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rabbit anti cd14 monoclonal antibody (Bioss)

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Bioss rabbit anti cd14 monoclonal antibody
Rabbit Anti Cd14 Monoclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti+cd14+monoclonal+antibody/CD14+(31G4)+Monoclonal+Antibody/pm37061741-63-36-44
Average 93 stars, based on 2 article reviews

rabbit anti cd14 monoclonal antibody - by Bioz Stars, 2026-09

93/100 stars

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Article Title: Neutrophil-inspired photothermo-responsive drug delivery system for targeted treatment of bacterial infection and endotoxins neutralization.
Article Snippet: Mouse anti-ICAM-1 antibody (ab171123) and rabbit anti-integrin β1 monoclonal antibody (ab179471) were bought from Abcam, U.K. Rabbit anti-integrin β2 polyclonal antibody (#47598) was bought from cell signing technology (CST), U.S.A. Rabbit anti-TLR4 polyclonal antibody (bs-20594R) and Rabbit anti-CD14 monoclonal antibody (bsm-52556R) were purchased from Bioss Biotechnology Co., Ltd, Beijing, China.

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Pparα deficiency in intestinal epithelium promotes hepatic steatosis and fibrosis in mice fed a high-fat plus high-sucrose diet (HFHS). (A) Schematic representation of HFHS experimental design. (B) Representative images of liver tissue stained with H&E and Oil Red O after short-term HFHS treatment ( n = 5). (C) Relative mRNA levels of Col1a1 , β-Pdgfr , Tgf-β , and Timp-1 in the liver after short-term HFHS treatment ( n = 5). (D) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver after short-term HFHS treatment ( n = 5). (E) Body weight of mice after long-term HFHS treatment ( n = 15). (F) Liver weight of mice after long-term HFHS treatment ( n = 15). (G) The length of the small intestine after long-term HFHS treatment ( n = 15). (H) Serum endotoxin levels after long-term HFHS treatment ( n = 15). (I) The endotoxin levels in the liver after long-term HFHS treatment ( n = 15). (J) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver after short-term HFHS treatment ( n = 5). (K) Relative mRNA levels of Col1a1, β-Pdgfr , Tgf-β , and Timp1 in the liver after the HFHS treatment for 16 weeks ( n = 5). (L) Representative images of liver tissue stained with H&E, Oil Red O, and Masson's trichrome and immunohistochemical staining for α -SMA and TGF- β after long-term HFHS treatment ( n = 5). (M) Levels of α -SMA and TGF- β were quantified using Image J software and expressed as AODs. Data are shown as the mean ± SD. For the two groups, statistical significance was tested by unpaired Student's t -test; for more than two groups, statistical significance was tested by one-way ANOVA followed by the least significant difference (LSD) test; ∗ P < 0.05 , ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: Acta Pharmaceutica Sinica. B

Article Title: PPAR α affects hepatic lipid homeostasis by perturbing necroptosis signals in the intestinal epithelium

doi: 10.1016/j.apsb.2024.08.021

Figure Lengend Snippet: Pparα deficiency in intestinal epithelium promotes hepatic steatosis and fibrosis in mice fed a high-fat plus high-sucrose diet (HFHS). (A) Schematic representation of HFHS experimental design. (B) Representative images of liver tissue stained with H&E and Oil Red O after short-term HFHS treatment ( n = 5). (C) Relative mRNA levels of Col1a1 , β-Pdgfr , Tgf-β , and Timp-1 in the liver after short-term HFHS treatment ( n = 5). (D) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver after short-term HFHS treatment ( n = 5). (E) Body weight of mice after long-term HFHS treatment ( n = 15). (F) Liver weight of mice after long-term HFHS treatment ( n = 15). (G) The length of the small intestine after long-term HFHS treatment ( n = 15). (H) Serum endotoxin levels after long-term HFHS treatment ( n = 15). (I) The endotoxin levels in the liver after long-term HFHS treatment ( n = 15). (J) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver after short-term HFHS treatment ( n = 5). (K) Relative mRNA levels of Col1a1, β-Pdgfr , Tgf-β , and Timp1 in the liver after the HFHS treatment for 16 weeks ( n = 5). (L) Representative images of liver tissue stained with H&E, Oil Red O, and Masson's trichrome and immunohistochemical staining for α -SMA and TGF- β after long-term HFHS treatment ( n = 5). (M) Levels of α -SMA and TGF- β were quantified using Image J software and expressed as AODs. Data are shown as the mean ± SD. For the two groups, statistical significance was tested by unpaired Student's t -test; for more than two groups, statistical significance was tested by one-way ANOVA followed by the least significant difference (LSD) test; ∗ P < 0.05 , ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: These samples were incubated overnight with a polyclonal rabbit anti-mouse F4/80 (1:1000, #A1256, ABclonal), polyclonal rabbit anti-mouse APOA1 (1:2000, #A14211, ABclonal), polyclonal rabbit anti-mouse ABCA1 (1:1000, #NB400-105, Novus Biological, Centennial), monoclonal rabbit anti-mouse CD14 (1:1000, #A19011, ABclonal), or polyclonal rabbit anti-mouse PV1 (1:2000, #A15906, ABclonal).

