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Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance
Published in Gabriel Virella, Medical Immunology, 2019
Scott Sugden, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, Virginia Litwin
HSCs give rise to the common myeloid progenitors (CMPs), which in turn give rise to the monocyte/dendritic cell progenitors (MDPs) or the granulocyte/monocyte progenitors (GMPs). Maturation then occurs in three stages: monoblast, promonocyte, and monocyte. Monoblasts expressing CD64, CD33, HLA-DR, CD34, and CD4 are derived from both MDP and GMP. As differentiation progresses transition toward promonocytes, there is a loss of CD34 expression and increased expression of CD4 (Figure 10.2). Changes in the expression levels of CD34, HLA-DR, CD117/c-kit, CD64, CD45, CD36, CD14, and CD300 are used to delineate monocyte maturation stages (Table 10.1). Monocytic-myeloid-derived suppressor cells (M-MDSCs) are also differentiated from MDPs.
Chronic Leukemias
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
Scott J. Graham, James D. Cotelingam
Peripheral blood evaluation reveals a mild normocytic, normochromic anemia. The total WBC count varies from low to increased, up to about 25 × 109/L. Thrombocytopenia is present in about half of patients. Absolute monocytosis develops immediately, or up to 2 years after splenectomy. Circulating monocytes have normal morphology (Fig. 14). Occasionally, promonocytes are identified. No monoblasts, Auer rods, or myelodysplastic changes are observed. Infiltration of parenchymal organs frequently occurs.
The Influence of Pituitary-Adrenal Axis on the Immune System
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
Cortisol acetate rapidly reduced bone marrow promonocytes to about 65% over a period of 96 hr. However, the mitotic activity of promonocytes was not decreased, and the production of monocytes was only moderately diminished to about 80% of normal. After in vivo labeling with 3H-thymidine, the monocyte labeling indices were initially significantly higher in cortisol treated mice. Therefore, a decreased production of monocytes in the bone marrow cannot account for the prolonged monocytopenia after cortisol administration. However, cortisol interferes with the release of newly-formed monocytes from the bone marrow.183
Importance of distinguishing the promonocyte in leukemia
Published in Baylor University Medical Center Proceedings, 2020
John R. Krause, Arthur Bredeweg
This case illustrates that promonocytes may have a morphologic picture resembling promyelocytes. As in this case, the granules may be quite prominent and may resemble a promyelocyte, particularly the microgranular variant (Figure 1c). As the treatment for acute monocytic leukemia and promyelocytic leukemia are different, it is important to distinguish between the two. However, there are some situations when it may be reasonable to start treatment for a suspected promyelocytic leukemia even if the diagnosis has not been confirmed with laboratory tests, as patients with APL can quickly develop life-threatening blood clots or bleeding problems if not treated.4,5 Our patient was started on all-trans retinoic acid (ATRA). APL is frequently associated with severe hemorrhagic events, and prompt treatment with ATRA is desirable to avoid early death.4–6 As in our case, if the diagnosis is not found to be APL, ATRA can be stopped and a myeloid regimen started without dire effects.
BCG-induced trained immunity in macrophage: reprograming of glucose metabolism
Published in International Reviews of Immunology, 2020
Yuntong Liu, Shu Liang, Ru Ding, Yuyang Hou, Feier Deng, Xiaohui Ma, Tiantian Song, Dongmei Yan
Monocyte-macrophage system includes promonocytes in bone marrow, monocytes in peripheral blood, and macrophages in tissue, which are all derived from hematopoietic stem cells in the bone marrow. Signals from different tissues can initiate various macrophage polarization. Now it is universally accepted that macrophages in the spectrum of its polarization have two main terminal phenotypic: the classically activated (or M1) or the alternatively activated (or M2) phenotypes.31 The former usually plays a role in clearing pathogens and limiting tumor growth, while the latter can mainly participate in anti-inflammatory responses, tissue healing, fibrosis, tumor survival and other pathological processes. Recently, there is an increased attention on the epigenetic changes that regulate macrophage polarization.31
A new approach for diagnosing chronic myelomonocytic leukemia using structural parameters of Sysmex XNTM analyzers in routine laboratory practice
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2018
Françoise Schillinger, Elise Sourdeau, Marouane Boubaya, Lucile Baseggio, Sylvain Clauser, Edouard Cornet, Camille Debord, Jean-Pierre Defour, Frédérique Dubois, Marion Eveillard, Anne-Cécile Galoisy, Marie-Odile Geay, François Mullier, Vanessa Nivaggioni, Valérie Soenen, Pascal Morel, Francine Garnache-Ottou, Emily Ronez, Valérie Bardet, Eric Deconinck
Chronic myelomonocytic leukemia (CMML) is a rare disease, with an estimated annual incidence of 0.4 cases per 100,000 individuals [1–3]. The biological diagnosis, defined in 2008 by the World Health Organization (WHO) and revised in 2016 is based on positive non-specific criteria: persistent monocytosis greater or equal to 1.0 × 109/L with monocytes accounting for ≥10% of the WBC count, dysplasia affecting at least one lineage in blood or bone marrow, blasts in bone marrow and/or in blood less than 20% and/or presence of a clonal abnormality. All other differential indications are negative criteria, namely: absence of reactive etiology to the monocytosis, absence of WHO criteria for myeloproliferative neoplasms and absence of PDGFRα/β or FGFR1 rearrangement [4–6]. Diagnosis of CMML requires a bone marrow examination, cytogenetic and molecular analysis, performed after blood smear examination. Bone marrow usually shows dysplastic abnormalities and excess of monocytes often with promonocytes and/or blasts. Cytogenetic abnormalities are present in 30–40% of cases [7] while molecular analysis shows abnormalities in more than 90% of CMML cases [8]. Identification of gene mutation markers permits risk stratification and may improve clinical decision making [9,10].