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R&D Systems anti cd5l aim
Anti Cd5l Aim, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+cd5l/CD5L+Antibody/pmc10133315__41467_2023_36910_MOESM3_ESM-35-1-18
Average 94 stars, based on 6 article reviews

anti cd5l aim - by Bioz Stars, 2026-11

94/100 stars

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Incubation:

Article Title: CD5L is upregulated upon infection with Mycobacterium tuberculosis with no effect on disease progression.
Article Snippet: i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, Porto, Portugal ESS, Politécnico do Porto, Porto, Portugal Doctoral Program in Molecular and Cell Biology, ICBAS-Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal IBMC—Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal Innate Immunity Group, Germans Trias i Pujol Research Institute (IGTP), Badalona, Spain

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CD5L -KO cells have reduced inflammatory state. Deletion of CD5L led to decrease in basal and LPS-induced cytokine mRNA levels. TNF and IL-1β levels in unstimulated cells were decreased nearly 300-fold, with average basal levels of 0.003 for knockout cells compared to the value of 1 set for the controls. A total of 2.5 × 10 5 cells in 24-well plates were differentiated using 50 ng/mL PMA for 48 hours. Stimulation was performed after 24 hours of rest in PMA-free media with 100 ng/mL LPS for 4 hours. Inflammatory cytokine expression levels were determined using qRT-PCR of RNAs isolated from cell lysates. Graphs are representative of at least three independent experiments. PMA, phorbol 12-myristate 13-acetate. (* p<0.05, ** p<0.01, *** p<0.001).

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: CD5L -KO cells have reduced inflammatory state. Deletion of CD5L led to decrease in basal and LPS-induced cytokine mRNA levels. TNF and IL-1β levels in unstimulated cells were decreased nearly 300-fold, with average basal levels of 0.003 for knockout cells compared to the value of 1 set for the controls. A total of 2.5 × 10 5 cells in 24-well plates were differentiated using 50 ng/mL PMA for 48 hours. Stimulation was performed after 24 hours of rest in PMA-free media with 100 ng/mL LPS for 4 hours. Inflammatory cytokine expression levels were determined using qRT-PCR of RNAs isolated from cell lysates. Graphs are representative of at least three independent experiments. PMA, phorbol 12-myristate 13-acetate. (* p<0.05, ** p<0.01, *** p<0.001).

Article Snippet: The primary antibodies against CD5L (mouse monoclonal F1 clone, 1/1,000, sc-514283, Santa Cruz Biotechnology), GAPDH (1/2000, sc-47724, Santa Cruz Biotechnology, Santa Cruz, CA USA), RORA (1/1,000 PP-H3910-00, R&D Systems), and the HRP-conjugated goat anti-mouse secondary antibody (1/5000, #P0447, Dako) were diluted in 0.5× blocking buffer/PBS.

Techniques: Knock-Out, Expressing, Quantitative RT-PCR, Isolation

RORα is epistatic to CD5L . Induction of inflammatory TNF (A) and IL-1β (B) gene expression in CD5L/RORA DKO cells is similar to that observed in RORA deletion cells (n = 3, ± SEM). Paired two-tailed t -test of three biological replicates has been used to evaluate statistical significance of differences between RORAko and CD5L/RORA DKO cell lines. Both RORAko and CD5L/RORA DKO cells produce similarly higher levels of TNF than the CD5Lko cells at 3 and 6 hours after LPS stimulation (C) . CD5Lko cells produce significantly lower amounts of IL-6 at both the 3- and 6-hour timepoints, while RORAko and CD5L/RORA DKO secrete similar levels of this cytokine (D) (n = 6, ± SEM, representative of two independent experiments * p<0.05, ** p<0.01).

