Thank you for joining the Adicet webcast. Before we begin, a quick reminder: This webcast will include forward-looking statements as detailed on this slide. Please refer to the Risk Factors section of Adicet's most recent quarterly report on Form 10-Q and subsequent SEC filings for more details. This call is being recorded. Thank you all for joining me today. I'm Blake Aftab, Chief Scientific Officer at Adicet Bio. Today, I'm going to provide you with an update covering new and compelling translational data that we've recently generated in conjunction with the phase I GLEAN trial of ADI-001 in lymphoma, that underpin core aspects of our gamma delta 1 CAR T cell platform, and that we believe position Adicet with a differentiated profile as we focus development of ADI-001 in autoimmune diseases. An important and significant advantage of gamma delta 1 T cells is their ability to traffic to tissues, and with today's data, we can confirm that ADI-001 has been shown to deplete B-cell populations within these tissues. The new clinical biomarker data we will present here represent an additional level of evidence for ADI-001's trafficking and pharmacodynamic effects within tissues. Specifically, the data that we are sharing today facilitate both visualization and quantitation of high concentrations of ADI-001 in lymph node biopsies across multiple dose levels, and exceeding levels previously reported from published studies in patients who received autologous alpha- beta CAR T. Importantly, within this new analysis of secondary lymphoid tissue, ADI-001 also demonstrated complete depletion of CD19- positive B cells, concurrent with the trafficking and functional CAR T activation observed at these sites of action. In context of the totality of our studies to date, we believe ADI-001 is emerging as a highly differentiated product candidate with a potentially best-in-class profile as an off-the-shelf cell therapy, consisting of multiple levels of evidence, and that establishes a robust opportunity for resetting the immune system in both blood and, importantly, within tissue for patients with autoimmune disease. Additionally, we'll also draw your attention to recently published clinical data with obinutuzumab and rituximab, both CD20-targeting antibodies, which we believe complements our observations and further validates our CD20-based approach for ADI-001 in autoimmune disease. These data clearly show that CD20 targeting with an antibody can deplete CD19-positive B-cell compartments in blood, inclusive of plasmablast, memory, and naive B-cell populations, but also, that these antibody-based modalities failed to achieve similar levels of B-cell depletion within tissues, a function that appears to be required for generation of long-term immunosuppressant-free responses in autoimmune patients. With these supporting data in hand, we are well-positioned to advance our broad development plan of ADI-001 in four autoimmune diseases, and look forward to sharing preliminary clinical data in the first half of next year. Let me first start on slide five by reminding you about the biomarker data for ADI-001 in peripheral blood. Starting with pharmacokinetics here, the two graphs on this slide from patients enrolled in the GLEAN trial show the expansion and overall exposure of ADI-001 using two distinct methods of detection. With flow cytometry on the left, reported as CAR T cells per microliter, and with PCR on the right, reported as CAR T copies per microgram of DNA. These data demonstrated robust expansion of ADI-001 in the clinic, that we believe is one of the most compelling profiles observed to date in the field, and is clearly differentiated as a potential off-the-shelf cell therapy. Using these complementary detection methods allow for the bridging of available data across the landscape of autologous and allogeneic cell therapies. As an example, we show on the left axis the relevant reference point for the mean Cmax for responders to axi-cel, at 44 cells per microliter. As you can appreciate, the mean Cmax for all patients treated with ADI-001 at both 3E8 and 1E9 doses exceeded this benchmark. Importantly, these are the dose levels in our protocol exploring ADI-001 in the initial four autoimmune indications. Let's move to slide six. Adding B-cell depletion profile to the picture, in lymphoma, ADI-001 exposure and its depletion of CD19- positive B cells in the peripheral blood were similarly consistent with the autologous alpha- beta CAR T experience in autoimmune disease. In this instance, in systemic lupus erythematosus, or SLE. On the left, you can see the result of ADI-001 regimen on CD19- positive B cells in the blood. Following dosing with ADI-001 in the GLEAN trial, 23 of 24 of these patients experienced consecutive undetectable CD19- positive B cell counts in peripheral blood. These data of the CD19 B-cell compartment depletion on the left are overall indistinguishable from the anti-CD19 autologous CAR T experience reported in SLE patients, represented on the right. Overall, this strongly supports our expectations for a compelling efficacy of ADI-001 in the autoimmune setting. Let's go to the next slide. Extending this potential for B-cell depletion, now in the context of relevant autoimmune diseases, this slide shows ADI-001's potent killing capacity of CD19- positive B cells derived from patients in five autoimmune diseases, using two independent clinical lots of ADI-001. As you can see, ADI-001 demonstrated potent ex vivo killing of patient-derived B-cells across multiple autoimmune diseases, including SLE, systemic sclerosis, rheumatoid arthritis, multiple sclerosis, and Sjögren's syndrome. These data are further supported by third-party clinical data, which are shown on the next slide. This slide summarizes published phase II