Techniques: Staining, Immunohistochemical staining, Software

Pparα deficiency in intestinal epithelium activates inflammatory signaling pathways in both the ileum and liver. (A) Endotoxin in serum and liver ( n = 10). (B) Immunofluorescent staining of F4/80 (red) in the liver of 8-week-old mice ( n = 5). (C) Protein levels of F4/80 in the liver of 8-week-old mice ( n = 3). (D) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver of 8-week-old mice ( n = 5). (E) Relative mRNA levels of Il-1β and Tnf-α in the liver of 8-week-old mice ( n = 5). (F) Relative mRNA levels of Lbp in the liver of 8-week-old mice ( n = 5). (G) Representative H&E staining, immunohistochemical staining for AP, and immunofluorescent staining for CD14 (green) in the ileum of 8-week-old mice ( n = 5). (H) Protein levels of CD14 and relative mRNA levels of Lbp and CD14 in the ileum of 8-week-old mice ( n = 5). (I) Enrichment graph of NOD-like receptor signaling dataset performed with ileum samples from 8-week-old Pparα ΔIE mice ( n = 3). (J) Heatmap representation of genes involved in innate antibacterial defense in 8-week-old Pparα ΔIE ileum relative to Pparα fl/fl ( n = 3). (K) Relative mRNA levels of Defa21 , Defa22 , Defa3 , Defa5 , and Reg3β in the ileum from 8-week-old mice ( n = 5). (L) Schematic representation of high-fructose corn syrup (HFCS) experimental design. (M) Representative images stained with H&E and Oil Red O, and immunofluorescent staining for F4/80 (red) in liver tissue from 8-week-old mice exposed to HFCS for 14 days ( n = 5). (N) Representative H&E image and immunohistochemical staining for AP in the ileum of 8-week-old mice exposed to HFCS for 14 days ( n = 5). (O) Serum endotoxin levels in 8-week-old mice exposed to HFCS for 14 days ( n = 8). AP: alkaline phosphatase staining. Data are shown as the mean ± SD. An unpaired two-tailed Student's t -test; ∗ P < 0.05 , ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: Acta Pharmaceutica Sinica. B

Article Title: PPAR α affects hepatic lipid homeostasis by perturbing necroptosis signals in the intestinal epithelium

