological studies, this offers a way to correct for cellular composition that previously required complex bioinformatic deconvolution of whole-genome data.

Perhaps the most provocative part of the study is what the biomarkers reveal about published disease research. Because immune cells drive inflammation, genuine leukocyte-specific methylation markers should appear repeatedly in methylation studies of inflammatory diseases, even when the diseased tissue itself is not blood-derived. Searching the EWAS Atlas database, the team found 28 disease traits associated with their markers, with psoriasis, inflammatory bowel disease and Alzheimer disease topping the list. A deeper PubMed search of twelve publications found that seven of the eleven studies using the standard methylation array platform reported at least one differentially methylated position or region overlapping the leukocyte-specific sites. Strikingly, many of these studies never mentioned leukocyte infiltration as a possible confound, and only one investigated the proportion of leukocytes in its samples at all.

The Alzheimer disease connection is particularly striking. Several independent studies have reported that a 48-kilobase region spanning the HOXA gene cluster from HOXA2 to HOXA6 becomes progressively hypermethylated in the brain as disease severity increases, measured by Braak stage. When the Otago team overlaid that hypermethylation pattern with methylation data from purified leukocytes and cortical neurons, the genomic locations matched almost exactly: leukocytes are heavily methylated across the HOXA cluster, neurons are not. The authors hypothesise that the methylation signal in the Alzheimer brain comes from infiltrating leukocytes, a phenomenon known to occur as the ageing blood-brain barrier becomes leaky, rather than from any change in the methylation of the brain cells themselves. A simple calculation based on a single CpG site suggested that by Braak stage 6, an additional 13.9 percent of cells in the prefrontal cortex could be leukocyte-derived.

The biomarkers also performed well in cancer. Using more than 8,000 tumour samples from 30 cancer types in The Cancer Genome Atlas, the team compared methylation at the HOXA3 marker with published estimates of leukocyte content. Across all cancers combined the correlation was modest, because cancer cells frequently acquire their own hypermethylation at the HOXA cluster. But in six tumour types, including uveal melanoma, mesothelioma, thyroid carcinoma, testicular germ cell tumours, bladder urothelial carcinoma and ovarian serous cystadenocarcinoma, a single CpG site showed a strong linear relationship with the leukocyte estimate, meaning that in these cancers one methylation measurement may be enough to quantify immune infiltration without any complex deconvolution.

The implications reach well beyond a single laboratory technique. The study demonstrates that methylation differences attributed to diseased cells may sometimes simply reflect the immune cells living among them, and it offers a concrete remedy: researchers studying inflammatory diseases could sort pure cell populations, spike in known amounts of leukocyte DNA as controls, or compare their samples against reference methylation data from healthy tissues and blood. Looking forward, the authors suggest that because colonic epithelium is virtually unmethylated at both loci, a stool-based test for intestinal inflammation could one day complement or even replace invasive colonoscopy for diagnosing inflammatory bowel disease. What began as a search for molecular fingerprints of blood cells has ended up casting doubt on a whole class of disease methylation signals, and providing the tools to tell them apart.

Subject of Research: Leukocyte-specific DNA methylation biomarkers for detecting immune cell infiltration in tissue samples

Article Title: Leukocyte-specific DNA methylation biomarkers and their implication for pathological epigenetic analysis

Article References: Dunnet, M. J., Ortega-Recalde, O. J., Waters, S. A., Weeks, R. J., Morison, I. M., & Hore, T. A. (2022). Leukocyte-specific DNA methylation biomarkers and their implication for pathological epigenetic analysis. Epigenetics Communications, 2(1), Article 5. https://doi.org/10.1186/s43682-022-00011-z

Image Credits: AI Generated

DOI: 10.1186/s43682-022-00011-z

Keywords: DNA methylation, leukocytes, epigenetics, biomarkers, HOXA3, MAP4K1, inflammation, Alzheimer disease, inflammatory bowel disease, cancer immunology, bisulphite sequencing, saliva

