T cell receptor (TCR)

T 细胞受体 (TCR)
  • 文章类型: Journal Article
    T细胞受体(TCR)通过快速准确地识别外源和非自身抗原,在调节T细胞反应中起着至关重要的作用。该过程涉及多个分子和调节机制,形成复杂的网络以实现有效的抗原识别。数学建模技术可以帮助解开复杂的TCR信令网络,并确定控制它的关键监管机构。在这次审查中,我们介绍并简要讨论了TCR初始触发的相关数学模型,重点研究具有不同修改结构的动态校对(KPR)模型。我们比较拓扑结构,生物学假设,参数选择,以及每个模型的仿真性能,并总结它们的优点和局限性。TCR建模设计的进一步研究,旨在优化特异性和灵敏度的平衡,预计将有助于开发新的治疗策略。
    T cell receptors (TCRs) play crucial roles in regulating T cell response by rapidly and accurately recognizing foreign and non-self antigens. The process involves multiple molecules and regulatory mechanisms, forming a complex network to achieve effective antigen recognition. Mathematical modeling techniques can help unravel the intricate network of TCR signaling and identify key regulators that govern it. In this review, we introduce and briefly discuss relevant mathematical models of TCR initial triggering, with a focus on kinetic proofreading (KPR) models with different modified structures. We compare the topology structures, biological hypotheses, parameter choices, and simulation performance of each model, and summarize the advantages and limitations of them. Further studies on TCR modeling design, aiming for an optimized balance of specificity and sensitivity, are expected to contribute to the development of new therapeutic strategies.
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  • 文章类型: Journal Article
    活性氧(ROS)是细胞间和细胞内信号传导的核心。它们的局部和瞬时效应是由于它们的半衰期短,特别是在受控数量的情况下。T细胞受体(TCR)激活后,调节的ROS信号传导主要由电子传递链(ETC)的复合物I和III启动。随后的ROS产生引发烟酰胺腺嘌呤二核苷酸磷酸氧化酶2(NADPH氧化酶2)的激活,延长氧化信号。然后,该信号参与激酶信号级联反应,例如丝裂原激活的蛋白激酶(MAPK)途径,并增加对REDOX敏感的转录因子的活性,例如核因子κB(NF-κB)和激活蛋白1(AP-1)。为了限制ROS的过度生产和防止氧化应激,核因子红系2相关因子2(Nrf2)和抗氧化蛋白如超氧化物歧化酶(SODs)精细调节信号强度,并能够在需要时终止氧化信号。因此,氧化信号,比如T细胞激活,控制良好,对蜂窝通信至关重要。
    Reactive oxygen species (ROS) are central to inter- and intracellular signaling. Their localized and transient effects are due to their short half-life, especially when generated in controlled amounts. Upon T cell receptor (TCR) activation, regulated ROS signaling is primarily initiated by complexes I and III of the electron transport chain (ETC). Subsequent ROS production triggers the activation of nicotinamide adenine dinucleotide phosphate oxidase 2 (NADPH oxidase 2), prolonging the oxidative signal. This signal then engages kinase signaling cascades such as the mitogen-activated protein kinase (MAPK) pathway and increases the activity of REDOX-sensitive transcription factors such as nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1). To limit ROS overproduction and prevent oxidative stress, nuclear factor erythroid 2-related factor 2 (Nrf2) and antioxidant proteins such as superoxide dismutases (SODs) finely regulate signal intensity and are capable of terminating the oxidative signal when needed. Thus, oxidative signals, such as T cell activation, are well-controlled and critical for cellular communication.
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  • 文章类型: Journal Article
    用于乳糜泻(CeD)的无麸质饮食是限制性的,并且通常不能诱导完全症状和/或粘膜疾病缓解。CeD发病机制的核心是谷蛋白特异性CD4+T细胞,在超过85%的CeD患者中受到HLA-DQ2.5的限制,使HLA-DQ2.5成为抑制谷蛋白依赖性免疫的有吸引力的靶标。最近,开发了特异性识别HLA-DQ2.5和多个谷蛋白表位复合物的新型抗HLA-DQ2.5抗体(DONQ52).