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: RORα is epistatic to CD5L . Induction of inflammatory TNF (A) and IL-1β (B) gene expression in CD5L/RORA DKO cells is similar to that observed in RORA deletion cells (n = 3, ± SEM). Paired two-tailed t -test of three biological replicates has been used to evaluate statistical significance of differences between RORAko and CD5L/RORA DKO cell lines. Both RORAko and CD5L/RORA DKO cells produce similarly higher levels of TNF than the CD5Lko cells at 3 and 6 hours after LPS stimulation (C) . CD5Lko cells produce significantly lower amounts of IL-6 at both the 3- and 6-hour timepoints, while RORAko and CD5L/RORA DKO secrete similar levels of this cytokine (D) (n = 6, ± SEM, representative of two independent experiments * p<0.05, ** p<0.01).

Techniques: Gene Expression, Two Tailed Test

RNA-seq analysis of differentiated CD5L deletion cells. (A) Volcano plot of ANOVA results. Vertical cutoff line is at FDR-adjusted p = 0.05. Vertical cutoff lines are at fold difference = 2. A total of 1,165 annotated genes were found to be differentially expressed between CD5L deletion and control cell lines using these criteria. The majority of differentially expressed genes (879) were downregulated (blue). (B) Gene Ontology terms enriched by the differentially expressed dataset include regulation of intracellular processes as well as cell-to-cell signaling characteristic of immune cells. (C) All five most significantly enriched KEGG pathways mediate immune signaling. (D) The magnitude of changes in expression levels of genes that contribute to the top five enriched KEGG pathways. For genes that are not part of a specific pathway, the values are shown in gray. Colors represent fold difference change in gene expression when compared to controls. FDR, false discovery rate.

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: RNA-seq analysis of differentiated CD5L deletion cells. (A) Volcano plot of ANOVA results. Vertical cutoff line is at FDR-adjusted p = 0.05. Vertical cutoff lines are at fold difference = 2. A total of 1,165 annotated genes were found to be differentially expressed between CD5L deletion and control cell lines using these criteria. The majority of differentially expressed genes (879) were downregulated (blue). (B) Gene Ontology terms enriched by the differentially expressed dataset include regulation of intracellular processes as well as cell-to-cell signaling characteristic of immune cells. (C) All five most significantly enriched KEGG pathways mediate immune signaling. (D) The magnitude of changes in expression levels of genes that contribute to the top five enriched KEGG pathways. For genes that are not part of a specific pathway, the values are shown in gray. Colors represent fold difference change in gene expression when compared to controls. FDR, false discovery rate.

Techniques: RNA Sequencing, Control, Expressing, Gene Expression

Expression of genes in the TNF signaling pathway is impacted by deletion of CD5L . Deletion of CD5L results in downregulation (green) of transcription of nearly half of the genes comprising the TNF signaling pathway. Expression of signal propagating kinases is also affected by p38, and JNK is downregulated at the transcriptional level (adapted from KEGG TNF signaling pathway, hsa04668 6/25/18).

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: Expression of genes in the TNF signaling pathway is impacted by deletion of CD5L . Deletion of CD5L results in downregulation (green) of transcription of nearly half of the genes comprising the TNF signaling pathway. Expression of signal propagating kinases is also affected by p38, and JNK is downregulated at the transcriptional level (adapted from KEGG TNF signaling pathway, hsa04668 6/25/18).

Techniques: Expressing

Lipid remodeling function of CD5L. (A) Total levels of lipid classes analyzed in mutant and control cells. (B) Proportion of side acyl chains classified according to the extent of their saturation. MUFA: one or two double bonds in a 3-acyl chain lipid or one double bond in a 2-acyl chain lipid. MUFA1: number of double bonds and acyl chains is equal. PUFA2, PUFA3, and PUFA4: number of double bonds is two-, three-, and fourfold higher compared to number of acyl chains in the lipid, respectively. (C) Deletion of CD5L significantly (*** p < 0.001, Mann–Whitney test) increases levels of highly polyunsaturated [PUFA(3,4,5)] fatty acids. (D) CD5L deletion results in an increase of free cholesterol in mutant cells. PUFA, polyunsaturated fatty acid. (E) Corrected Total Cell Fluorescence (CTCF) values calculated for 10 randomly selected cells for each cell line (* p = 0.014 unpaired two-tailed t -test).

