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Comment
. 2023 Dec 1;108(12):3444-3448.
doi: 10.3324/haematol.2023.282739.

Specific blood monocyte distribution in histiocytoses correlates with vascular involvement and disease activity

Jerome Razanamahery  1 , Maxime Samson  2 , Julien Guy  3 , Jessica Racine  3 , Celine Row  3 , Hélène Greigert  2 , Barbara Nicolas  2 , Stephanie Francois  4 , Jean-François Emile  5 , Fleur Cohen-Aubart  6 , Sylvain Audia  2 , Julien Haroche  6 , Bernard Bonnotte  2
Affiliations
Comment

Specific blood monocyte distribution in histiocytoses correlates with vascular involvement and disease activity

Jerome Razanamahery et al. Haematologica. .
No abstract available

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Figures

Figure 1.
Figure 1.
Procedure for gating monocytes by flow cytometry. Monocytes were identified from peripheral blood mononucelar cells with CD45 and CD33 expression after successive exclusion of T lymphocytes, natural killer (NK) cells, residual lymphocytes and basophils. Then monocytes were analyzed regarding CD14/CD16 expression for classical, intermediate and non-classical monocytes. KO: knockout; SSC: side scatter.
Figure 2.
Figure 2.
Distribution of monocyte subsets in histiocytoses and myeloid neoplasms and according to molecular status. (A) Distribution of monocyte subsets in patients with histiocytoses (N=17), chronic myelomonocytic leukemia (CMML) (N=7), essential thrombocythemia (ET) (N=7) and heathy donors (HD) (N=21). (B) Distribution of monocyte subsets in histiocytoses with clonal hematopoiesis (CH+) (N=6), without clonal hematopoiesis (CH-) (N=9) and CMML patients (N=7). Percentages are given among total monocytes. Horizontal bars show the median and error bars the interquartile range. P value is the result of the ANOVA test. *P<0.05; **P<0.01; ns: non-significant.
Figure 3.
Figure 3.
Distribution of monocyte subsets in histiocytoses according to vascular injury and disease activity. Comparison of the distribution of monocyte subsets according to (A) the presence of vascular injury (N=7) or not (N=10), and (B) to the achievement of a metabolic response (N=10) or not (N=7). Disease activity was established using the last metabolic evaluation with fluorodeoxyglucose positron emission tomography-computed tomography according to PERCIST criteria. Complete metabolic response was defined by normalization of all lesions to at or below standardized uptake value (SUV) of liver background. Partial metabolic response was defined by a ≥50% decrease in the sum of all target lesion baseline SUV. Progressive metabolic disease was defined by a ≥50% increase in the nadir sum of all target or new evaluable lesion SUV. Stable metabolic disease was defined as condition that did not meet previous criteria. Patients with "complete metabolic response" and "partial metabolic response" were considered as responders and patients with "stable metabolic disease" and "progressive metabolic disease" considered as non-responders.
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