    目的:评估DONQ52抑制CeD患者来源的T细胞对包含免疫显性T细胞表位的免疫原性最强的谷蛋白肽反应的能力。
    方法:我们在CeD患者中采用了体内谷蛋白攻击模型,该模型提供了疾病相关谷蛋白特异性T细胞反应的定量读数。HLA-DQ2.5+CeD患者食用含有小麦的食物,大麦,或黑麦3天,在开始攻击之前(D1)和之后6天(D6)收集血液。分离外周血单核细胞,并在干扰素(IFN)-γ酶联免疫吸附斑点测定(ELISpot)中进行评估,测试对包含一系列免疫显性T细胞表位的谷蛋白肽的反应。评估DONQ52(4或40μg/mL)的抑制作用并与pan-HLA-DQ阻断(SPVL3抗体)进行比较。
    结果:在HLA-DQ2.5+CeD患者中,DONQ52将对所有小麦面筋肽的T细胞应答降低到与泛HLA-DQ抗体阻断相当或更有效的程度。它将T细胞对最具免疫显性小麦表位混合物的应答降低了中值87.3%(IQR72.4-92.4)。值得注意的是,DONQ52还显著降低了对显性大麦大麦醇溶蛋白和黑麦secalin衍生肽的T细胞应答。DONQ52对T细胞对非谷蛋白抗原的反应没有影响。
    结论:DONQ52可显著阻断HLA-DQ2.5限制性T细胞对CeD中免疫原性最强的谷蛋白肽的反应。我们的发现支持体外数据,即DONQ52对多种谷蛋白肽:HLA-DQ2.5复合物具有选择性和广泛的交叉反应性。这项工作提供了概念验证多特异性抗体阻断具有有意义地抑制CeD中致病性谷蛋白特异性T细胞反应的潜力,并支持正在进行的治疗开发。
    The gluten-free diet for celiac disease (CeD) is restrictive and often fails to induce complete symptom and/or mucosal disease remission. Central to CeD pathogenesis is the gluten-specific CD4+ T cell that is restricted by HLA-DQ2.5 in over 85% of CeD patients, making HLA-DQ2.5 an attractive target for suppressing gluten-dependent immunity. Recently, a novel anti-HLA-DQ2.5 antibody that specifically recognizes the complexes of HLA-DQ2.5 and multiple gluten epitopes was developed (DONQ52).
    OBJECTIVE: To assess the ability of DONQ52 to inhibit CeD patient-derived T-cell responses to the most immunogenic gluten peptides that encompass immunodominant T cell epitopes.
    METHODS: We employed an in vivo gluten challenge model in patients with CeD that affords a quantitative readout of disease-relevant gluten-specific T-cell responses. HLA-DQ2.5+ CeD patients consumed food containing wheat, barley, or rye for 3 days with collection of blood before (D1) and 6 days after (D6) commencing the challenge. Peripheral blood mononuclear cells were isolated and assessed in an interferon (IFN)-γ enzyme-linked immunosorbent spot assay (ELISpot) testing responses to gluten peptides encompassing a series of immunodominant T cell epitopes. The inhibitory effect of DONQ52 (4 or 40 μg/mL) was assessed and compared to pan-HLA-DQ blockade (SPVL3 antibody).
    RESULTS: In HLA-DQ2.5+ CeD patients, DONQ52 reduced T cell responses to all wheat gluten peptides to an equivalent or more effective degree than pan-HLA-DQ antibody blockade. It reduced T cell responses to a cocktail of the most immunodominant wheat epitopes by a median of 87% (IQR 72-92). Notably, DONQ52 also substantially reduced T-cell responses to dominant barley hordein and rye secalin derived peptides. DONQ52 had no effect on T-cell responses to non-gluten antigens.
    CONCLUSIONS: DONQ52 can significantly block HLA-DQ2.5-restricted T cell responses to the most highly immunogenic gluten peptides in CeD. Our findings support in vitro data that DONQ52 displays selectivity and broad cross-reactivity against multiple gluten peptide:HLA-DQ2.5 complexes. This work provides proof-of-concept multi-specific antibody blockade has the potential to meaningfully inhibit pathogenic gluten-specific T-cell responses in CeD and supports ongoing therapeutic development.
