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Background The purpose of this study is to determine if Haralick texture analysis on CT imaging of mucoepidermoid carcinomas (MEC) can differentiate low-grade and high-grade tumors. Methods A retrospective review of 18 patients with MEC of the salivary glands, corresponding CT imaging and pathology report was performed. Tumors were manually segmented and image analysis was performed to calculate radiomic features. Radiomic features were compared between low-grade and high-grade MEC. A multivariable logistic regression model and receiver operating characteristic analysis was performed. Results A total of 18 patients (mean age, 51, range 9-83 years, 8 men and 10 women) were included. Nine patients had low-grade pathology and nine patients had high-grade pathology. Of the 18 cases, 7 (39%) occurred in the parotid gland and 11 (61%) occurred in minor salivary glands. No individual feature was significantly different between low-grade and high-grade MEC. A logistic regression model including surface regularity, energy and information measure II of correlation was performed and was able to predict high-grade MEC accurately (sensitivity 89%, specificity 68%). The area under the receiver operating characteristic curve was 0.802. Conclusions High-grade MEC tend to have a low energy, high correlation texture as well as surface irregularity. Together, these three features may comprise a tumor phenotype that is able to predict high-grade pathology in MECs.

Zeeshan Haq,1 Michael H Zhang,1 Mark J Benjamin,2 Kamran M Riaz1 1Department of Ophthalmology and Visual Science, University of Chicago, Chicago, IL, USA; 2Benjamin Eye Care Center, La Grange, IL, USACorrespondence: Kamran M RiazDean McGee Eye Institute, University of Oklahoma, 608 Stanton L. Young Blvd, Suite 313, OK 73104, Oklahoma City Tel +1 405 271-1095Fax +1 405 271-3680Email Kamran-Riaz@dmei.orgPurpose: To compare short-term non-infectious clinical outcomes after cataract surgery with an intraoperative pars plana intravitreal antibiotic-steroid (IVAS) injection of triamcinolone, moxifloxacin, and vancomycin (TMV) versus a standard postoperative topical regimen.Patients and Methods: A retrospective comparative case series of 1058 eyes (control = 487, treatment = 571) undergoing cataract surgerywere included. Endpoints included best-corrected visual acuity (BCVA), intraocular pressure (IOP), and the unplanned use of anti-inflammatory topical medication in the postoperative period. The follow-up period ranged from 1 to 6 months.Results: A final monocular BCVA of 20/25 or better was achieved in 78.8% and 87.4% of eyes in the control and treatment groups, respectively (p = 0.001). The overall incidence of an IOP spike (Δ ≥ 10 mm Hg) was not significantly different between the two groups (0.4% versus 1.9%, p = 0.027). The rates of persistent anterior chamber inflammation (PACI), rebound anterior chamber inflammation (RACI), and cystoid macular edema (CME) in the control and treatment groups were 8.0% vs 2.6% (p < 0.001), 6.4% vs 2.6% (p = 0.003), and 3.9% vs 4.7% (p = 0.511), respectively. The use of an IVAS injection of TMV conferred an increased risk of CME (odds ratio [OR] = 3.21, 95% confidence interval [CI] = 1.42 to 7.23) but no significant effect on the risk of PACI (OR = 0.34, 95% CI = 0.10 to 1.14) or RACI (OR = 0.52, 95% CI = 0.18 to 1.54) when compared to a topical regimen.Conclusion: An intraoperative IVAS injection after uncomplicated cataract surgery may be as safe and effective as a standard topical regimen in terms of postoperative IOP and anterior chamber inflammatory events, respectively. However, the efficacy of a TMV formulation for CME prophylaxis appears to be unsatisfactory. Future studies with prospective and randomized designs are needed to further evaluate this technique.Keywords: dropless cataract surgery, inflammation prophylaxis, intraocular pressure spike, cystoid macular edema

