Abstract:Background: We investigated the potential role of several pattern-recognition receptors (PRRs; CD11b, CD11c, CD32, CD206, CD209, and dectin-1) in adult-onset Still’s disease (AOSD). Methods: The study included 13 untreated AOSD patients, 19 rheumatoid arthritis (RA) patients (as a disease control), and 19 healthy controls (HCs). The PRRs were quantified in peripheral blood using flow cytometry. The serum levels of interleukin-17 (IL-17), IL-18, and IL-23 were measured by enzyme-linked immunosorbent assay. Resu… Show more
“…Primary granulocytes and promyelocytic cells in the bone marrow do not express CD11b and mature myeloid cells and neutrophils is consistently high, this feature can be used to distinguish between promyelocytic cells and other myeloid cell populations. CD11b also plays a role in the maintenance of autoreactive B cell tolerance, which is linked to the pathogenesis of systemic lupus erythematosus and adult‐onset Still's disease . In our study, the expression rate of CD11b was 7% in the APL group, which was different from that reported by Dong et al, and was statistically different from the expression rate in other types of AML (35%).…”
Section: Discussioncontrasting
confidence: 99%
“…CD11b also plays a role in the maintenance of autoreactive B cell tolerance, which is linked to the pathogenesis of systemic lupus erythematosus 16 and adult-onset Still's disease. 17,18 In our study, the expression rate of CD11b was 7% in the APL group, which was different from Acute promyelocytic leukemia is characterized by lack of HLA-DR antigen expression. 19 However, absence of HLA-DR expression is rare in non-APL-AML cases.…”
Objective
To investigate the immunophenotypic characteristics of acute promyelocytic leukemia (APL) and explore the sensitivity and specificity of various antibody combinations for the timely and accurate diagnosis APL.
Methods
A retrospective analysis was performed using morphological, immunological, genetic, and molecular biological data from 92 patients diagnosed with APL and 190 controls diagnosed with non‐APL acute myeloid leukemia.
Results
For APL diagnosis, the CD9/CD11b/human leukocyte antigen (HLA)‐DR antibody combination had 85% sensitivity and 95% specificity, AUC = 0.85. However, the sensitivity and specificity were 39% and 92%, AUC = 0.65, respectively, for the HLA‐DR/CD34/CD117 combination, and 80% and 80%, AUC = 0.80, respectively for the CD11b/HLA‐DR combination. Significant differences were observed between the different antibody combinations.
Conclusions
The CD9/CD11b/HLA‐DR antibody combination displays high sensitivity and specificity and can be used to diagnose APL.
“…Primary granulocytes and promyelocytic cells in the bone marrow do not express CD11b and mature myeloid cells and neutrophils is consistently high, this feature can be used to distinguish between promyelocytic cells and other myeloid cell populations. CD11b also plays a role in the maintenance of autoreactive B cell tolerance, which is linked to the pathogenesis of systemic lupus erythematosus and adult‐onset Still's disease . In our study, the expression rate of CD11b was 7% in the APL group, which was different from that reported by Dong et al, and was statistically different from the expression rate in other types of AML (35%).…”
Section: Discussioncontrasting
confidence: 99%
“…CD11b also plays a role in the maintenance of autoreactive B cell tolerance, which is linked to the pathogenesis of systemic lupus erythematosus 16 and adult-onset Still's disease. 17,18 In our study, the expression rate of CD11b was 7% in the APL group, which was different from Acute promyelocytic leukemia is characterized by lack of HLA-DR antigen expression. 19 However, absence of HLA-DR expression is rare in non-APL-AML cases.…”
Objective
To investigate the immunophenotypic characteristics of acute promyelocytic leukemia (APL) and explore the sensitivity and specificity of various antibody combinations for the timely and accurate diagnosis APL.
Methods
A retrospective analysis was performed using morphological, immunological, genetic, and molecular biological data from 92 patients diagnosed with APL and 190 controls diagnosed with non‐APL acute myeloid leukemia.
Results
For APL diagnosis, the CD9/CD11b/human leukocyte antigen (HLA)‐DR antibody combination had 85% sensitivity and 95% specificity, AUC = 0.85. However, the sensitivity and specificity were 39% and 92%, AUC = 0.65, respectively, for the HLA‐DR/CD34/CD117 combination, and 80% and 80%, AUC = 0.80, respectively for the CD11b/HLA‐DR combination. Significant differences were observed between the different antibody combinations.
Conclusions
The CD9/CD11b/HLA‐DR antibody combination displays high sensitivity and specificity and can be used to diagnose APL.