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: Lipid remodeling function of CD5L. (A) Total levels of lipid classes analyzed in mutant and control cells. (B) Proportion of side acyl chains classified according to the extent of their saturation. MUFA: one or two double bonds in a 3-acyl chain lipid or one double bond in a 2-acyl chain lipid. MUFA1: number of double bonds and acyl chains is equal. PUFA2, PUFA3, and PUFA4: number of double bonds is two-, three-, and fourfold higher compared to number of acyl chains in the lipid, respectively. (C) Deletion of CD5L significantly (*** p < 0.001, Mann–Whitney test) increases levels of highly polyunsaturated [PUFA(3,4,5)] fatty acids. (D) CD5L deletion results in an increase of free cholesterol in mutant cells. PUFA, polyunsaturated fatty acid. (E) Corrected Total Cell Fluorescence (CTCF) values calculated for 10 randomly selected cells for each cell line (* p = 0.014 unpaired two-tailed t -test).

Techniques: Mutagenesis, Control, MANN-WHITNEY, Fluorescence, Two Tailed Test

FASN activity in knockout and control cells. Deletion of CD5L does not significantly change the overall FASN activity of human macrophages. Lysates from 10 6 cells were used to measure FASN activity by monitoring NADPH oxidation over 15 minutes. Activity is presented as an average of replicates from three independent experiments. FASN, fatty acid synthase.

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: FASN activity in knockout and control cells. Deletion of CD5L does not significantly change the overall FASN activity of human macrophages. Lysates from 10 6 cells were used to measure FASN activity by monitoring NADPH oxidation over 15 minutes. Activity is presented as an average of replicates from three independent experiments. FASN, fatty acid synthase.

Techniques: Activity Assay, Knock-Out, Control

Differences in gene expression in CD5L and RORA deletion cells. (A) Self-organizing map (SOM) clustering identified six distinct patterns of changes in gene expression between respective mutant and control cells. (B) GO term analysis of genes in highlighted divergently regulated clusters identifies terms characteristic of immune response. (C) Eight out of 10 KEGG pathways enriched by genes from highlighted clusters are central to shaping the inflammatory signaling of immune cells. Genes contributing to the TNF (D) and NF-κB (E) signaling pathways are downregulated in CD5L mutant cells and upregulated in RORA mutants. GO, Gene Ontology.

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: Differences in gene expression in CD5L and RORA deletion cells. (A) Self-organizing map (SOM) clustering identified six distinct patterns of changes in gene expression between respective mutant and control cells. (B) GO term analysis of genes in highlighted divergently regulated clusters identifies terms characteristic of immune response. (C) Eight out of 10 KEGG pathways enriched by genes from highlighted clusters are central to shaping the inflammatory signaling of immune cells. Genes contributing to the TNF (D) and NF-κB (E) signaling pathways are downregulated in CD5L mutant cells and upregulated in RORA mutants. GO, Gene Ontology.

Techniques: Gene Expression, Mutagenesis, Control, Protein-Protein interactions

CD5L deletion induces transcriptional changes in undifferentiated monocytes. (A) Deletion of CD5L in undifferentiated monocytic THP-1 cells significantly changed expression of 52 genes more than twofold up and 95 genes twofold down (in color). (B) Expression of atherogenesis-related genes involved in interaction of monocytes with ECM is changed in CD5Lko cells. (C) CD52 expression is significantly increased in undifferentiated (FDR = 3e−14) and differentiated (FDR = 2.9e−35) CD5Lko cells. (D) Cellular CD52 protein levels are increased in undifferentiated CD5Lko THP-1 monocytes. ECM, extracellular matrix; FDR, false discovery rate.

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: CD5L deletion induces transcriptional changes in undifferentiated monocytes. (A) Deletion of CD5L in undifferentiated monocytic THP-1 cells significantly changed expression of 52 genes more than twofold up and 95 genes twofold down (in color). (B) Expression of atherogenesis-related genes involved in interaction of monocytes with ECM is changed in CD5Lko cells. (C) CD52 expression is significantly increased in undifferentiated (FDR = 3e−14) and differentiated (FDR = 2.9e−35) CD5Lko cells. (D) Cellular CD52 protein levels are increased in undifferentiated CD5Lko THP-1 monocytes. ECM, extracellular matrix; FDR, false discovery rate.