Antigen presenting cells (APCs) have been extensively studied for treating cancers and autoimmune diseases. Dendritic cells (DCs) are potent APCs that uptake and present antigens (Ags) to activate immunity or tolerance. Despite their active use in cellular immunotherapies, DCs face several challenges that hinder clinical translation, such as inability to control Ag dosing for tuning immune responses and low abundance in peripheral blood. B cells are a potential alternative to DCs, but their poor non-specific Ag uptake capabilities compromise controllable priming of T cells. We developed phospholipid-conjugated Ags (L-Ags) and lipid-polymer hybrid nanoparticles (L/P-Ag NPs) as Ag delivery platforms to expand the range of accessible APCs for use in priming CD4+and CD8+T cells. These delivery platforms were evaluated using DCs, CD40-activated B cells, and resting B cells as a diverse set of APCs to understand the impact of various Ag delivery mechanisms for generation of Ag-specific T cell responses. L-Ag delivery (termed depoting) of MHC class I and II-restricted Ags successfully loaded all APC types in a tunable manner and primed both Ag-specific CD8+and CD4+T cells, respectively. Incorporating L-Ags and polymer-conjugated Ags (P-Ag) into NPs can direct Ags to different uptake pathways to engineer the dynamics of presentation and shape T cell responses. DCs were capable of processing and presenting Ag delivered from both L- and P-Ag NPs yet B cells could only utilize Ag delivered from L-Ag NPs. Multivariate analysis of cytokines secreted from APC:T cell co-cultures indicated that L-Ag NPs primed different T cell responses than P-Ag NPs. Altogether, we show that L-Ags and P-Ags can be rationally paired within a single NP to leverage distinct delivery mechanisms to access multiple Ag processing pathways in two APC types, offering a modular delivery platform for engineering immunotherapies.

An HIV vaccine capable of eliciting durable neutralizing antibody responses continues to be an important unmet need. Multivalent nanoparticles displaying a high density of envelope trimers may be promising immunogen forms to elicit strong and durable humoral responses to HIV, but critical particle design criteria remain to be fully defined. To this end, we developed strategies to covalently anchor a stabilized gp140 trimer, BG505 MD39, on the surfaces of synthetic liposomes to study the effects of trimer density and vesicle stability on vaccine-elicited humoral responses in mice. CryoEM imaging revealed homogeneously distributed and oriented MD39 on the surface of liposomes irrespective of particle size, lipid composition, and conjugation strategy. Immunization with covalent MD39-coupled liposomes led to increased germinal center and antigen-specific T follicular helper cell responses and significantly higher avidity serum MD39-specific IgG responses compared to immunization with soluble MD39 trimers. A priming immunization with liposomal-MD39 was important for elicitation of high avidity antibody responses, regardless of whether booster immunizations were administered with either soluble or particulate trimers. The stability of trimer anchoring to liposomes was critical for these effects, as germinal center and output antibody responses were further increased by liposome compositions incorporating sphingomyelin that exhibited high in vitro stability in the presence of serum. Together these data highlight key liposome design features for optimizing humoral immunity to lipid nanoparticle immunogens.

BACKGROUND AND OBJECTIVE: To report ocular and neurodevelopmental outcomes among infants treated for retinopathy of prematurity (ROP) in a nationwide health insurance claims database. PATIENTS AND METHODS: Retrospective cohort study of 298 infants treated with laser or anti-vascular endothelial growth factor (VEGF) injection identified in the MarketScan database (2011–2017) with 2-year follow-up. RESULTS: A review of claims data found 298 patients with International Classification of Diseases and Common Procedural Technology codes for ROP treatment and 2 years of continuous insurance coverage. Of these, 63 infants received injections and 235 received laser. Overall, the anti-VEGF group had higher rates of underlying neurological comorbidities (35% vs. 23%; P = .05) and thrombocytopenia (17% vs. 8%; P = .02). Most ocular outcomes were similar, including retinal detachment ( P = .87). There were higher rates of second procedures after injection (44% vs. 10%; P < .001). Rates of language, motor, and cognitive delays were similar. Rates of cerebral palsy were higher with injections but were not statistically significant after adjusting for comorbidities (odds ratio = 1.88; P = .10). CONCLUSIONS: The prevalence of retinal detachment after 2 years was similar comparing anti-VEGF to laser. Despite the higher rates of underlying neurologic comorbidity in the injection group, there were no differences in language, motor, or cognitive delays. [ Ophthalmic Surg Lasers Imaging Retina . 2020;51:486–493.]

The goal of this study is to characterize the normal size of parotid lymph nodes among healthy adult patients on CT. This was a single-center retrospective observational study of 543 patients who underwent maxillofacial CT scans between January 2019 and July 2019. The long and short axis diameters of the largest lymph nodes in the bilateral superficial parotid glands were measured. Among the 543 patients, 407 subjects with a mean age of 47.0 ± 18.4 years had a total of 719 detectable intraparotid lymph nodes. The mean patient age was 47.0 ± 18.4 years. Of all 719 measured intraparotid lymph nodes, the measured long and short axis diameter means were 4.4 ± 1.4 mm and 3.3 ± 1.1 mm, respectively. In our study, 96% (689/719) of all lymph nodes had a long axis diameter of 7 mm or less and 93% (671/719) of all lymph nodes had a short axis diameter of 5 mm or less. Younger patients had significantly larger lymph nodes than older patients in both long axis (4.5 vs 4.3 mm; P = 0.03) and short axis (3.4 vs 3.1 mm, P = 0.01) measurements. Our findings suggest 5 mm as an upper limit of normal for the short axis diameter of superficial intraparotid lymph nodes.