doi: 10.1016/j.apsb.2024.08.021

Figure Lengend Snippet: Pparα deficiency in intestinal epithelium activates inflammatory signaling pathways in both the ileum and liver. (A) Endotoxin in serum and liver ( n = 10). (B) Immunofluorescent staining of F4/80 (red) in the liver of 8-week-old mice ( n = 5). (C) Protein levels of F4/80 in the liver of 8-week-old mice ( n = 3). (D) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver of 8-week-old mice ( n = 5). (E) Relative mRNA levels of Il-1β and Tnf-α in the liver of 8-week-old mice ( n = 5). (F) Relative mRNA levels of Lbp in the liver of 8-week-old mice ( n = 5). (G) Representative H&E staining, immunohistochemical staining for AP, and immunofluorescent staining for CD14 (green) in the ileum of 8-week-old mice ( n = 5). (H) Protein levels of CD14 and relative mRNA levels of Lbp and CD14 in the ileum of 8-week-old mice ( n = 5). (I) Enrichment graph of NOD-like receptor signaling dataset performed with ileum samples from 8-week-old Pparα ΔIE mice ( n = 3). (J) Heatmap representation of genes involved in innate antibacterial defense in 8-week-old Pparα ΔIE ileum relative to Pparα fl/fl ( n = 3). (K) Relative mRNA levels of Defa21 , Defa22 , Defa3 , Defa5 , and Reg3β in the ileum from 8-week-old mice ( n = 5). (L) Schematic representation of high-fructose corn syrup (HFCS) experimental design. (M) Representative images stained with H&E and Oil Red O, and immunofluorescent staining for F4/80 (red) in liver tissue from 8-week-old mice exposed to HFCS for 14 days ( n = 5). (N) Representative H&E image and immunohistochemical staining for AP in the ileum of 8-week-old mice exposed to HFCS for 14 days ( n = 5). (O) Serum endotoxin levels in 8-week-old mice exposed to HFCS for 14 days ( n = 8). AP: alkaline phosphatase staining. Data are shown as the mean ± SD. An unpaired two-tailed Student's t -test; ∗ P < 0.05 , ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Techniques: Protein-Protein interactions, Staining, Immunohistochemical staining, Two Tailed Test

Pparα deficiency in intestinal epithelium increases the translocation of gut-derived antigens into the liver. (A) Intestinal permeability assessment (FITC-dextran, 4 kD) in 8-week-old mice ( n = 10). (B) Relative mRNA levels of Zo-1 and Cldn8 in the ileum from 8-week-old mice ( n = 5). (C) The relative proportion of bacterial species in the cecum content by 16S rRNA gene sequencing ( n = 6). (D) Bugbase phenotypic prediction of gut microbiota in 8-week-old mice ( n = 6). (E) The mRNA and protein levels of PV1 in the ileum of 8-week-old mice ( n = 5). (F) Transmission electron microscopy images of the diaphragm (red star) in the capillaries from ileum sections in 24-week-old mice ( n = 3). (G) Representative images of fluorescence microscopy and transmission electron in 8-week-old mice treated with FITC-LPS (green) or Au-LPS ( n = 3–5). (H) Portal HDL-C levels in 8-week-old mice ( n = 10). (I) The protein levels of APOA1 and ABCA1 in the ileum of 8-week-old mice ( n = 5). (J) Relative mRNA levels of Apoa1 , Pon1 , and Pon3 in the ileum of 8-week-old mice ( n = 5). (K) Serum APOA1 levels in 8-, 16- and 32-week-old mice ( n = 8–10). (L) Serum APOA1 levels in 8-week-old mice exposed to HFCS for 14 days ( n = 8). (M) Serum APOA1 levels in 16-week-old Pparα Δhep mice ( n = 10). (N) Schematic representation of a cocktail of broad-spectrum antibiotics (Abx) experimental design. (O) Representative images stained with H&E and Oil Red O, and immunofluorescent staining for F4/80 (red) in the liver from 8-week-old mice treated with Abx ( n = 5). (P) Triglyceride in serum and liver treated with Abx ( n = 10). (Q) Relative mRNA levels of genes related to triglyceride accumulation in the liver from 8-week-old mice treated with Abx ( n = 5). (R) Hepatic levels of cytokines from 8-week-old mice treated with Abx ( n = 5). (S) Protein levels of F4/80 in the liver of 8-week-old mice treated with Abx ( n = 3). (T) Relative mRNA levels of F4/80, Clec4f , and Cd14 in the liver of 8-week-old mice treated with Abx ( n = 5). LD: lipid droplet; M: mitochondria; FITC-LPS: fluorescein isothiocyanate (FITC)-LPS; Au-LPS: LPS-gold-complexes. Data are shown as the mean ± SD. An unpaired two-tailed Student's t -test; ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: Acta Pharmaceutica Sinica. B