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  • 文章类型: Journal Article
    粘膜相关的不变T(MAIT)细胞是一组非常规T细胞,可识别MHC-I相关蛋白1(MR1)呈递的小分子代谢物,通过αβT细胞受体(TCR)。MAITTCR具有基本上不变的TCRα链,这在哺乳动物之间是高度保守的。同样,MR1是最高度保守的MHC-I样分子。这种极端的保护,包括MAITTCR和MR1之间的相互作用模式,已显示允许T细胞生物学中独特的物种错配反应性,从而允许在比较免疫学研究中使用选定的物种错配MR1抗原(MR1-Ag)四聚体。然而,物种错配MR1-Ag四聚体在鉴定不同物种MAIT细胞时的交叉反应模式尚未得到正式评估.我们开发了新的牛和猪MR1-Ag四聚体,并利用这些与先前开发的人类,小鼠和猪尾猕猴MR1-Ag四聚体表征跨物种四聚体反应性。来自每个物种的MR1-Ag四聚体以与物种匹配的MR1-Ag四聚体相当的特异性鉴定了远亲物种中的T细胞群体。然而,染色特征存在细微差异,对MAIT细胞的准确鉴定具有实际意义。猪MR1在物种中充分保守,猪MR1-Ag四聚体鉴定了来自其他物种的MAIT细胞。然而,猪的MAIT细胞处于表型检测的极限。在没有绵羊MR1-Ag四聚体的情况下,通过表型鉴定了绵羊血液中的MAIT细胞群,利用物种错配的MR1-Ag四聚体。总的来说,我们的结果验证了物种错配MR1-Ag四聚体在比较免疫学研究中的用途和局限性.
    Mucosal-associated invariant T (MAIT) cells are a subset of unconventional T cells that recognize small molecule metabolites presented by major histocompatibility complex class I related protein 1 (MR1), via an αβ T cell receptor (TCR). MAIT TCRs feature an essentially invariant TCR α-chain, which is highly conserved between mammals. Similarly, MR1 is the most highly conserved major histocompatibility complex-I-like molecule. This extreme conservation, including the mode of interaction between the MAIT TCR and MR1, has been shown to allow for species-mismatched reactivities unique in T cell biology, thereby allowing the use of selected species-mismatched MR1-antigen (MR1-Ag) tetramers in comparative immunology studies. However, the pattern of cross-reactivity of species-mismatched MR1-Ag tetramers in identifying MAIT cells in diverse species has not been formally assessed. We developed novel cattle and pig MR1-Ag tetramers and utilized these alongside previously developed human, mouse, and pig-tailed macaque MR1-Ag tetramers to characterize cross-species tetramer reactivities. MR1-Ag tetramers from each species identified T cell populations in distantly related species with specificity that was comparable to species-matched MR1-Ag tetramers. However, there were subtle differences in staining characteristics with practical implications for the accurate identification of MAIT cells. Pig MR1 is sufficiently conserved across species that pig MR1-Ag tetramers identified MAIT cells from the other species. However, MAIT cells in pigs were at the limits of phenotypic detection. In the absence of sheep MR1-Ag tetramers, a MAIT cell population in sheep blood was identified phenotypically, utilizing species-mismatched MR1-Ag tetramers. Collectively, our results validate the use and define the limitations of species-mismatched MR1-Ag tetramers in comparative immunology studies.