Cell-based immunotherapies have tremendous potential to treat many diseases, such as activating immunity in cancer or suppressing it in autoimmune diseases. Most cell-based cancer immunotherapies in the clinic provide adjuvant signals through genetic engineering to enhance T cell functions. However, genetically encoded signals have minimal control over dosing and persist for the life of a cell lineage. These properties make it difficult to balance increasing therapeutic efficacy with reducing toxicities. Here, we demonstrated the potential of phospholipid-coupled ligands as a non-genetic system for immune cell engineering. This system provides simple, controlled, non-genetic adjuvant delivery to immune cells via lipid-mediated insertion into plasma membranes. Lipid-mediated insertion (depoting) successfully delivered Toll-like receptor (TLR) ligands intracellularly and onto cell surfaces of diverse immune cells. These ligands depoted into immune cells in a dose-controlled fashion and did not compete during multiplex pairwise loading. Immune cell activation could be enhanced by autocrine and paracrine mechanisms depending on the biology of the TLR ligand tested. We determined that depoted ligands can functionally persist on plasma membranes for up to four days in naïve and activated T cells, enhancing their activation, proliferation, and skewing cytokine secretion. Depoted ligands provide a persistent yet non-permanent adjuvant signal to immune cells that may minimize the intensity and duration of toxicities compared to permanent genetic delivery. Altogether, these findings demonstrate potential for lipid-mediated insertion (depoting) as a universal cell engineering approach with unique, complementary advantages to other cell engineering methods.

The current model of murine innate lymphoid cell (ILC) development holds that mouse ILCs are derived downstream of the common lymphoid progenitor through lineage-restricted progenitors. However, corresponding lineage-restricted progenitors in humans have yet to be discovered. Here we identified a progenitor population in human secondary lymphoid tissues (SLTs) that expressed the transcription factor, RORγt, and was unique in its ability to generate all known ILC subsets, including natural killer (NK) cells, but not other leukocyte populations. In contrast to murine fate-mapping data, which indicate that only ILC3 cells express Rorγt, these human progenitor cells as well as human peripheral blood NK cells and all mature ILC populations expressed RORγt. Thus, all human ILCs can be generated through an RORγt+ developmental pathway from a common progenitor in SLTs. These findings help establish the developmental signals and pathways involved in human ILC development.

PURPOSE: To assess the effects of the American Academy of Ophthalmology’s 2015 patient education video on patient information retention and anxiety preoperatively, on the day of surgery and postoperatively. METHODS: This is a prospective, surgeon-blinded randomized controlled trial at the University of Chicago Medical Center. Ninety-one patients with a diagnosis of first-eye cataract were randomized into either a video or control group. Subjects in both groups received face-to-face discussion with the surgeon and an informational brochure at the preoperative evaluation. Participants in the video group then viewed a four-minute educational video at the preoperative evaluation and on the day of surgery. Both groups completed an information retention quiz and a state anxiety assessment at the preoperative visit, on the day of surgery, and on the postoperative week one visit. Subject understanding of cataract surgery was measured using a twelve-question multiple choice quiz. State anxiety was measured by State Trait Anxiety Inventory-Y1 survey score. RESULTS: Participants in the video group did not score significantly higher on the information retention quiz compared to the control group at the preoperative evaluation (8.7±2.4 vs 7.7±2.5, P = 0.07), but did so on the day of surgery (11.2±0.8 vs 8.4±1.7, P < 0.001) and postoperative week one visit (10.8±1.5 vs 9.0±2.0, P < 0.001). Subjects in the video group were significantly less anxious on the day of surgery (26.4±5.1 vs 41.1±10.3, P < 0.001). CONCLUSIONS: Video supplementation to the traditional informed consent process demonstrated animprovement in patient understanding of cataract surgery at multiple time points and decreased anxiety on day of surgery.