Article Title: PPAR α affects hepatic lipid homeostasis by perturbing necroptosis signals in the intestinal epithelium

doi: 10.1016/j.apsb.2024.08.021

Figure Lengend Snippet: Pparα deficiency in intestinal epithelium increases the translocation of gut-derived antigens into the liver. (A) Intestinal permeability assessment (FITC-dextran, 4 kD) in 8-week-old mice ( n = 10). (B) Relative mRNA levels of Zo-1 and Cldn8 in the ileum from 8-week-old mice ( n = 5). (C) The relative proportion of bacterial species in the cecum content by 16S rRNA gene sequencing ( n = 6). (D) Bugbase phenotypic prediction of gut microbiota in 8-week-old mice ( n = 6). (E) The mRNA and protein levels of PV1 in the ileum of 8-week-old mice ( n = 5). (F) Transmission electron microscopy images of the diaphragm (red star) in the capillaries from ileum sections in 24-week-old mice ( n = 3). (G) Representative images of fluorescence microscopy and transmission electron in 8-week-old mice treated with FITC-LPS (green) or Au-LPS ( n = 3–5). (H) Portal HDL-C levels in 8-week-old mice ( n = 10). (I) The protein levels of APOA1 and ABCA1 in the ileum of 8-week-old mice ( n = 5). (J) Relative mRNA levels of Apoa1 , Pon1 , and Pon3 in the ileum of 8-week-old mice ( n = 5). (K) Serum APOA1 levels in 8-, 16- and 32-week-old mice ( n = 8–10). (L) Serum APOA1 levels in 8-week-old mice exposed to HFCS for 14 days ( n = 8). (M) Serum APOA1 levels in 16-week-old Pparα Δhep mice ( n = 10). (N) Schematic representation of a cocktail of broad-spectrum antibiotics (Abx) experimental design. (O) Representative images stained with H&E and Oil Red O, and immunofluorescent staining for F4/80 (red) in the liver from 8-week-old mice treated with Abx ( n = 5). (P) Triglyceride in serum and liver treated with Abx ( n = 10). (Q) Relative mRNA levels of genes related to triglyceride accumulation in the liver from 8-week-old mice treated with Abx ( n = 5). (R) Hepatic levels of cytokines from 8-week-old mice treated with Abx ( n = 5). (S) Protein levels of F4/80 in the liver of 8-week-old mice treated with Abx ( n = 3). (T) Relative mRNA levels of F4/80, Clec4f , and Cd14 in the liver of 8-week-old mice treated with Abx ( n = 5). LD: lipid droplet; M: mitochondria; FITC-LPS: fluorescein isothiocyanate (FITC)-LPS; Au-LPS: LPS-gold-complexes. Data are shown as the mean ± SD. An unpaired two-tailed Student's t -test; ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Techniques: Translocation Assay, Derivative Assay, Permeability, Sequencing, Transmission Assay, Electron Microscopy, Fluorescence, Microscopy, Staining, Two Tailed Test

Butyric acid attenuates PPAR α -induced necroptosis in HIEC-6 cells and ameliorates hepatic steatosis in Pparα ΔIE mice. (A) Relative CREB3L3 mRNA level in HIEC-6 cells transfected with the PPAR α expression vector ( n = 3). (B) Relative mRNA level of apoptotic and necroptosis signaling components in HIEC-6 cells transfected with the CREB3L3 expression vector ( n = 3). (C) Relative mRNA level of apoptotic and necroptosis signaling components in HIEC-6 cells treated with TNF- α ( n = 3). (D) Effects of GW6471 on RIPK3 and MLKL promoter-driven luciferase activities in human intestinal epithelial HIEC-6 cells ( n = 3). (E) Relative CREB3L3 mRNA level in HIEC-6 cells treated with butyric acid ( n = 3). (F) Relative mRNA level of necroptosis signaling components in HIEC-6 cells treated with TNF- α and butyric acid ( n = 3). (G) Schematic representation of the experimental design for butyric acid treatment. H, Relative CREB3L3 mRNA level in Pparα fl/fl and Pparα ΔIE mice treated with butyric acid ( n = 5). (I) Relative mRNA level of necroptosis signaling components in Pparα ΔIE mice treated with butyric acid ( n = 5). (J) Representative immunohistochemical staining for cleaved-caspase 3 and MLKL, and immunofluorescent staining for cleaved-caspase 8 (green), p-RIPK3 (red), and p-MLKL (red) in the ileum after butyric acid treatment ( n = 5). (K) Representative images stained with H&E and Oil Red O, and immunofluorescent staining for F4/80 (red) in liver tissue after butyric acid treatment ( n = 5). (L) Relative mRNA levels of genes related with lipolysis, lipogenesis, and lipid droplet proteins in the liver after butyric acid treatment ( n = 5). (M) Triglyceride in serum and liver after butyric acid treatment ( n = 10). (N) Hepatic levels of cytokines in mice after butyric acid treatment ( n = 5). (O) Protein levels of F4/80 in the liver after butyric acid treatment ( n = 3). (P) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver after butyric acid treatment ( n = 5). Buty: butyric acid. Data are shown as the mean ± SD. For the two groups, statistical significance was tested by unpaired Student's t -test; for more than two groups, statistical significance was tested by one-way ANOVA followed by the least significant difference (LSD) test; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

