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Bone marrow cellular composition in Listeria monocytogenes infected mice detected using ER-MP12 and ER-MP20 antibodies: a flow cytometric alternative to differential counting.

Detailed assessment of bone marrow cellular composition is essential in the evaluation of various experimental in vivo systems, such as expr … ected, the bone marrow composition changed dramatically during infection, leading to an increase of myeloid cells which peaked after 1 week of infection. Data determined by ER-MP12/20 flow cytometric analysis appeared to be in close agreement with both morphology and lineage marker analysis. In addition, ER-MP12/20 analysis provided more detailed information wi …

Продольное иммунное профилирование после аутологической трансплантации стволовых клеток при множественном склерозе: изучение иммунной реконструкции и модуляции болезней.

ВВЕДЕНИЕ: Автономная трансплантация стволовых клеток (AHSCT) представляет собой эффективное средство для повторного переноса множественных склерозов, однако механизмы, лежащие в основе перезагрузки иммунной системы и устойчивой ремиссии, по-прежнему не до конца понятны. Это исследование дает продольное иммунное профилирование пациентов, проходящих АКСХТ, с уделением особого внимания восстановлению иммунной системы в течение двух лет после АХССТ. МЕТОДЫ: Периферальные моноядерные клетки крови (ПБДК) были собраны у 22 пациентов с множественным склерозом в исходном и многовременном порядке после

Совпадение в аннотации оригинала
INTRODUCTION: Autologous hematopoietic stem cell transplantation (AHSCT) is an effective treatment for relapsing remitting multiple sclerosi … nal mass cytometry (CyTOF) and flow cytometry to assess phenotypic changes in B cells, T cells, and myeloid cells. RESULTS: AHSCT led to profound alterations in immune cell populations. B-cell recovery was marked by a rapid expansion of naïve B cells, while memory B cells and plasmablasts remained depleted. Notably, patients with evidence of inflammatory disea …

The Inflamed Niche: A Double-Edged Sword in AML?

Although inflammation has long been recognized as a hallmark of many cancers, including acute myeloid leukemia (AML), how it affects individual cells of the tumor microenvironment and their interaction with normal and neoplastic cells is incompletely understood. A comprehensive single-cell transcriptomic analysis of human bone marrow from patients with AML and healthy individuals identified skewing of stem cell and stromal cell populations in AML toward proinflammatory states associated with reduced risk of relapse, paralleling previous findings in mouse models and suggesting that inflamed bon

Cure of aplastic anaemia in paroxysmal nocturnal haemoglobinuria by marrow transfusion from identical twin: Failure of peripheral-leucocyte transfusion to correct marrow aplasia.

The ability of syngeneic peripheral leucocytes to cure marrow aplasia was tested in a patient with paroxysmal nocturnal haemoglobinuria (P.N.H.). Transfusion of 7.1X10(10) white cells obtained by leucopheresis from an identical-twin donor, providing 3.4X10(4) myeloid progenitors (C.F.U.-C)/kg, failed to improve marrow function within two months. In contrast, transfusion of 1.3X10(10) nucleated bone-marrow cells, representing 6.4X10(4) C.F.U.-C/kg, from the same donor resulted in prompt bone-marrow recovery. These observations support the hypothesis that aplastic anaemia in P.N.H. is a stem-cel

"Galectin-9: A double-edged sword in Acute Myeloid Leukemia".

Acute Myeloid Leukemia (AML) presents a formidable challenge in the realm of hematologic malignancies, characterized by the unregulated proliferation of myeloid progenitor cells, leading to severe disruptions in normal hematopoiesis. This review examines the multifaceted role of Galectin-9, a crucial glycan-binding protein in the pathophysiology of AML, emphasizing its potential as both a prognostic biomarker and a therapeutic target. Recent insights into the molecular underpinnings of AML, particularly those involving genetic mutations and cytogenetic abnormalities, illuminate the complex lan

MALNC: a new mutant NPM1/IDH2R140 and PML-RARA-associated lncRNA with impact on AML cell proliferation, maturation and drug response.

As the non-coding genome remains poorly characterized in acute myeloid leukemia (AML), we aimed to identify and functionally characterize novel long non-coding RNAs (lncRNAs) relevant to AML biology and treatment. We first identified lncRNAs overexpressed in AML blasts and, among them, discovered a novel transcript, which we named myeloid and AML-associated intergenic long non-coding RNA (MALNC). MALNC is overexpressed in AML, particularly in cases with the PML-RARA fusion or IDH2R140/NPM1 co-mutations, and is associated with a distinct gene expression profile. Functional studies showed that M

Dual-action membrane-chimeric liposomes with self-reinforcing targeting for acute lung injury treatment.