“…Interestingly, increased CD206 from whole blood cells were increased in patients with active adult-onset Still's disease (AOSD), a rare systemic autoinflammatory disease when compared to healthy controls. The increased expression of CD206 was in lymphocytes of AOSD patients ( 60 ). The true expression of CD206 in T2DM remains to be elucidated.…”
Background: Although peripheral blood mononuclear cells (PBMC) have been demonstrated to be in a pro-inflammatory state in obesity and type 2 Diabetes Mellitus (T2DM), characterization of circulating PBMC phenotypes in the obese and T2DM and the effect of Metformin on these phenotypes in humans is still ill-defined and remains to be determined.Methods: Thirty normal healthy adult volunteers of normal weight, 30 obese subjects, 20 obese newly diagnosed diabetics and 30 obese diabetics on Metformin were recruited for the study. Fasting blood samples were collected and PBMC were isolated from whole blood. Polarization markers (CD86, IL-6, TNFα, iNOS, CD36, CD11c, CD169, CD206, CD163, CD68, CD11b, CD16, and CD14) were measured by RT-qPCR. Gene expression fold changes were calculated using the 2−ΔΔCT method for RT-qPCR.Results: Obesity and T2DM are associated an increased CD68 marker in PBMC. mRNA expression of CD11b, CD11c, CD169, and CD163 were significantly reduced in PBMC from T2DM subjects whereas CD11c was significantly inhibited in PBMC from obese subjects. On the other hand, macrophage M1-like phenotype was observed in T2DM circulation as demonstrated by increased mRNA expression of CD16, IL-6, iNOS, TNFα, and CD36. There were no significant changes in CD14 and CD86 in the obese and T2DM when compared to the lean subjects. Metformin treatment in T2DM reverted CD11c, CD169, IL-6, iNOS, TNFα, and CD36 to levels comparable to lean subjects. CD206 mRNA expression was significantly upregulated in PBMC of T2DM while Metformin treatment inhibited CD206 expression levels.Conclusions: These data support the notion that PBMC in circulation in T2DM express different pattern of phenotypic markers than the patterns typically present in M1 and M2 like cells. These phenotypic markers could be representative of metabolically activated macrophages (MMe)-like cells. Metformin, on the other hand, reduces MMe-like cells in circulation.
“…The systemic scoring system of Pouchot et al . 2 assigns a score from 0 to 12, with 1 point for each of the following manifestations: fever, typical rash, pleuritis, pneumonia, pericarditis, hepatomegaly or abnormal liver function test data, splenomegaly, lymphadenopathy, leukocytosis (⩾ 15,000/mm 2 ), sore throat, myalgia, and abdominal pain. Supplement Figure 1.…”
Section: Supplement Tablementioning
confidence: 99%
“…Further activation of innate immune cells is triggered by the interaction of specific damage-associated molecular patterns (DAMPs) and pattern recognition receptors (PRRs), and several PRRs are responsible for the pathological pathways of JIA and AOSD. 2 …”
We examined the expression of human leukocyte antigen (HLA) and composition of differentiated T cells in the peripheral blood to understand the characteristics of the immune changes in patients with adult-onset Still’s disease (AOSD). This study enrolled patients with AOSD (n = 14), patients with rheumatoid arthritis (RA, n = 20), and healthy controls (HC, n = 20). The percentage of surface-stained cells with HLA-DP, DQ, and DR alleles and the composition of differentiated T cells in peripheral blood leukocytes (PBLs) were evaluated by flow cytometry. AOSD patients exhibited significantly higher percentages of lymphocytes presenting HLA-DP and HLA-DR, and lower percentages of cells presenting HLA-DQ, than RA patients or HC. The proportions of CD4+, CD4+CCR7+, CD4+CD62L–, and CD8+CD62L– cells from PBLs were decreased in AOSD patients relative to RA patients or HCs. By contrast, AOSD patients had higher proportions of CD8+naïve T cells in whole blood relative to RA patients or HC. The proportions of CD4+ effector memory T cells, CD8+ naïve T cells, and CD8+ effector memory T cells in whole blood cells and CD4+ effector memory T cell in lymphocytes were significantly associated with the systemic score. While the proportions of CD4+, CD8+, CCR7+, CD4+CCR7+, CD4+CD62L–, and CD8+CD62L– cells were significantly decreased in AOSD patients, and the proportion of CD8+naïve T cells was elevated in AOSD and correlated with the systemic score. Further studies of a large cohort of AOSD patients will be necessary to evaluate these markers in the pathogenesis of AOSD.
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