Techniques: Expressing

Model for the role of CD5L in mediating inflammatory state of human macrophages. (A) CD5L induces changes in macrophages’ lipid content, reducing the availability of RORα ligands and subsequent RORα inactivation. Thus, no inhibitory effect of RORα is applied on inflammatory signaling. (B) In the absence of CD5L, there are sufficient levels of RORα ligands driving its activation and downregulation of inflammatory signaling.

Journal: Frontiers in Immunology

Article Title: Endogenous CD5L controls the metabolic and inflammatory state of human macrophages

doi: 10.3389/fimmu.2025.1677948

Figure Lengend Snippet: Model for the role of CD5L in mediating inflammatory state of human macrophages. (A) CD5L induces changes in macrophages’ lipid content, reducing the availability of RORα ligands and subsequent RORα inactivation. Thus, no inhibitory effect of RORα is applied on inflammatory signaling. (B) In the absence of CD5L, there are sufficient levels of RORα ligands driving its activation and downregulation of inflammatory signaling.

Techniques: Activation Assay

CD5L promotes the uptake of free fatty acids (FFAs) by hepatocytes and stellate cells. A: Uptake of BODIPY-labeled palmitate acid (BODIPY-PA) in a time-dependent manner. Top four panels: Images taken at indicated time of PA exposure. Bottom panel: Quantitative analysis of the images. B: Cultured mouse hepatocytes ( top panel ) and HepG2 cells ( bottom panel ) were pretreated with CD5L (2000 ng/mL) or vehicle for 25 minutes. Uptake of free fatty acids was then measured by incubating BODIPY-PA for the indicated period. CD5L pretreatment enhanced the uptake of BODIPY-PA with 0.25, 0.5, and 1 hour of uptake but not 2 and 4 hours of uptake. C: Cultured LX-2 cells were pretreated with CD5L (2000 ng/mL) or vehicle for 25 minutes. Uptake of free fatty acids was then measured by incubating BODIPY-PA for the indicated period. CD5L pretreatment facilitated the uptake of BODIPY-PA with 15 minutes, 30 minutes, and 1 hour of uptake but not 2 and 4 hours of uptake. No differences were observed with 4 hours of uptake. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001. Scale bars = 50 μm ( A ). NS, not significant.

Journal: The American Journal of Pathology

Article Title: Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

doi: 10.1016/j.ajpath.2025.06.003

Figure Lengend Snippet: CD5L promotes the uptake of free fatty acids (FFAs) by hepatocytes and stellate cells. A: Uptake of BODIPY-labeled palmitate acid (BODIPY-PA) in a time-dependent manner. Top four panels: Images taken at indicated time of PA exposure. Bottom panel: Quantitative analysis of the images. B: Cultured mouse hepatocytes ( top panel ) and HepG2 cells ( bottom panel ) were pretreated with CD5L (2000 ng/mL) or vehicle for 25 minutes. Uptake of free fatty acids was then measured by incubating BODIPY-PA for the indicated period. CD5L pretreatment enhanced the uptake of BODIPY-PA with 0.25, 0.5, and 1 hour of uptake but not 2 and 4 hours of uptake. C: Cultured LX-2 cells were pretreated with CD5L (2000 ng/mL) or vehicle for 25 minutes. Uptake of free fatty acids was then measured by incubating BODIPY-PA for the indicated period. CD5L pretreatment facilitated the uptake of BODIPY-PA with 15 minutes, 30 minutes, and 1 hour of uptake but not 2 and 4 hours of uptake. No differences were observed with 4 hours of uptake. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001. Scale bars = 50 μm ( A ). NS, not significant.

Article Snippet: Then, cells were treated with rabbit anti-mouse CD5L as primary antibody (ABclonal, Woburn, MA) and BV421 labeled donkey anti-rabbit IgG as the secondary antibody (clone: Poly4064; BioLegend) subsequently.