Acute myeloid leukemia (AML) can evade the mouse and human innate immune system by suppressing natural killer (NK) cell development and NK cell function. This is driven in part by the overexpression of microRNA (miR)-29b in the NK cells of AML patients, but how this occurs is unknown. In the current study, we demonstrate that the transcription factor aryl hydrocarbon receptor (AHR) directly regulates miR-29b expression. We show that human AML blasts activate the AHR pathway and induce miR-29b expression in NK cells, thereby impairing NK cell maturation and NK cell function, which can be reversed by treating NK cells with an AHR antagonist. Finally, we show that inhibition of constitutive AHR activation in AML blasts lowers their threshold for apoptosis and decreases their resistance to NK cell cytotoxicity. Together, these results identify the AHR pathway as a molecular mechanism by which AML impairs NK cell development and function. The results lay the groundwork in establishing AHR antagonists as potential therapeutic agents for clinical development in the treatment of AML.

An effective preventive vaccine is highly sought after in order to stem the current HIV-1 pandemic. Both conservation of contiguous gp41 membrane-proximal external region (MPER) amino acid sequences across HIV-1 clades and the ability of anti-MPER broadly neutralizing antibodies (BNAbs) to block viral hemifusion/fusion establish the MPER as a prime vaccination target. In earlier studies, we described the development of an MPER vaccine formulation that takes advantage of liposomes to array the MPER on a lipid bilayer surface, paralleling its native configuration on the virus membrane while also incorporating molecular adjuvant and CD4 T cell epitope cargo. Here we demonstrate that several immunizations with MPER/liposomes induce high levels of bone marrow long-lived plasma cell (LLPC) antibody production. Single-cell immunoglobulin gene retrieval analysis shows that these plasma cells are derived from a germ line repertoire of B cells with a diverse representation of immunoglobulin genes, exhibiting antigen-driven positive selection. Characterization of LLPC recombinant monoclonal antibodies (rMAbs) indicates that antigen recognition is achieved through convergence on a common epitopic focus by utilizing various complementarity-determining region H3 (CDRH3) lengths. Importantly, the vast majority of rMAbs produced from these cells lack polyreactivity yet manifest antigen specificity in the context of lipids, shaping MPER-specific paratopes through selective pressure. Taken together, these findings demonstrate that the MPER is a vaccine target with minimal risk of generating off-target autoimmunity. IMPORTANCE A useful vaccine must generate desired long-term, antigen-specific antibody responses devoid of polyreactivity or autoreactivity. The common polyreactive features of some HIV-1 BNAbs have raised concern about elicitation of anti-MPER antibodies. Utilizing single-LLPC repertoire analysis and biophysical characterization of anti-MPER rMAbs, we show that their fine specificities require a structural fitness of the antibody combining site involving heavy and light chain variable domains shaped by somatic hypermutation and affinity maturation of B cells in the germinal center. Perhaps more importantly, our results demonstrate that the majority of MPER-specific antibodies are not inherently polyspecific and/or autoreactive, suggesting that polyreactivity of MPER-specific antibodies is separable from their antigen specificity., Bill & Melinda Gates Foundation (Grant OPP1108179), National Institute of Allergy and Infectious Diseases (U.S.) (Grant U19 AI091693), Howard Hughes Medical Institute

Acute myeloid leukemia (AML) is a deadly disease in need of novel therapeutic avenues to improve outcomes. Natural killer (NK) cells have the potential to be curative in the setting of AML, although successful strategies to deploy NK cells in patients have been limited to date, likely due in part to cancer-derived immune suppression. Recently, we showed that NK cell development is impaired in the presence of AML. In our present study, we uncover a novel mechanism by which AML releases aryl hydrocarbon receptor (AHR) ligands that in turn activate the NK cells to induce expression of microRNA (miR)-29b, resulting in impaired NK cell development and function. This developmental block was dependent on miR-29b in NK cells, as miR-29b deficient NK cells were resistant to these changes in the presence of AML and miR-29b knockout mice engrafted with AML showed improved survival. In support of these findings in mice, AML patients with a transcriptional profile consistent with an activated AHR pathway had more aggressive disease and decreased survival (p=0.006). AML-derived AHR ligands impaired NK cell development by repressing Tbet and Eomes, two master regulators of late-stage NK cell maturation. We also show that agonist-bound AHR binds a dioxin-responsive element (DRE) located in the promoter of miR-29b to directly induce its transcription as demonstrated by luciferase constructs and anti-AHR ChIP-PCR in primary NK cells. Indeed, transwell co-cultures of AML and immature NK cells found increased miR-29b in NK cells and impaired development that was contact independent. These effects were reversed with addition of the AHR antagonist CH-223191. Finally, we show that AML cells pretreated with CH-223191 and then cultured with NK cells lead to more NK cell IFN-γ production and higher cytotoxicity against AML. Collectively, these data show that AML blasts secrete AHR ligands and AHR is a significant contributor to AML-induced immune suppression by upregulating miR-29b in NK cells and delaying their development, blunting their IFN-γ production and decreasing their cytotoxicity. Furthermore, we demonstrate that targeting AHR may be an effective novel therapeutic avenue because it promotes NK cell maturation while also enhancing NK cell-mediated activation and killing of AML cells. Citation Format: Steven D. Scoville, Ansel Nalin, Luxi Chen, Li Chen, Kathleen McConnell, Susana Beceiro Casas, Abd Al-Rahman, Naima Hashi, Michael Zhang, Jennifer Saultz, Jianhua Yu, Aharon Freud, Michael Caligiuri, Bethany Mundy-Bosse. The aryl hydrocarbon receptor directly regulates microRNA-29b to inhibit human natural killer cell development and function in acute myeloid leukemia [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 4729.