Acute lung injury (ALI) is a common acute and critical syndrome with high mortality. The uncontrollable feedback loop of inflammation is the primary cause of death in patients with ALI. Therefore, targeting the inflammatory site and breaking the inflammatory loop are key strategies for ALI treatment. Our work developed a myeloid cell membrane-chimeric liposome containing dexamethasone (DEX) and leukocyte adhesin-1 (LA-1), abbreviated as ML/LA@DEX NPs. During the preparation of ML/LA@DEX NPs, LA-1 could activate CD11b on the myeloid cell membrane, thereby improving the binding ability of ML/LA@

Vitamin D Derivatives in Acute Myeloid Leukemia: The Matter of Selecting the Right Targets.

Acute myeloid leukemia (AML) is an aggressive and often fatal hematopoietic malignancy. A very attractive way to treat myeloid leukemia, called "differentiation therapy", was proposed when in vitro studies showed that some compounds are capable of inducing differentiation of AML cell lines. One of the differentiation-inducing agents, all-trans-retinoic acid (ATRA), which can induce granulocytic differentiation in AML cell lines, has been introduced into clinics to treat patients with acute promyelocytic leukemia (APL) in which a PML-RARA fusion protein is generated by a chromosomal translocati

The tumor suppressor RASSF1A modulates inflammation and injury in the reperfused murine myocardium.

Inflammation is a central feature of cardiovascular disease, including myocardial infarction and heart failure. Reperfusion of the ischemic myocardium triggers a complex inflammatory response that can exacerbate injury and worsen heart function, as well as prevent myocardial rupture and mediate wound healing. Therefore, a more complete understanding of this process could contribute to interventions that properly balance inflammatory responses for improved outcomes. In this study, we leveraged several approaches, including global and regional ischemia/reperfusion (I/R), genetically modified mic

Outcome of myeloablative allogeneic peripheral blood hematopoietic stem cell transplantation for refractory/relapsed AML patients in NR status.

To further find effective method to improve the long term survival of refractory or relapsed acute myeloid leukemia (AML) patients, we retrospectively analyzed the outcomes of myeloablative hematopoietic stem cell transplantation (HSCT) for 133 consecutive patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS) therapy related AML(t-AML) in not remission status. The overall 3-year OS and DFS were 40.9% and 35.6% respectively. The variables associated with improved long term DFS were a bone marrow blast cell count less than 20% and an intensified conditioning regimen. In ad

Securinine, a myeloid differentiation agent with therapeutic potential for AML.

As the defining feature of Acute Myeloid Leukemia (AML) is a maturation arrest, a highly desirable therapeutic strategy is to induce leukemic cell maturation. This therapeutic strategy has the potential of avoiding the significant side effects that occur with the traditional AML therapeutics. We identified a natural compound securinine, as a leukemia differentiation-inducing agent. Securinine is a plant-derived alkaloid that has previously been used clinically as a therapeutic for primarily neurological related diseases. Securinine induces monocytic differentiation of a wide range of myeloid l

The Interaction of Hemopoiesis and Immunogenesis in Immunopathology Development.

A great number of authors consider as "stem cell disorders" the following immunopathologies: immunodeficiency, lymphoproliferative diseases, systemic and organ-specific autoimmune diseases. A participation of early hemopoietic precursors in immunopathology development was analyzed on the next models: age-related immunodeficiency in CBF1 mice, autoimmune hemolytic anemia in NZB mice and leukemia in AKR mice. NZB mice have an augmented number of CFUs in S-phase, as a prerequisit for elevated sensitivity to Rauscher leukemia virus, as well to autoimmune disorder development. The increased stem ce

Lymphatic CD49a is a driver of meningeal immune aging and cognitive decline.

Aging is associated with progressive accumulation and dysregulation of dural immune cells, coinciding with impaired CSF drainage and lymphatic function. Prior work has shown that improving lymphatic function in aged mice is sufficient to ameliorate age-associated cognitive decline, and that local immune cells can directly regulate lymphatic draining function. Yet, the endothelial-intrinsic mechanisms driving lymphatic dysfunction remain unclear. Here we found that the integrin CD49a is upregulated in aged lymphatic endothelial cells and regulates CCL21 release. Accordingly, genetic deletion of

Stem-cell gene therapy for the Wiskott-Aldrich syndrome.