Techniques: Labeling, Cell Culture

Expression of Cd5l in liver tissues from mouse models of steatotic liver injury. A: Expression of Cd5l is concurrently induced with Clec4f , a marker for liver macrophages in high-fat diet (HFD) induced steatotic livers. Low-fat diet (LFD) serves as control. B: Expression of Cd5l and Clec4f in ethanol (EtOH) induced steatotic livers. C : Expression of Cd5l and Clec4f in steatotic livers induced by high-fat and high-sucrose (HFHC) feeding versus normal chow (NC) control. D : Expression of Cd5l in steatohepatitis LiPten livers. E: Correlation of Clec4f and Cd5l expression in all mice analyzed in A – D regardless of diet and genotype. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. Con, control.

Journal: The American Journal of Pathology

Article Title: Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

doi: 10.1016/j.ajpath.2025.06.003

Figure Lengend Snippet: Expression of Cd5l in liver tissues from mouse models of steatotic liver injury. A: Expression of Cd5l is concurrently induced with Clec4f , a marker for liver macrophages in high-fat diet (HFD) induced steatotic livers. Low-fat diet (LFD) serves as control. B: Expression of Cd5l and Clec4f in ethanol (EtOH) induced steatotic livers. C : Expression of Cd5l and Clec4f in steatotic livers induced by high-fat and high-sucrose (HFHC) feeding versus normal chow (NC) control. D : Expression of Cd5l in steatohepatitis LiPten livers. E: Correlation of Clec4f and Cd5l expression in all mice analyzed in A – D regardless of diet and genotype. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. Con, control.

Techniques: Expressing, Marker, Control

Identification of Clec4f + liver macrophages (LMacs) as the dominant cell population expressing CD5L in the liver. A: Analysis of CD5L in all CD45 + cell populations identified a CD5L hi versus a CD5L low population. B: Analysis of CD11b and F4/80 in all CD45 + cell populations to identify CD11b hi F4/80 low (yellow) versus CD11b intermediate F4/80 hi (red) population LMacs. C: Overlay of A and B shows that CD5L hi population overlaps with CD11b intermediate F4/80 hi population LMacs. D: Analysis of CD5L and CLEC4F shows CD5L high expression cells also express high CLEC4F. E: Quantification of CD5L expression in the two LMac populations in LiPten versus control mouse livers. ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001. FSC, forward scatter; MFI, mean fluorescent intensity.

Journal: The American Journal of Pathology

Article Title: Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

doi: 10.1016/j.ajpath.2025.06.003

Figure Lengend Snippet: Identification of Clec4f + liver macrophages (LMacs) as the dominant cell population expressing CD5L in the liver. A: Analysis of CD5L in all CD45 + cell populations identified a CD5L hi versus a CD5L low population. B: Analysis of CD11b and F4/80 in all CD45 + cell populations to identify CD11b hi F4/80 low (yellow) versus CD11b intermediate F4/80 hi (red) population LMacs. C: Overlay of A and B shows that CD5L hi population overlaps with CD11b intermediate F4/80 hi population LMacs. D: Analysis of CD5L and CLEC4F shows CD5L high expression cells also express high CLEC4F. E: Quantification of CD5L expression in the two LMac populations in LiPten versus control mouse livers. ∗∗ P < 0.01, ∗∗∗∗ P < 0.0001. FSC, forward scatter; MFI, mean fluorescent intensity.

Techniques: Expressing, Control

Colocalization of CD5L with CLEC4F in mouse livers. A: Immunofluorescence staining of CD5L and CLEC4F in LiPten versus genotype control (Con) livers showing more CD5L and CLEC4F staining in the injured livers of LiPten mice. Most CD5L is colocalized in cell expression CLEC4F. Blue, DAPI for nuclei. Quantification of positively stained cells. Boxed areas are shown in the bottom three panels as enlarged images. Arrows point to CD5L and CLEC4F positive stained cells. B: Three random sections per animal were counted for double-stained cells versus total CLEC4F staining cells in the LiPten and control mice. The fold change difference between LiPten livers and controls is reported. C: Expression of Clec4f , Cd5l , and TimD4 in livers of mice treated with clodronate (CLD) to depleted macrophages. D: Alamar Blue fluorescent signal in Raw264.7 cells treated with 250 μmol/L palmitic acid with or without CD5L (2000 ng/mL). n = 3 ( B ). ∗ P < 0.05, ∗∗∗∗ P < 0.0001. Scale bars = 100 μm ( A ). PBS, phosphate-buffered saline.