This paper discusses solution techniques for the morning commute problem that is formulated as a discrete variational inequality (VI). Various heuristics have been proposed to solve this problem, mostly because the analytical properties of the path travel time function have not yet been well understood. Two groups of ''non-heuristic'' algorithms for general VIs, namely projection-type algorithms and ascent direction algorithms, were examined. In particular, a new ascent direction method is introduced and implemented with a heuristic line search procedure. The performance of these algorithms are compared on simple instances of the morning commute problem. The implications of numerical results are discussed.

Checkpoint blockade with antibodies specific for cytotoxic T lymphocyte–associated protein (CTLA)-4 or programmed cell death 1 (PDCD1; also known as PD-1) elicits durable tumor regression in metastatic cancer, but these dramatic responses are confined to a minority of patients. This suboptimal outcome is probably due in part to the complex network of immunosuppressive pathways present in advanced tumors, which are unlikely to be overcome by intervention at a single signaling checkpoint. Here we describe a combination immunotherapy that recruits a variety of innate and adaptive immune cells to eliminate large tumor burdens in syngeneic tumor models and a genetically engineered mouse model of melanoma; to our knowledge tumors of this size have not previously been curable by treatments relying on endogenous immunity. Maximal antitumor efficacy required four components: a tumor-antigen-targeting antibody, a recombinant interleukin-2 with an extended half-life, anti-PD-1 and a powerful T cell vaccine. Depletion experiments revealed that CD8⁺ T cells, cross-presenting dendritic cells and several other innate immune cell subsets were required for tumor regression. Effective treatment induced infiltration of immune cells and production of inflammatory cytokines in the tumor, enhanced antibody-mediated tumor antigen uptake and promoted antigen spreading. These results demonstrate the capacity of an elicited endogenous immune response to destroy large, established tumors and elucidate essential characteristics of combination immunotherapies that are capable of curing a majority of tumors in experimental settings typically viewed as intractable., National Cancer Institute (U.S.) (P30-CA14051), United States. National Institutes of Health (CA174795), United States. National Institutes of Health (NIH #T32GM008334), United States. National Institutes of Health (CA180586)

Although materials and engineered surfaces are broadly utilized in creating assays and devices with wide applications in diagnostics, preservation of these immuno-functionalized surfaces on microfluidic devices remains a significant challenge to create reliable repeatable assays that would facilitate patient care in resource-constrained settings at the point-of-care (POC), where reliable electricity and refrigeration are lacking. To address this challenge, we present an innovative approach to stabilize surfaces on-chip with multiple layers of immunochemistry. The functionality of microfluidic devices using the presented method is evaluated at room temperature for up to 6-month shelf life. We integrated the preserved microfluidic devices with a lensless complementary metal oxide semiconductor (CMOS) imaging platform to count CD4+ T cells from a drop of unprocessed whole blood targeting applications at the POC such as HIV management and monitoring. The developed immunochemistry stabilization method can potentially be applied broadly to other diagnostic immuno-assays such as viral load measurements, chemotherapy monitoring and biomarker detection for cancer patients at the POC.

We have developed a rapid negative selection method to enrich rare mononuclear cells from human tissues. Unwanted and antibody-tethered cells are selectively depleted during a Ficoll separation step and there is no need for magnetic-based reagents and equipment. The new method is fast, customizable, inexpensive, remarkably efficient and easy to perform and per sample the overall cost is less than one-tenth the cost associated with a magnetic column-based method.