The logic behind the advance rests on radiochemistry that is deceptively simple. Since the mid-1970s, clinicians have labeled white blood cells with gamma emitters such as technetium-99m and indium-111, then reinjected them to locate abscesses and inflammatory lesions. Indium-111, with a physical half-life of about 2.8 days, became the workhorse for this purpose because it persists long enough to follow cells for days. Zirconium-89, with a half-life of 3.3 days, offers a nearly identical temporal window but emits positrons, enabling PET imaging, which delivers substantially higher sensitivity and better spatial and temporal resolution than SPECT. The UAB team exploited 8-hydroxyquinoline, known as oxine, a lipophilic chelator that shuttles zirconium-89 across cell membranes, allowing the radionuclide to become trapped inside the leukocytes rather than merely attached to their surfaces.

The trial enrolled four healthy adult women between 37 and 53 years of age, a deliberate choice grounded in radiation protection logic. Extrapolations from decades of indium-111 oxine dosimetry predicted a higher effective-dose coefficient for females, 1.14 mSv/MBq, than for males, 0.855 mSv/MBq, so studying women represented the more conservative test of safety. There was also a clinical rationale: the team’s longer-term goal is to image neuroinflammation in myalgic encephalomyelitis/chronic fatigue syndrome, a condition that disproportionately affects women. Each participant donated roughly 120 milliliters of blood, from which leukocytes were isolated, incubated with zirconium-89 oxine, washed, and returned intravenously within strict time limits. The mean administered activity was 10.9 plus or minus 2.9 MBq, a modest amount by nuclear medicine standards.

Quality control was rigorous. Every labeled cell preparation had to meet predefined release criteria before reinjection, including radiochemical purity of at least 95 percent, radionuclidic purity of at least 99.5 percent, verified leukocyte viability before and after labeling, sterility, and endotoxin testing. The radiolabeling itself was performed at a licensed commercial radiopharmacy under USP Chapter 797 standards, while the zirconium-89 oxine was produced in the UAB Cyclotron PET Production Facility under USP Chapter 823 guidelines. Only products passing every specification were administered, a framework designed to mirror the established clinical workflow for FDA-approved indium-111 oxine labeling and thereby ease eventual regulatory translation.

Imaging followed a demanding schedule. Each participant underwent whole-body PET/CT at five time points: immediately after injection, then at 4 to 6, 24, 48, and 72 hours. The scans captured a dynamic biological story. Early images showed the labeled cells concentrated in the liver, spleen, heart, and blood pool, as would be expected for cells still circulating. By 24 hours and increasingly at 48 and 72 hours, uptake shifted to the liver, spleen, and red marrow, particularly within the pelvis and iliac crests, reflecting the physiological homing of leukocytes to the organs where they are naturally cleared and stored. The pattern was qualitatively similar to that long documented for indium-111 oxine-labeled leukocytes and consistent with prior mouse and non-human primate studies of zirconium-89 oxine labeling.

The dosimetry numbers carry the study’s headline significance. The highest mean absorbed-dose coefficients appeared in the spleen at 3.52 plus or minus 1.38 mGy/MBq, followed by the liver at 2.1 plus or minus 0.45, the adrenals at 1.62 plus or minus 0.24, the uterus at 1.48 plus or minus 0.98, and the kidneys at 1.36 plus or minus 0.12 mGy/MBq. The mean effective-dose coefficient came out to 0.92 plus or minus 0.06 mSv/MBq, numerically lower than the predicted 1.14 mSv/MBq, a difference that reached statistical significance in an exploratory one-sample t-test with a P value of 0.006. The measured biodistribution also diverged from the assumptions used for prediction: roughly 32 percent of activity localized to the liver, 8 percent to the spleen, and 15 percent to red marrow, rather than the 30-30-34 split assumed from indium-111 data. The authors attribute much of the discrepancy to methodological differences, since PET/CT-based whole-organ dosimetry is inherently more direct than the SPECT-only methods used historically.