Journal: Acta Pharmaceutica Sinica. B

Article Title: PPAR α affects hepatic lipid homeostasis by perturbing necroptosis signals in the intestinal epithelium

doi: 10.1016/j.apsb.2024.08.021

Figure Lengend Snippet: Butyric acid attenuates PPAR α -induced necroptosis in HIEC-6 cells and ameliorates hepatic steatosis in Pparα ΔIE mice. (A) Relative CREB3L3 mRNA level in HIEC-6 cells transfected with the PPAR α expression vector ( n = 3). (B) Relative mRNA level of apoptotic and necroptosis signaling components in HIEC-6 cells transfected with the CREB3L3 expression vector ( n = 3). (C) Relative mRNA level of apoptotic and necroptosis signaling components in HIEC-6 cells treated with TNF- α ( n = 3). (D) Effects of GW6471 on RIPK3 and MLKL promoter-driven luciferase activities in human intestinal epithelial HIEC-6 cells ( n = 3). (E) Relative CREB3L3 mRNA level in HIEC-6 cells treated with butyric acid ( n = 3). (F) Relative mRNA level of necroptosis signaling components in HIEC-6 cells treated with TNF- α and butyric acid ( n = 3). (G) Schematic representation of the experimental design for butyric acid treatment. H, Relative CREB3L3 mRNA level in Pparα fl/fl and Pparα ΔIE mice treated with butyric acid ( n = 5). (I) Relative mRNA level of necroptosis signaling components in Pparα ΔIE mice treated with butyric acid ( n = 5). (J) Representative immunohistochemical staining for cleaved-caspase 3 and MLKL, and immunofluorescent staining for cleaved-caspase 8 (green), p-RIPK3 (red), and p-MLKL (red) in the ileum after butyric acid treatment ( n = 5). (K) Representative images stained with H&E and Oil Red O, and immunofluorescent staining for F4/80 (red) in liver tissue after butyric acid treatment ( n = 5). (L) Relative mRNA levels of genes related with lipolysis, lipogenesis, and lipid droplet proteins in the liver after butyric acid treatment ( n = 5). (M) Triglyceride in serum and liver after butyric acid treatment ( n = 10). (N) Hepatic levels of cytokines in mice after butyric acid treatment ( n = 5). (O) Protein levels of F4/80 in the liver after butyric acid treatment ( n = 3). (P) Relative mRNA levels of F4/80 , Clec4f , and Cd14 in the liver after butyric acid treatment ( n = 5). Buty: butyric acid. Data are shown as the mean ± SD. For the two groups, statistical significance was tested by unpaired Student's t -test; for more than two groups, statistical significance was tested by one-way ANOVA followed by the least significant difference (LSD) test; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001.

Techniques: Transfection, Expressing, Plasmid Preparation, Luciferase, Immunohistochemical staining, Staining

CD14 high CD90 int cells in RA tissues. (A) and (B) show the sublining layer of RA synovial tissues. (C) and (D) show the cartilage/pannus junction where the synovial tissues invade the bone. (A) and (C) show HE staining. (B) and (D) show double immunofluorescence staining for CD14 (red) and CD90 (green). Scale bar, 100 μm. HE, hematoxylin and eosin; RA, rheumatoid arthritis.

Journal: ACR Open Rheumatology

Article Title: CD14 + Dendritic‐Shaped Cells Functioning as Dendritic Cells in Rheumatoid Arthritis Synovial Tissues

doi: 10.1002/acr2.11670

Figure Lengend Snippet: CD14 high CD90 int cells in RA tissues. (A) and (B) show the sublining layer of RA synovial tissues. (C) and (D) show the cartilage/pannus junction where the synovial tissues invade the bone. (A) and (C) show HE staining. (B) and (D) show double immunofluorescence staining for CD14 (red) and CD90 (green). Scale bar, 100 μm. HE, hematoxylin and eosin; RA, rheumatoid arthritis.

