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Article Abstract

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://www.ncbi.nlm.nih.gov/pmc/articles/PMC11524003PMC
http://dx.doi.org/10.1186/s13256-024-04844-1DOI Listing

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Article Synopsis
  • Segregated-nucleus-containing atypical monocytes have been identified in mice and are believed to induce fibrosis in drug-injured lungs, with a human counterpart potentially existing in primary myelofibrosis.
  • A 74-year-old male patient with primary myelofibrosis had anemia and elevated lactate dehydrogenase, and his bone marrow showed histological features consistent with the disease.
  • Immunohistochemical analysis revealed the presence of some CD16MSR1CEACAM1 cells in the patient's bone marrow, suggesting a possible connection to murine atypical monocyte characteristics.
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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.

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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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