clinical data from obinutuzumab, or obi, a CD20-targeted antibody in 125 patients with lupus nephritis when given in combination with standard of care. In this study, obi was dosed on day one and weeks 2, 24, and 26. If you look at the graph on the right, you can see that CD20 targeting with obi depleted CD19-positive B-cells in peripheral blood after each cycle with obi. This depletion was inclusive of memory B-cells, naive B-cells, and importantly, plasmablast populations, all defined as CD19-positive. While this is encouraging to see in blood for a CD20-targeted modality, it is equally important to understand what is occurring in tissues. Let's take a look at this on Slide nine. Data initially presented by Schett et al. at EULAR this year, and later published this month, demonstrated that in five patients treated with the CD20 targeting antibody rituximab versus five patients treated with CAR-T, both were capable of achieving this complete CD19-positive B-cell depletion in the blood. However, for the antibody, this level of complete depletion failed to be realized within secondary lymphoid tissues, like lymph nodes, and for these patients, this failure to achieve complete depletion at the tissue level was also associated with suboptimal potential for generating complete immune reset or immunosuppressant-free remissions. Let's now look at the exposure of ADI-001 in tissues on the next slide. This slide summarizes newly generated data from secondary lymphoid tissue from patients treated with ADI-001 in the GLEAN trial. As you can see on the left, in lymph node biopsies on day 10, robust tissue trafficking of ADI-001 CAR T cells was observed, marked in yellow, including significant levels of ADI-001 CAR T cell activation, marked in red by detection of granzyme B. These tissues were also quantified for exposure and demonstrated that ADI-001 represented 27%-64% of the total cellular material detected by ddPCR at the 1E9 dose level. Clear data sets like this are not commonly found or referenced in published or presented materials. As such, it is difficult to find benchmarks for these quantitative exposures in tissues. Despite this rarity for reporting, as you can see on the right, the number of ADI-001 CAR T cells per million total cells exceeded published data reported for autologous CAR T cells in lymph node biopsies, further confirming the significant trafficking to tissues of gamma delta 1 T cells, which is a function that is well documented in the literature, and indeed, this exposure of ADI-001 in tissue led to complete CD19- positive B-cell depletion. Let's take a look at that on the next slide. On the left of this slide, you can appreciate the abundance of CD19- positive cells within lymph nodes at baseline, shown in green, prior to administration of ADI-001. On the neighboring panel, by day 10, following a single dose of ADI-001, and in conjunction with this high level of active ADI-001 trafficking, complete depletion of CD19- positive B-cells was observed in secondary lymphoid tissue. By day 10 after dosing, no CD19- positive B-cells were detected in the lymph node. Of note, on the right of this slide, we have also previously seen functional evidence for extranodal tissue responses. In this case, we are seeing a PET-CT from a DLBCL patient treated with ADI-001, demonstrating complete clinical response in an extranodal lesion in the leg. The bottom line here is that we have now reported and seen unequivocal data with ADI-001 that demonstrated significant trafficking to tissues and its ability to completely deplete CD19- positive B-cells within these tissues. Although novel, this is not completely unexpected for the platform. On slide 12, we summarize data from nine third-party publications, illustrating the critical advantage of gamma delta 1 T cells in trafficking to organs and tissues, which is potentially highly advantageous for the treatment of many autoimmune diseases. This trafficking to tissues was also confirmed in preclinical testing, which is shown on the next slide. Here, we can see that within four days of receiving our gamma delta 1 T cells, the cells distributed to target lesions, tissues, and blood in mice. Over time, the gamma delta 1 T cells continued to proliferate in the target lesion and continued to remain resident, with a strong preference for accumulation in solid tissues over the peripheral blood. Let's finish with Slide 14. In summary, we believe our data uniquely positions ADI-001 as an off-the-shelf cell therapy candidate and has demonstrated clear potential for achieving robust expansion in peripheral blood to levels consistent with that of autologous CAR T. This expansion has also demonstrated complete depletion of CD19-positive cells in the blood and the capacity for ADI-001 to similarly target B-cells ex vivo, derived from patients with autoimmune disease. This capacity is further underpinned by learnings from CD20 targeted antibodies in the clinic, both demonstrating complete B-cell depletion in blood, including CD19- positive plasmablast populations. Importantly, these antibody-based modalities failed to replicate this level of depletion within tissues. For ADI-001, we have now demonstrated unequivocal evidence for robust trafficking and activation within these lymphoid tissues, and concurrent with this trafficking, ADI-001 indeed resulted in complete CD19- positive B-cell depletion within the same tissue. Together, these data provide multiple levels of evidence supporting our approach and our ongoing clinical development activities with ADI-001 in multiple autoimmune diseases. We look forward to continuing the journey with our ongoing clinical activities and reporting initial clinical data in the first half of 2025. With that, I thank you all for sharing your time and for joining me today.