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  • 文章类型: Journal Article
    在外部和内部因素的影响下,个体的T细胞库不断变化。不接受刺激信号的细胞死亡,而那些遇到并识别病原体或接受共刺激信号的人分裂,导致克隆扩张。可以通过监测其独特的T细胞受体(TCR)序列的存在来追踪T细胞克隆,通过称为V(D)J重排的过程从头组装。追踪T细胞可以提供对造血干细胞移植(HSCT)或癌症治疗反应后细胞存活的有价值的见解,并且可以指示通过疫苗接种诱导保护性免疫。在这项研究中,我们报道了一种从TCR测序数据定量T细胞库动态的生物信息学方法.我们通过测量健康供体的T细胞库稳定性来证明其实用性,通过量化供体淋巴细胞输注(DLI)的效果,并通过追踪HSCT患者中不同T细胞亚群的命运以及接种疫苗个体中病原体特异性克隆的扩增。
    An individual\'s T-cell repertoire constantly changes under the influence of external and internal factors. Cells that do not receive a stimulatory signal die, while those that encounter and recognize a pathogen or receive a co-stimulatory signal divide, resulting in clonal expansions. T-cell clones can be traced by monitoring the presence of their unique T-cell receptor (TCR) sequence, which is assembled de novo through a process known as V(D)J rearrangement. Tracking T cells can provide valuable insights into the survival of cells after hematopoietic stem cell transplantation (HSCT) or cancer treatment response and can indicate the induction of protective immunity by vaccination. In this study, we report a bioinformatic method for quantifying the T-cell repertoire dynamics from TCR sequencing data. We demonstrate its utility by measuring the T-cell repertoire stability in healthy donors, by quantifying the effect of donor lymphocyte infusion (DLI), and by tracking the fate of the different T-cell subsets in HSCT patients and the expansion of pathogen-specific clones in vaccinated individuals.
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  • 文章类型: Editorial
    暂无摘要。
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  • 文章类型: Journal Article
    表征新诊断的特发性炎性肌病(IIM)的未治疗患者的外周血和肌肉组织中的T细胞受体(TCRβ)库。
    在20名新诊断的初治IIM患者的外周血和肌肉组织中进行了TCRβ链的高通量RNA测序(9名DM,5NM/OM,5IMNM和1ASys)和健康对照。其结果与疾病活动的标志物相关。
    当与IIM的外周血以及健康对照相比时,IIM患者的肌肉组织显示出更多的TCRβ克隆扩增和降低的多样性(均p=0.0001)。肌肉中的几个扩增的TCRβ克隆是组织限制性的,无法在外周血中检索。与循环中发现的克隆(也)相比,这些克隆具有明显更长的CDR3区域(p=0.0002),而它们的CDR3区更疏水(p<0.01)。网络分析显示,患者之间共享克隆TCRβ特征。肌肉组织中克隆扩张的增加与CK水平的增加显着相关(p=0.03),而它往往与肌肉力量下降相关(p=0.08)。
    对IIM患者肌肉中克隆的网络分析显示,患者之间共有序列簇。肌肉限制性CDR3TCRβ克隆在其T细胞受体中显示特定结构特征。我们的结果表明,肌肉组织中的克隆TCRβ扩增可能与疾病活动有关。总的来说,这些发现支持肌肉组织中特异性克隆性T细胞反应在所研究的IIM亚型发病机制中的作用.
    To characterize the T cell receptor (TCRβ) repertoire in peripheral blood and muscle tissues of treatment naïve patients with newly diagnosed idiopathic inflammatory myopathies (IIMs).
    High throughput RNA sequencing of the TCRβ chain was performed in peripheral blood and muscle tissue in twenty newly-diagnosed treatment-naïve IIM patients (9 DM, 5 NM/OM, 5 IMNM and 1 ASyS) and healthy controls. Results thereof were correlated with markers of disease activity.
    Muscle tissue of IIM patients shows more expansion of TCRβ clones and decreased diversity when compared to peripheral blood of IIM as well as healthy controls (both p=0.0001). Several expanded TCRβ clones in muscle are tissue restricted and cannot be retrieved in peripheral blood. These clones have significantly longer CDR3 regions when compared to clones (also) found in circulation (p=0.0002), while their CDR3 region is more hydrophobic (p<0.01). Network analysis shows that clonal TCRβ signatures are shared between patients. Increased clonal expansion in muscle tissue is significantly correlated with increased CK levels (p=0.03), while it tends to correlate with decreased muscle strength (p=0.08).
    Network analysis of clones in muscle of IIM patients shows shared clusters of sequences across patients. Muscle-restricted CDR3 TCRβ clones show specific structural features in their T cell receptor. Our results indicate that clonal TCRβ expansion in muscle tissue might be associated with disease activity. Collectively, these findings support a role for specific clonal T cell responses in muscle tissue in the pathogenesis of the IIM subtypes studied.