A power law relating bed-form magnitudes (lengths or heights) to time, with all parameters normalized by equilibrium values, is promoted to describe ripple or dune growth with time from plane-bed to equilibrium conditions. In order to use this relation for prediction purposes, new expressions are presented herein for both the times required for ripples and dunes to achieve equilibrium magnitudes, and also the respective growth exponents for the development of bed-form heights and lengths. These new relations have been determined based on 15 new and 76 previously published laboratory experiments covering ranges of sands and flow strengths, although additional work is warranted to confirm these expressions for field scales. The power-law relation for bed-form growth from a plane bed is also extended in concept herein to describe changes in bed-form size from nonzero initial magnitudes. In preliminary tests, this modified power-law expression was found to provide reasonable descriptions of trends in increasing and decreasing bed-form heights and lengths with changes in flow strength. At this stage, application of this modified expression is principally conceptual in nature, with further work required to facilitate prediction for changes in flow of both times to achieve equilibrium magnitudes and also height and length growth exponents.

The need for sensitive, robust, portable and inexpensive biosensing platforms is of significant interest in clinical applications for disease diagnosis and treatment monitoring at the point-of-care (POC) settings. Rapid, accurate POC diagnostic assays play a crucial role in developing countries, where there are limited laboratory infrastructure, trained personnel and financial support. However, current diagnostic assays commonly require long assay time, sophisticated infrastructure and expensive reagents that are not compatible with resource-constrained settings. Although paper and flexible material-based platform technologies provide alternative approaches to develop POC diagnostic assays for broad applications in medicine, they have technical challenges integrating to different detection modalities. Here, we address the limited capability of current paper and flexible material-based platforms by integrating cellulose paper and flexible polyester films as diagnostic biosensing materials with various detection modalities through the development and validation of new widely applicable electrical and optical sensing mechanisms using antibodies and peptides. By incorporating these different detection modalities, we present selective and accurate capture and detection of multiple biotargets including viruses (Human Immunodeficieny Virus-1), bacteria (Escherichia coli and Staphylococcus aureus) and cells (CD4+ T lymphocytes) from fingerprick volume equivalent of multiple biological specimens such as whole blood, plasma and peritoneal dialysis effluent with clinically relevant detection and sensitivity.

Remote medical monitoring is of increasing importance as it enables low cost in-situ monitoring of patients regardless of their location. Realization of this technology requires that medical sensors (forming a body sensor network, BSN) are capable of detecting physiological data and transferring this data to physicians via wireless links. In this paper, we will present a wireless communication platform to provide a reliable and secure pathway for transferring health informatics data from on-body medical sensors to a mobile device or remote database server.

Transplantation of engineered vascular grafts has emerged as a potential therapeutic solution for cardiovascular disease treatment. Although engineered vascular grafts hold the potential to satisfy a large clinical need, thrombosis remains a major risk with the small-diameter grafts (

Natural killer (NK) cells are innate effector cells that can spontaneously recognize and kill cancer cells. While important in inducing long-term disease free survival (DFS) in the setting of killer immunoglobulin-like receptor (KIR) mismatch for acute myeloid leukemia (AML), harnessing NK cells to kill autologous or self AML blasts to extend DFS has had no success. In this study, we uncover one potential mechanism by which AML blasts can evade NK cell cytotoxicity. The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that has now been shown to be expressed in immature human NK cells. Furthermore, activation of AHR in these immature cells suppresses human NK cell maturation and function. We and others have shown that human AML blasts secrete ligands that can activate AHR, leading us to hypothesize that AML may evade autologous NK cell cytotoxicity in part by inhibiting NK cell maturation. Expression of microRNA (miR)-29b has previously been shown to suppress the expression of transcription factors Tbx21 (TBET) and Eomesodermin (EOMES), both of which are critical for terminal NK cell differentiation and function. Here we show that AHR is able to directly regulate the expression of miR-29b and thus may serve as the link between AML and immune evasion of NK cells. We first identified putative AHR binding sites within the proximal promoter of miR-29b, suggesting that AHR may directly regulate miR-29b expression. To test this, we transfected the AHR responsive HepG2 human cell line with a miR-29b promoter driven luciferase reporter and measured luciferase activity after treatment with the known AHR agonist, FICZ, compared to vehicle control. We discovered that cells treated with 6-formylindolol[3,2-b]carbazole (FICZ) had increased luciferase activity compared to cells treated with vehicle control (P Figure 1. Figure 1. Disclosures No relevant conflicts of interest to declare.