Article Snippet: After heat‐induced antigen retrieval, fluorescent immunostaining was conducted using an anti‐CD14 rabbit monoclonal antibody (1:200; Abcam) and an anti‐CD90 mouse monoclonal antibody (1:1,000; ProteinTech), then visualized using goat anti‐rabbit immunoglobulin G (IgG) (1:200, Alexa Fluor 594; Abcam) and goat anti‐mouse IgG (1:200, Alexa Fluor 488; Abcam) as second antibodies.

Techniques: Staining, Double Immunofluorescence Staining

Percentages of CD14 high CD90 int cells in peripheral blood samples and synovial tissues. (A) Percentages of CD14 high CD90 int cells in the peripheral blood samples are shown. (B) Percentages of CD14 high CD90 int cells in the synovial tissues are shown. Flow cytometry data shown in the bottom are representative data for each group. Each frame in data indicates CD14 high CD90 int cells. The regions of these frames were determined and fixed by comparison with OA controls. The bars show average values and SDs. The Mann–Whitney U test and Spearman's rank correlation coefficient were used to assess significant differences. * P < 0.05. OA, osteoarthritis (n = 5); RA in rem, RA in clinical remission (n = 10); RA, rheumatoid arthritis; untreated active RA, untreated and active RA (n = 10).

Journal: ACR Open Rheumatology

Article Title: CD14 + Dendritic‐Shaped Cells Functioning as Dendritic Cells in Rheumatoid Arthritis Synovial Tissues

doi: 10.1002/acr2.11670

Figure Lengend Snippet: Percentages of CD14 high CD90 int cells in peripheral blood samples and synovial tissues. (A) Percentages of CD14 high CD90 int cells in the peripheral blood samples are shown. (B) Percentages of CD14 high CD90 int cells in the synovial tissues are shown. Flow cytometry data shown in the bottom are representative data for each group. Each frame in data indicates CD14 high CD90 int cells. The regions of these frames were determined and fixed by comparison with OA controls. The bars show average values and SDs. The Mann–Whitney U test and Spearman's rank correlation coefficient were used to assess significant differences. * P < 0.05. OA, osteoarthritis (n = 5); RA in rem, RA in clinical remission (n = 10); RA, rheumatoid arthritis; untreated active RA, untreated and active RA (n = 10).

Techniques: Flow Cytometry, Comparison, MANN-WHITNEY

(A) Dendritic cell–differentiation induction of RA synovial cells is shown. Subpanels show representative flow cytometry data from independent experiments (n = 7). Blue color in each subpanel indicates isotype control. (B) CD83 and HLA‐DR expression after dendritic cell–differentiation induction on day 7 is shown. The CD14 high CD90 int cell group showed significantly increased expression of CD83 and HLA‐DR compared with the non‐CD14 high CD90 int cell group. (C) Expression levels of IL‐6 and TNF‐α in the supernatant of both cell groups were significantly increased by dendritic cell–differentiation induction on day 4 and day 7 compared with day 1. These results suggest that CD14 high CD90 int cells have the potential to differentiate into CD83+ and HLA‐DR+ dendritic cells. The bars show average values and SDs. Scale bar, 100 μm. RA, rheumatoid arthritis; HLA‐DR, human leukocyte antigen‐DR; IL‐6, interleukin‐6; TNF‐α, tumor necrosis factor‐α.

Journal: ACR Open Rheumatology

Article Title: CD14 + Dendritic‐Shaped Cells Functioning as Dendritic Cells in Rheumatoid Arthritis Synovial Tissues

doi: 10.1002/acr2.11670

Figure Lengend Snippet: (A) Dendritic cell–differentiation induction of RA synovial cells is shown. Subpanels show representative flow cytometry data from independent experiments (n = 7). Blue color in each subpanel indicates isotype control. (B) CD83 and HLA‐DR expression after dendritic cell–differentiation induction on day 7 is shown. The CD14 high CD90 int cell group showed significantly increased expression of CD83 and HLA‐DR compared with the non‐CD14 high CD90 int cell group. (C) Expression levels of IL‐6 and TNF‐α in the supernatant of both cell groups were significantly increased by dendritic cell–differentiation induction on day 4 and day 7 compared with day 1. These results suggest that CD14 high CD90 int cells have the potential to differentiate into CD83+ and HLA‐DR+ dendritic cells. The bars show average values and SDs. Scale bar, 100 μm. RA, rheumatoid arthritis; HLA‐DR, human leukocyte antigen‐DR; IL‐6, interleukin‐6; TNF‐α, tumor necrosis factor‐α.