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  • 文章类型: Journal Article
    腹主动脉瘤(AAA)是一种危及生命的心血管疾病。尽管对其发病机制仍知之甚少,最近的证据表明,AAA表现出自身免疫性疾病的特征。特别是,对主动脉壁中的AAA相关抗原作出反应的T细胞可能有助于初始免疫应答。单细胞RNA(scRNA)T细胞受体(TCR)和B细胞受体(BCR)测序是研究克隆性的有力工具。然而,在实施和数据分析过程中必须考虑有限数量的孤立细胞等困难,使生物学解释具有挑战性。这里,我们在实验性小鼠AAA中进行了代表性的单细胞免疫库分析,并显示了可靠的生物信息学处理流程,突出了这种方法的机会和局限性.
    我们在AAA诱导后3、7、14和28天通过弹性蛋白酶灌注主动脉对来自雄性C57BL/6J小鼠的肾下主动脉的分离的淋巴细胞进行了scRNATCR和BCR测序。在第3天和第28天假手术小鼠和非手术小鼠作为对照。
    179个B细胞和796个T细胞的互补决定区(CDR3)长度分布的比较显示AAA和对照之间以及疾病阶段之间都没有差异。我们在AAA中没有发现B细胞的克隆扩增。对于T细胞,我们在16个AAA样本中的11个和8个对照样本中的一个中鉴定出几个克隆.免疫受体库比较表明,在单个AAA样品之间仅共享少数克隆。AAA中TCRβ链中最常用的V基因是TRBV3、TRBV19和剪接变体TRBV12-2+TRBV13-2。
    我们没有发现B细胞的克隆扩增,但有证据表明在小鼠中弹性蛋白酶诱导的AAA中T细胞的克隆扩增。我们的发现暗示,TCR和BCR分布的更精确表征需要更多数量的淋巴细胞来防止采样不足并可能检测稀有克隆。因此,需要进一步的实验来证实我们的发现。总之,本文研究了TCR和BCR测序结果,确定限制和陷阱,并为未来的研究提供指导。
    UNASSIGNED: An abdominal aortic aneurysm (AAA) is a life-threatening cardiovascular disease. Although its pathogenesis is still poorly understood, recent evidence suggests that AAA displays autoimmune disease characteristics. Particularly, T cells responding to AAA-related antigens in the aortic wall may contribute to an initial immune response. Single-cell RNA (scRNA) T cell receptor (TCR) and B cell receptor (BCR) sequencing is a powerful tool for investigating clonality. However, difficulties such as limited numbers of isolated cells must be considered during implementation and data analysis, making biological interpretation challenging. Here, we perform a representative single-cell immune repertoire analysis in experimental murine AAA and show a reliable bioinformatic processing pipeline highlighting opportunities and limitations of this approach.
    UNASSIGNED: We performed scRNA TCR and BCR sequencing of isolated lymphocytes from the infrarenal aorta of male C57BL/6J mice 3, 7, 14, and 28 days after AAA induction via elastase perfusion of the aorta. Sham-operated mice at days 3 and 28 and non-operated mice served as controls.
    UNASSIGNED: Comparison of complementarity-determining region (CDR3) length distribution of 179 B cells and 796 T cells revealed neither differences between AAA and control nor between the disease stages. We found no clonal expansion of B cells in AAA. For T cells, we identified several clones in 11 of 16 AAA samples and one of eight control samples. Immune receptor repertoire comparison indicated that only a few clones were shared between the individual AAA samples. The most frequently used V-genes in the TCR beta chain in AAA were TRBV3, TRBV19, and the splicing variant TRBV12-2 + TRBV13-2.
    UNASSIGNED: We found no clonal expansion of B cells but evidence for clonal expansion of T cells in elastase-induced AAA in mice. Our findings imply that a more precise characterization of TCR and BCR distribution requires a more extensive number of lymphocytes to prevent undersampling and potentially detect rare clones. Thus, further experiments are necessary to confirm our findings. In summary, this paper examines TCR and BCR sequencing results, identifies limitations and pitfalls, and offers guidance for future studies.
