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Heterogeneity of Macrophages in Skin Granulomas
Published in Brian J. Nickoloff, Dermal Immune System, 2019
Normal monocytopoiesis occurs through a complex, orderly, and closely regulated system in the bone marrow. Although some heterogeneity may be detected in the early developmental phases, it is not until mature monocytes venture into the organs as macrophages that the well-known heterogeneity of tissue macrophages asserts itself. This marvelous degree of diversity of macrophages undoubtedly bestows major survival and defense value on the animal and the specific organ.
Genetic Control of Macrophage Antitumor Responses
Published in Gloria H. Heppner, Amy M. Fulton, Macrophages and Cancer, 2019
Mary M. Stevenson, Emil Skamene
Induction of inflammation, for example, in the peritoneal cavity by injection of nonspecific, sterile stimuli, is characterized by the accumulation of young, recently blood-derived macrophages. This response is accompanied by monocytosis in the peripheral blood as a result of increased bone marrow production of mononuclear phagocytes in response to a soluble factor, factor increasing monocytopoiesis (FIM), produced by macrophages at the site of inflammation.23,24
Macrophages As Effectors Of Cell-Mediated Immunity
Published in Hans H. Gadebusch, Phagocytes and Cellular Immunity, 2020
The origin, structure, and general activities of macrophages have been widely reviewed23,31,35 and will be treated here only in outline. Ther term “mononuclear phagocytic system” (MPS) has been proposed36 to embrace the cells generally referred to as macrophages or members of the reticuloendothelial system and their precursors. Mature macrophages include those found in connective tissue as histiocytes; the liver as Kupffer cells; the pulmonary alveoli, the spleen lymph nodes, and bone marrow as free and fixed macrophages and sinusoidal lining cells; serous cavities as peritoneal macrophages; bone tissues as osteoclasts; and the nervous system, probably as microglia. These cells are derived ultimately from a rapidly dividing precursor (promonocyte) in bone marrow by way of monocytes in blood.37"39 It has been suggested that macrophages may, in some circumstances, arise from precursors with the morphology of lymphocytes.40,41 This suggestion was made, in part, on the basis of experiments with thoracic duct “lymphocytes,” but it is now clear that thoracic duct lymph contains macrophages.42 Lymphocyte to macrophage transformation, if it occurs at all, probably makes only a minor contribution to the body’s supply of macrophages. Mature macrophages are capable of division (see Reference 23 and discussion below) and this may be important in increasing the number of macrophages available as effectors. An increased demand is, however, more likely to be met by increases in the number and activity of monocyte precursors, mainly in the bone marrow.38 Humoral factors — such as colony stimulating factor (CSF) and inhibitors thereof — are probably important in the regulation of monocytopoiesis, though their precise roles are not known.43-45
Fever-range whole body hyperthermia leads to changes in immune-related genes and miRNA machinery in Wistar rats
Published in International Journal of Hyperthermia, 2023
Henryk Mikołaj Kozłowski, Justyna Sobocińska, Tomasz Jędrzejewski, Bartosz Maciejewski, Artur Dzialuk, Sylwia Wrotek
We further investigated the effects of FRH on the count of monocytes. As G-CSF is a key regulator of granulocytopoiesis and monocytopoiesis [48], we anticipated downstream effects of FRH on monocyte number. Surprisingly, we observed a modest but nonsignificant change in the number of monocytes in blood samples. We additionally evaluated the expression of Mif, and observed decreased levels in all examined organs after 24 h of FRH. Despite its obvious role in the regulation of the migration of macrophages, MIF regulates the expression of pro-inflammatory cytokines. Furthermore, it is a key regulator of the innate immune system, most notably the inflammatory response to microbial infection [9]. These findings suggest that FRH acts as an immunomodulatory factor responsible for the maintenance of immune homeostasis. FRH has been shown to influence the expression of anti-inflammatory cytokines including IL-10 [12]. Consistent with these studies, we observed that its expression in PBMCs and spleen significantly increased following FRH. Thus, we found that FRH regulates both pro-inflammatory and anti-inflammatory factors.
Improving the accuracy of prognostication in chronic myelomonocytic leukemia
Published in Expert Review of Anticancer Therapy, 2020
Jennifer Kaivers, Esther Schuler, Barbara Hildebrandt, Beate Betz, Christina Rautenberg, Rainer Haas, Guido Kobbe, Norbert Gattermann, Ulrich Germing
In 1982, FAB-classification considered CMML as a subgroup of myelodysplastic syndromes (MDS). Since 1999, revisions by the World Health Organization (WHO) working group reclassified CMML as member of a group of myelodysplastic/myeloproliferative neoplasms, together with atypical chronic myeloid leukemia (aCML) and refractory anemia with ring sideroblasts and thrombocytosis (RARS-T). This reclassification of CMML reflects awareness of disease heterogeneity: 50% of patients present with features of a myeloproliferative disease, whereas the other half show signs and symptoms similar to myelodysplastic syndromes. Myelodysplastic CMML (CMML-MD) is characterized by hematopoietic insufficiency, mild monocytosis, and a white blood cell (WBC) count < 13 × 109/l, whereas the proliferative type (CMML-MP) shows increased granulocytopoiesis and monocytopoiesis, with a WBC count ≥ 13 × 109/l, and is often accompanied by constitutional symptoms like fever, sweating, weight loss, and autoimmune disorders. The elevated WBC counts in CMML-MP often require cytoreductive treatment. Patients with CMML-MP have a shorter overall survival (OS) and a higher risk for leukemic progression than patients with CMML-MD [4,5].
Deciphering the genotype and phenotype of hairy cell leukemia: clues for diagnosis and treatment
Published in Expert Review of Clinical Immunology, 2019
Margot C.E. Polderdijk, Michiel Heron, Saskia Kuipers, Ger T. Rijkers
Which features do monocytes and hairy cells share? Firstly, they are found in the same region on a flow cytometry forward-side scatter plot, indicating that their size and cytoplasmic complexity are comparable (also see panel A of Figure 2). Secondly, hairy cells typically express CD11c, a surface antigen that is naturally expressed on monocytes, but only on limited populations of normal B-cells [32]. Hairy cells also adhere to glass or nylon, and they have the ability to phagocytose particles, which are both characteristics of monocytes [96]. No direct explanation for the apparent depletion of blood monocytes in HCL can be given, but it is interesting to note that dendritic cells are also barely present in blood of HCL patients. It seems likely that this phenomenon is related to the monocytopenia [33]. After successful treatment of the disease, both monocyte and dendritic cell numbers normalize slowly. In isolated cases of HCL monocytosis rather than monocytopenia can be observed. In such a case, as reported by Williams, Taute, Dunlap, and Fan [34] it is proposed that a concurrent disease (myelodysplastic syndrome) can override whatever mechanism hairy cells employ, so that monocytosis develops. Treatment with blood transfusions can also correct the monocytopenia, with complete normalization that persists for several months [35]. In this case, the patient was treated with leukocyte transfusions at doses of 2.9–5.8 *109 cells, with 1–15% monocytes. This number of cells is not sufficient to still be detected in the blood at normal levels after several months, so the transfusion must have caused a change in the patient’s monocytopoiesis.