Journal: The American Journal of Pathology

Article Title: Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

doi: 10.1016/j.ajpath.2025.06.003

Figure Lengend Snippet: Colocalization of CD5L with CLEC4F in mouse livers. A: Immunofluorescence staining of CD5L and CLEC4F in LiPten versus genotype control (Con) livers showing more CD5L and CLEC4F staining in the injured livers of LiPten mice. Most CD5L is colocalized in cell expression CLEC4F. Blue, DAPI for nuclei. Quantification of positively stained cells. Boxed areas are shown in the bottom three panels as enlarged images. Arrows point to CD5L and CLEC4F positive stained cells. B: Three random sections per animal were counted for double-stained cells versus total CLEC4F staining cells in the LiPten and control mice. The fold change difference between LiPten livers and controls is reported. C: Expression of Clec4f , Cd5l , and TimD4 in livers of mice treated with clodronate (CLD) to depleted macrophages. D: Alamar Blue fluorescent signal in Raw264.7 cells treated with 250 μmol/L palmitic acid with or without CD5L (2000 ng/mL). n = 3 ( B ). ∗ P < 0.05, ∗∗∗∗ P < 0.0001. Scale bars = 100 μm ( A ). PBS, phosphate-buffered saline.

Techniques: Immunofluorescence, Staining, Control, Expressing, Saline

CD5L promotes chemotaxis of natural killer T (NKT) cells. A: Schematics of the Transwell assay. B: Transwell assay performed with primary liver immune cells in the insert with or without 2000 ng/mL CD5L in the bottom chamber. No CD5L wells contain media and 0.1% fetal bovine serum (FBS). Cells recovered in the bottom were analyzed for immune cell types using flow cytometry and reported as percentage of cell distributions. C: Transwell assay performed with primary liver immune cells in the insert with or without liver macrophage (LMac) in the bottom chamber. No LMac wells contain media and 0.1% FBS. Cells recovered in the bottom were analyzed for immune cell types using flow cytometry and reported as percentage of cell distributions. Each dot is one mouse. Data are not significant (NS), P = 0.057. D: Transwell assay performed with Jurkat cells in the insert and 2% FBS with indicated doses of CD5L in the bottom chamber. E: Transwell assay performed with primary liver immune cells in the insert and LMac in the bottom chamber. Treatment with or without CD5L neutralizing antibody or CD36 inhibitor SMS121 is compared with vehicle treatment (0.1% FBS). F: Schematic representation of the overall function of CD5L in the liver: CD5L produced by LMacs facilitates lipid uptake in hepatocytes and stellate cells and regulates the migration of NKT cells. G: Correlation of CD5L with Nk1.1, a marker of NKT in liver injury models. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001; # P < 0.05 only detected in experimental group.

Journal: The American Journal of Pathology

Article Title: Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

doi: 10.1016/j.ajpath.2025.06.003

Figure Lengend Snippet: CD5L promotes chemotaxis of natural killer T (NKT) cells. A: Schematics of the Transwell assay. B: Transwell assay performed with primary liver immune cells in the insert with or without 2000 ng/mL CD5L in the bottom chamber. No CD5L wells contain media and 0.1% fetal bovine serum (FBS). Cells recovered in the bottom were analyzed for immune cell types using flow cytometry and reported as percentage of cell distributions. C: Transwell assay performed with primary liver immune cells in the insert with or without liver macrophage (LMac) in the bottom chamber. No LMac wells contain media and 0.1% FBS. Cells recovered in the bottom were analyzed for immune cell types using flow cytometry and reported as percentage of cell distributions. Each dot is one mouse. Data are not significant (NS), P = 0.057. D: Transwell assay performed with Jurkat cells in the insert and 2% FBS with indicated doses of CD5L in the bottom chamber. E: Transwell assay performed with primary liver immune cells in the insert and LMac in the bottom chamber. Treatment with or without CD5L neutralizing antibody or CD36 inhibitor SMS121 is compared with vehicle treatment (0.1% FBS). F: Schematic representation of the overall function of CD5L in the liver: CD5L produced by LMacs facilitates lipid uptake in hepatocytes and stellate cells and regulates the migration of NKT cells. G: Correlation of CD5L with Nk1.1, a marker of NKT in liver injury models. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001; # P < 0.05 only detected in experimental group.