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  • 文章类型: Journal Article
    新抗原反应性细胞毒性T淋巴细胞在精确消除癌细胞中起着至关重要的作用。在这项研究中,我们证明了个性化的基于新抗原的T细胞治疗在诱导两名负担沉重的转移性卵巢癌患者的肿瘤消退中的有效性.我们的方法涉及新抗原反应性T淋巴细胞离体扩增的强大管道的开发。基于肿瘤的体细胞突变及其预测的HLA结合亲和力来设计和合成新抗原肽。然后通过与新抗原负载的树突状细胞共培养将这些肽呈递给T淋巴细胞用于离体扩增。在细胞治疗之后,两名患者的肿瘤标志物水平均显著降低,并且肿瘤明显消退.一名患者通过输注从新鉴定的新抗原产生的T细胞产物实现了重复的癌症消退。转录组学分析显示,细胞治疗后患者外周血中新抗原反应性细胞毒性淋巴细胞显着增加。这些细胞毒性T淋巴细胞表达针对新抗原的多克隆T细胞受体(TCR),以及丰富的细胞毒性蛋白和促炎细胞因子。新抗原靶向的功效与免疫原性和TCR多克隆性显著相关。值得注意的是,新抗原特异性TCR克隆型在细胞治疗后在外周血中持续存在.我们的发现表明,个性化的基于新抗原的T细胞治疗触发了表达抗卵巢癌的多克隆TCR的细胞毒性淋巴细胞,表明其在癌症免疫疗法中的潜力。
    Neoantigen-reactive cytotoxic T lymphocytes play a vital role in precise cancer cell elimination. In this study, we demonstrate the effectiveness of personalized neoantigen-based T cell therapy in inducing tumor regression in two patients suffering from heavily-burdened metastatic ovarian cancer. Our approach involved the development of a robust pipeline for ex vivo expansion of neoantigen-reactive T lymphocytes. Neoantigen peptides were designed and synthesized based on the somatic mutations of the tumors and their predicted HLA binding affinities. These peptides were then presented to T lymphocytes through co-culture with neoantigen-loaded dendritic cells for ex vivo expansion. Subsequent to cell therapy, both patients exhibited significant reductions in tumor marker levels and experienced substantial tumor regression. One patient achieved repeated cancer regression through infusions of T cell products generated from newly identified neoantigens. Transcriptomic analyses revealed a remarkable increase in neoantigen-reactive cytotoxic lymphocytes in the peripheral blood of the patients following cell therapy. These cytotoxic T lymphocytes expressed polyclonal T cell receptors (TCR) against neoantigens, along with abundant cytotoxic proteins and pro-inflammatory cytokines. The efficacy of neoantigen targeting was significantly associated with the immunogenicity and TCR polyclonality. Notably, the neoantigen-specific TCR clonotypes persisted in the peripheral blood after cell therapy. Our findings indicate that personalized neoantigen-based T cell therapy triggers cytotoxic lymphocytes expressing polyclonal TCR against ovarian cancer, suggesting its promising potential in cancer immunotherapy.
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  • 文章类型: Journal Article
    T细胞受体(TR)支持T细胞活性的多样性和特异性。因此,TR库数据作为适应性免疫生物标志物都是有价值的,并作为确定候选治疗性TR的方法。TR库的分析在很大程度上依赖于计算分析,因此,数据标准化和计算机可读是至关重要的。然而在实践中,在不同的数据集中使用不同的缩写和非标准术语使得这些数据预处理变得不平凡。Tidytcells是一个轻量级的,独立于平台的Python包,提供专门为TR命名设计的易于使用的标准化工具。该软件在MIT许可下是开源的,可以从Python包索引(PyPI)安装。在出版的时候,tidytcells是2.0.0版本。
    T cell receptors (TR) underpin the diversity and specificity of T cell activity. As such, TR repertoire data is valuable both as an adaptive immune biomarker, and as a way to identify candidate therapeutic TR. Analysis of TR repertoires relies heavily on computational analysis, and therefore it is of vital importance that the data is standardized and computer-readable. However in practice, the usage of different abbreviations and non-standard nomenclature in different datasets makes this data pre-processing non-trivial. tidytcells is a lightweight, platform-independent Python package that provides easy-to-use standardization tools specifically designed for TR nomenclature. The software is open-sourced under the MIT license and is available to install from the Python Package Index (PyPI). At the time of publishing, tidytcells is on version 2.0.0.
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