Techniques: Cell Differentiation, Flow Cytometry, Control, Expressing

(A) Overview of the co‐culture experiments of RA synovial cells and lymphocytes is shown. (B) shows pictures of phase contrast microscopy and HE‐stained histology after co‐culture of CD14 high CD90 int cells, non‐CD14 high CD90 int cells, CD14 high CD90 int cells after DC induction, and non‐CD14 high CD90 int cells after DC induction, with lymphocytes, respectively. In co‐culture of synovial cells after DC induction and lymphocytes (Bc and Bd), both synovial cells and lymphocytes proliferated remarkably. (C) IL‐6 and TNF‐α in the supernatant were also most highly expressed in the groups of synovial cells after DC induction. Experiments were performed three times for each condition. (D) shows the percentages of cell area occupied by synovial cells and lymphocytes relative to culture dish. Scale bar = 100 μm. The bars show average values and SDs. DC, dendritic cell; HE, hematoxylin and eosin; IL‐6, interleukin‐6; RA, rheumatoid arthritis; TNF‐α, tumor necrosis factor‐α.

Journal: ACR Open Rheumatology

Article Title: CD14 + Dendritic‐Shaped Cells Functioning as Dendritic Cells in Rheumatoid Arthritis Synovial Tissues

doi: 10.1002/acr2.11670

Figure Lengend Snippet: (A) Overview of the co‐culture experiments of RA synovial cells and lymphocytes is shown. (B) shows pictures of phase contrast microscopy and HE‐stained histology after co‐culture of CD14 high CD90 int cells, non‐CD14 high CD90 int cells, CD14 high CD90 int cells after DC induction, and non‐CD14 high CD90 int cells after DC induction, with lymphocytes, respectively. In co‐culture of synovial cells after DC induction and lymphocytes (Bc and Bd), both synovial cells and lymphocytes proliferated remarkably. (C) IL‐6 and TNF‐α in the supernatant were also most highly expressed in the groups of synovial cells after DC induction. Experiments were performed three times for each condition. (D) shows the percentages of cell area occupied by synovial cells and lymphocytes relative to culture dish. Scale bar = 100 μm. The bars show average values and SDs. DC, dendritic cell; HE, hematoxylin and eosin; IL‐6, interleukin‐6; RA, rheumatoid arthritis; TNF‐α, tumor necrosis factor‐α.

Techniques: Co-Culture Assay, Microscopy, Staining

Diagram showing our hypothesis of RA chronic inflammation induced by CD14+ dendritic‐shaped cells. We hypothesized that the CD14+ cells in the bone marrow flow into the synovial tissues via the circulating blood. Some of these cells contribute to RA inflammation after differentiating into HLA‐DR+ dendritic cells. The yellow‐colored cells in the immunohistochemistry images indicate the CD14 high CD90 int cells. Scale bar, 100 μm. HLA‐DR, human leukocyte antigen‐DR; RA, rheumatoid arthritis.

Journal: ACR Open Rheumatology

Article Title: CD14 + Dendritic‐Shaped Cells Functioning as Dendritic Cells in Rheumatoid Arthritis Synovial Tissues

doi: 10.1002/acr2.11670

Figure Lengend Snippet: Diagram showing our hypothesis of RA chronic inflammation induced by CD14+ dendritic‐shaped cells. We hypothesized that the CD14+ cells in the bone marrow flow into the synovial tissues via the circulating blood. Some of these cells contribute to RA inflammation after differentiating into HLA‐DR+ dendritic cells. The yellow‐colored cells in the immunohistochemistry images indicate the CD14 high CD90 int cells. Scale bar, 100 μm. HLA‐DR, human leukocyte antigen‐DR; RA, rheumatoid arthritis.

Techniques: Immunohistochemistry

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