Techniques: Chemotaxis Assay, Transwell Assay, Flow Cytometry, Produced, Migration, Marker

Elevated plasma CD5L in high-fat diet (HFD)–induced liver injury and its association with hepatocellular carcinoma (HCC) response to immune checkpoint therapy. A: Plasma concentration of CD5L in patients with HCC versus healthy donors. A and B: Plasma concentration of CD5L is higher in patients with HCC with higher Child Pugh scores ( B ) versus lower scores ( A ). C: Plasma concentration of CD5L predicts patient response to therapy. Left panel: Plasma CD5L in patients showed clinical benefit versus those who did not show clinical benefit. Right panel: Plasma CD5L in patients who responded completely or partially versus those whose disease did not progress or progressed. Red dotted line shows a trend of progression. Data are not significant (NS), P = 0.0748. D: Plasma alanine aminotransferase (ALT) levels in mice fed low-fat diet (LFD) versus HFD at the indicated time points. Each dot represents one mouse. E: Detection of CD5L in serum of mice fed LFD versus HFD. HFD feeding for 5 and 9 months significantly increased the plasma levels of CD5l. Each dot represents one mouse. n = 50 patients with HCC ( A ); n = 5 healthy donors ( A ); n = 1 patient who responded completely ( C , right panel ); n = 8 patients who responded partially and patients whose disease progressed ( C , right panel ); n = 27 patients whose disease did not progress ( C , right panel ). ∗ P < 0.05, ∗∗∗ P < 0.001. CR, complete response; PD, progressive disease; PR, partial response; SD, stable disease.

Journal: The American Journal of Pathology

Article Title: Characterizing Kupffer Cell Production of CD5 Antigen-Like and Its Function on Regulating Migration of Natural Killer T Cells

doi: 10.1016/j.ajpath.2025.06.003

Figure Lengend Snippet: Elevated plasma CD5L in high-fat diet (HFD)–induced liver injury and its association with hepatocellular carcinoma (HCC) response to immune checkpoint therapy. A: Plasma concentration of CD5L in patients with HCC versus healthy donors. A and B: Plasma concentration of CD5L is higher in patients with HCC with higher Child Pugh scores ( B ) versus lower scores ( A ). C: Plasma concentration of CD5L predicts patient response to therapy. Left panel: Plasma CD5L in patients showed clinical benefit versus those who did not show clinical benefit. Right panel: Plasma CD5L in patients who responded completely or partially versus those whose disease did not progress or progressed. Red dotted line shows a trend of progression. Data are not significant (NS), P = 0.0748. D: Plasma alanine aminotransferase (ALT) levels in mice fed low-fat diet (LFD) versus HFD at the indicated time points. Each dot represents one mouse. E: Detection of CD5L in serum of mice fed LFD versus HFD. HFD feeding for 5 and 9 months significantly increased the plasma levels of CD5l. Each dot represents one mouse. n = 50 patients with HCC ( A ); n = 5 healthy donors ( A ); n = 1 patient who responded completely ( C , right panel ); n = 8 patients who responded partially and patients whose disease progressed ( C , right panel ); n = 27 patients whose disease did not progress ( C , right panel ). ∗ P < 0.05, ∗∗∗ P < 0.001. CR, complete response; PD, progressive disease; PR, partial response; SD, stable disease.

Techniques: Clinical Proteomics, Concentration Assay

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