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Background: Segregated-nucleus-containing atypical monocytes have recently been identified in mice. Segregated-nucleus-containing atypical monocytes are thought to originate from the bone marrow and induce fibrosis in the drug-injured lung. The Lyc6c murine monocyte subset is the counterpart to human CD14CD16 non-classical monocytes; however, the human counterpart to murine segregated-nucleus-containing atypical monocytes has not yet been identified. Primary myelofibrosis is a well-known disease of progressive marrow fibrosis, and atypical megakaryocytes are thought to be closely related to fibrosis in primary myelofibrosis bone marrow. However, recently, monocytes have been reported to play an important role in marrow fibrosis in primary myelofibrosis. We speculated that, if there is a human counterpart to murine segregated-nucleus-containing atypical monocytes, it would present the same markers as murine segregated-nucleus-containing atypical monocytes, such as CD14CD16 macrophage-1 antigen (CD11b/CD18 complex), MSR1, and CEACAM1, and it might exist in the bone marrow of patients with primary myelofibrosis.
Case Presentation: A 74-year-old Japanese male visited our hospital for clinical follow-up after total prostatectomy for prostatic cancer. Anemia, thrombocytosis, and elevated lactate dehydrogenase were suddenly observed in a periodic examination. CALR mutation type 2 (p.K385fs*47) was observed. The histological features of the patient's bone marrow were consistent with fibrotic primary myelofibrosis. We immunohistochemically studied the bone marrow in an attempt to identify a human counterpart to murine segregated-nucleus-containing atypical monocytes. We detected a few CD16MSR1CEACAM1 cells, but not CD14MSR1CEACAM1 cells, by triple immunostaining. The patient is in a good condition and does not require treatment for primary myelofibrosis.
Conclusion: There is a possibility that human segregated-nucleus-containing atypical monocytes exist in the bone marrow of primary myelofibrosis patients and might be related to marrow fibrosis.
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http://dx.doi.org/10.1186/s13256-024-04844-1 | DOI Listing |
J Med Case Rep
October 2024
Department of Diagnostic Pathology, Tokyo Women's Medical University Adachi Medical Center, 4-33-1, Kohoku, Adachi-ku, 123-8558, Tokyo, Japan.
Nihon Yakurigaku Zasshi
July 2023
Department of Immunology, Graduate School and Faculty of Medicine, Tokyo Medical and Dental University (TMDU).
Macrophages have been discovered more than 100 years ago. Recent studies indicated that monocytes and macrophages can be categorized into several distinct phenotypes and their respective differentiation mechanisms are known. We also reported that the Jmjd3 is critical for the macrophage subtype activated by allergic stimuli and that the tissue resident macrophage subtype in adipose tissue, which is controlled by Trib1, is responsible for maintaining homeostasis of peripheral tissues such as adipocyte.
View Article and Find Full Text PDFBiochem Biophys Rep
December 2021
Department of Respiratory Medicine and Allergology, Kindai University Faculty of Medicine, 377-2 Onohigashi, Osakasayama, Osaka, 589-8511, Japan.
Background: Idiopathic pulmonary fibrosis (IPF) is a form of chronic, progressive fibrosing interstitial pneumonia of unknown cause, with a poor prognosis. We previously showed the antifibrotic effects of a novel phosphodiesterase 4 (PDE4) inhibitor, AA6216. In this study, we examined the effect of AA6216 on the pulmonary accumulation of segregated-nucleus-containing atypical monocytes (SatMs), which produce tumor necrosis factor (TNF)-α and are involved in murine lung fibrosis.
View Article and Find Full Text PDFInt Immunol
November 2021
Department of Host Defense, Research Institute for Microbial Diseases (RIMD), Osaka University, Osaka, Japan.
Fibrosis is a life-threatening disorder with significant morbidity and mortality and is caused by excessive formation of connective tissue that can affect several important organs. Fibrosis in organ tissues is caused by an abnormal wound-healing process from repeated injuries. In our recent study using a mouse model of bleomycin-induced lung fibrosis, we examined the role of RNA-binding motif protein 7 (RBM7) on the development of lung fibrosis.
View Article and Find Full Text PDFDiagnostics (Basel)
July 2020
Department of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.
Fibrosis is a life-threatening disorder caused by excessive formation of connective tissue that can affect several critical organs. Innate immune cells are involved in the development of various disorders, including lung fibrosis. To date, several hematopoietic cell types have been implicated in fibrosis, including pro-fibrotic monocytes like fibrocytes and segregated-nucleus-containing atypical monocytes (SatMs), but the precise cellular and molecular mechanisms underlying its development remain unclear.
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