Safety results were unambiguous. No adverse events, clinically significant laboratory abnormalities, or pharmacological effects were observed in any participant through 72 hours, and follow-up contact 24 hours after protocol completion turned up nothing further. Vital signs remained stable throughout. One intriguing observation warrants mention: activity concentrations in plasma exceeded those in whole blood, especially at early time points, which the researchers suggest could reflect leukocyte lysis, efflux of the radionuclide from cells, or incomplete buffy coat formation during processing. This phenomenon, they note, deserves closer investigation in subsequent studies.

A key technical concern with any intracellular label is stability. Free zirconium-89 has a well-documented affinity for hydroxyapatite and accumulates in mineralized bone, so progressive cortical bone uptake would signal that the label was leaking from cells. To probe this, the team performed an exploratory skeletal analysis comparing marrow-rich regions of the spine and pelvis with cortical tibial bone. Uptake remained consistently higher in the marrow-rich compartment, while cortical tibial activity stayed low with no progressive accumulation, supporting the interpretation that skeletal signal reflects genuine leukocyte homing to red marrow rather than liberated radionuclide. The authors caution that low-level efflux beyond 72 hours cannot be fully excluded and that longer imaging windows will help settle the question.

The study also showcased a modern dosimetry workflow. Organ regions of interest were generated automatically on CT using an in-house deep learning segmentation tool, then manually refined and propagated across time points. This automation reduces interobserver variability and could make dosimetry scalable across larger, multi-institution cohorts. Time-integrated activity coefficients were computed with Simpson’s rule, and doses were calculated in OLINDA 2.1 using standard adult female phantoms and ICRP 103 tissue weighting factors. Beyond the final 72-hour scan, activity was assumed to decay only physically, a conservative assumption that likely overestimates doses for organs still clearing activity biologically.

Looking ahead, the implications stretch well beyond infection imaging. The same labeling strategy could track CAR T-cells and other cell-based therapies as they home to tumors, offering oncologists a real-time window into treatment delivery. It may prove especially valuable in neurology: animal models of stroke, traumatic brain injury, multiple sclerosis, and Alzheimer’s and Parkinson’s diseases all show leukocyte invasion of the brain, but these events have never been directly visualized in living humans because available PET tracers decay too quickly, while the critical window of immune cell infiltration spans three to four days. Zirconium-89’s half-life fits that window precisely. The research team plans to apply the technique to patients with suspected central nervous system inflammation, including multiple sclerosis and ME/CFS, while working to reduce the blood volume needed for labeling and to improve labeling efficiency. Limitations remain, including the small all-female cohort and the absence of functional testing of labeled cells beyond viability, but the foundation is now laid: for the first time, human dosimetry data confirm that PET imaging of a patient’s own immune cells is both safe and feasible, opening a new chapter in molecular imaging of the immune system.

Subject of Research: First-in-human radiation dosimetry and biodistribution of zirconium-89 oxine-labeled autologous leukocytes imaged with PET/CT

Article Title: First-in-human dosimetry and biodistribution of [89Zr]Zr-oxine-labeled autologous leukocytes using PET/CT

Article References: Gultekin, K., Bartels, J. L., Cardenas, C. E., Kumar, Y., Gimblet, G. R., Jones, C. L., Bankston, C., Jeffers, C. D., White, S. L., Lapi, S. E., Younger, J. W., & McConathy, J. E. (2026). First-in-human dosimetry and biodistribution of [89Zr]Zr-oxine-labeled autologous leukocytes using PET/CT. European Journal of Nuclear Medicine and Molecular Imaging. https://doi.org/10.1007/s00259-026-08158-w

Image Credits: AI Generated

DOI: 10.1007/s00259-026-08158-w

Keywords: zirconium-89, PET/CT, leukocytes, cell tracking, dosimetry, radiopharmaceuticals, nuclear medicine, oxine, immunimaging, neuroinflammation, CAR T-cells, first-in-human trial