The Wiskott-Aldrich syndrome (WAS) is an X-linked recessive primary immunodeficiency disorder associated with thrombocytopenia, eczema, and autoimmunity. We treated two patients who had this disorder with a transfusion of autologous, genetically modified hematopoietic stem cells (HSC). We found sustained expression of WAS protein expression in HSC, lymphoid and myeloid cells, and platelets after gene therapy. T and B cells, natural killer (NK) cells, and monocytes were functionally corrected. After treatment, the patients' clinical condition markedly improved, with resolution of hemorrhagic di…

Neutralization of inhibitory activity derived from cells of MDS patients and ML-2 cell line by monoclonal antibodies against H and L-subunit-rich ferritins.

Monoclonal antibody 2A4 against human heart ferritin and a polyclonal antibody against human placental ferritin inactivated the suppressor activity present in media conditioned by cells of patients with myelodysplastic syndrome (MDS). These antibodies also neutralized the inhibitory activity released by cells of myeloid leukemic ML-2 cell line. In contrast, a monoclonal antibody against the ferritin L subunit did not neutralize the inhibitory activity of the media conditioned either by the cells of patients with MDS or by the ML-2 cell line. Neutralization of the inhibitory activity present in

Release of high molecular weight-neutrophil chemotactic activity from human tissues, cells and secretion.

Release of high molecular weight-neutrophil chemotactic activity from human tissues, cells and secretion was studied in vivo and in vitro. Lung, nasal turbinate, nasal polyps, skin of neurofibromatosis, basophils from chronic myeloid leukemia and cultured basophilic cells from cord blood released this mediator following calcium ionophore, antigen, anti-IgE or homogenization in vitro. Its release was also demonstrated in human nasal secretions from patients with allergic rhinitis following antigen challenge. Regarding mononuclear cells no release of this mediator was observed from normal donors

[Tumor infiltrates suspicious of carcinoma in mediastinal lymph nodes].

Myelosarcomas are, due to their rarity, a difficult differential diagnosis. Not infrequently, extensive immunohistochemical staining for characterization of the tumor is performed, if one does not directly think of myelosarcoma. In the present case, there was a positivity of the myeloid blasts for cytokeratin. This may complicate the discrimination of myelosarcoma from carcinoma, in particular small cell carcinoma, not only in the mediastinum, but also in the skin, e.g., Merkel cell carcinoma.

Polyamine depletion limits progression of acute leukaemia.

Cancer cells are addicted to polyamines, polycations essential for cellular function. While dual targeting of cellular polyamine biosynthesis and polyamine uptake is under clinical investigation in solid cancers, preclinical and clinical studies into its potential in haematological malignancies are lacking. Here we investigated the preclinical efficacy of polyamine depletion in acute leukaemia. The polyamine biosynthesis inhibitor difluoromethylornithine (DFMO) inhibited growth of a molecularly diverse panel of acute leukaemia cell lines, while non-malignant cells were unaffected. Responsivene

Aberrant expression of miR-9/9* in myeloid progenitors inhibits neutrophil differentiation by post-transcriptional regulation of ERG.

Aberrant post-transcriptional regulation by microRNAs (miRNAs) has been shown to be involved in the pathogenesis of acute myeloid leukemia (AML). In a previous study, we performed a large functional screen using a retroviral barcoded miRNA expression library. Here, we report that overexpression of miR-9/9* in myeloid 32D cell line (32D-miR-9/9*) had profound impact on granulocyte colony-stimulating factor-induced differentiation. Further in vitro studies showed that enforced expression of miR-9/9* blocked normal neutrophil development in 32D and in primary murine lineage-negative bone marrow c

Clonal evolutions during long-term cultures of bone marrow from de novo acute myeloid leukaemia with trilineage myelodysplasia and with myelodysplastic remission marrow.

We previously established a long-term bone marrow culture (LTBMC) system in which novel abnormal karyotypes could emerge in vitro prior to the appearance of the same karyotypes in vivo in patients with myelodysplastic syndrome (MDS). We extended our study to examine whether acute myeloid leukaemia (AML) transformed from MDS (MDS/AML) and de novo AML with trilineage myelodysplasia (AML/TMDS) show clonal evolution in LTBMC similar to that of typical AML or MDS. We also analysed the cytogenetic changes in cultures with bone marrows from AML with myelodysplastic remission marrow (AML/MRM) as well