cxcl16 protein  (MedChemExpress)

Journal: Inflammation

Article Title: KANK4 Regulates CXCL16 Glycosylation Through TMEM260 to Modulate Microglial Activation in Sepsis-associated Encephalopathy

doi: 10.1007/s10753-026-02481-y

Figure Lengend Snippet: KANK4 regulated CXCL16 glycosylation and microglial activation via TMEM260. Microglia were isolated from the hippocampus of mice in Sham, SAE, SAE + AAV-NC, and SAE + AAV-KANK4 groups, followed by the following analyses: (A) IHC was performed to detect CXCL16 protein expression. Microglia were isolated from the Sham and SAE groups for the following assays: (B) Western blot analysis was conducted to assess CXCL16 glycosylation levels ( n = 3). (C) Co-IP was carried out to examine the interaction between TMEM260 and CXCL16. BV2 microglial cells were treated with LPS to establish a cell model. Control and LPS groups were subjected to the following analyses: (D) Western blot analysis was applied to detect CXCL16 expression using both anti-CXCL16 and anti-His-CXCL16 antibodies ( n = 3). (E) Co-IP was conducted to validate the interaction between TMEM260 and CXCL16. (F) Western blot was used to assess O-mannosylation of CXCL16 protein in LPS-treated microglia ( n = 3). (G) Effect of CXCL16 glycosylation site mutations on its glycosylation level. Wild-type (WT) and site-specific mutant (S137A, S117A, S139A) CXCL16 plasmids were transfected into microglia. CXCL16 glycosylation was assessed by Western blot ( n = 3). (H) Impact of CXCL16 glycosylation site mutation (S117A) on the expression of inflammatory factors. In an LPS-induced microglial inflammation model, cells were transfected with either WT or glycosylation-site mutant (S117A) CXCL16 plasmid. The levels of inflammatory cytokines IL-1β, IL-6, and TNF-α in the cells were measured by ELISA. BV2 cells were transfected for TMEM260 overexpression or knockdown. The groups included Control, si-NC, si-TMEM260, NC-OE, and TMEM260-OE, and the following analyses were performed: (I) Western blot analysis was used to detect the expression of TMEM260 and CXCL16 proteins ( n = 3). (J) CHX assay was performed to evaluate the stability of CXCL16 protein. LPS-treated BV2 cells were used to conduct KANK4 overexpression and TMEM260 knockdown rescue experiments, with six groups: Control, LPS, LPS + OE-NC, LPS+KANK4-OE, LPS+KANK4-OE + si-NC, and LPS+KANK4-OE + si-TMEM260. The following analysis was conducted: (K) Western blot analysis was performed to measure CXCL16 protein expression in BV2 cells ( n = 3). For overexpression of TMEM260 and CXCL16 in LPS-treated BV2 cells, the groups included: Control, LPS, LPS + OE-NC, LPS+TMEM260-OE, LPS+TMEM260-OE + OE-NC, and LPS+TMEM260-OE+CXCL16-OE. The following analyses were carried out: (L) Western blot analysis was conducted to detect TMEM260 and CXCL16 protein levels in each group ( n = 3). (M) CCK-8 assay was applied to evaluate microglial cell viability across groups. (N) IF staining was performed to assess the expression of Iba-1 (green) and CD11b (red), indicating microglial activation status (Scale bar = 50 μm). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. LPS/LPS + OE-NC/LPS+TMEM260-OE + OE-NC; ns, no significant difference vs. LPS/Control

Article Snippet: To assess the stability of CXCL16 protein, CHX (MCE, HY-12320) was used to block new protein synthesis, and a protein stability tracking experiment was conducted.

Techniques: Glycoproteomics, Activation Assay, Isolation, Expressing, Western Blot, Co-Immunoprecipitation Assay, Control, Mutagenesis, Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Over Expression, Knockdown, CCK-8 Assay, Staining

Journal: Inflammation

Article Title: KANK4 Regulates CXCL16 Glycosylation Through TMEM260 to Modulate Microglial Activation in Sepsis-associated Encephalopathy

doi: 10.1007/s10753-026-02481-y

Figure Lengend Snippet: KANK4 regulated CXCL16 glycosylation and microglial activation via TMEM260. Microglia were isolated from the hippocampus of mice in Sham, SAE, SAE + AAV-NC, and SAE + AAV-KANK4 groups, followed by the following analyses: (A) IHC was performed to detect CXCL16 protein expression. Microglia were isolated from the Sham and SAE groups for the following assays: (B) Western blot analysis was conducted to assess CXCL16 glycosylation levels ( n = 3). (C) Co-IP was carried out to examine the interaction between TMEM260 and CXCL16. BV2 microglial cells were treated with LPS to establish a cell model. Control and LPS groups were subjected to the following analyses: (D) Western blot analysis was applied to detect CXCL16 expression using both anti-CXCL16 and anti-His-CXCL16 antibodies ( n = 3). (E) Co-IP was conducted to validate the interaction between TMEM260 and CXCL16. (F) Western blot was used to assess O-mannosylation of CXCL16 protein in LPS-treated microglia ( n = 3). (G) Effect of CXCL16 glycosylation site mutations on its glycosylation level. Wild-type (WT) and site-specific mutant (S137A, S117A, S139A) CXCL16 plasmids were transfected into microglia. CXCL16 glycosylation was assessed by Western blot ( n = 3). (H) Impact of CXCL16 glycosylation site mutation (S117A) on the expression of inflammatory factors. In an LPS-induced microglial inflammation model, cells were transfected with either WT or glycosylation-site mutant (S117A) CXCL16 plasmid. The levels of inflammatory cytokines IL-1β, IL-6, and TNF-α in the cells were measured by ELISA. BV2 cells were transfected for TMEM260 overexpression or knockdown. The groups included Control, si-NC, si-TMEM260, NC-OE, and TMEM260-OE, and the following analyses were performed: (I) Western blot analysis was used to detect the expression of TMEM260 and CXCL16 proteins ( n = 3). (J) CHX assay was performed to evaluate the stability of CXCL16 protein. LPS-treated BV2 cells were used to conduct KANK4 overexpression and TMEM260 knockdown rescue experiments, with six groups: Control, LPS, LPS + OE-NC, LPS+KANK4-OE, LPS+KANK4-OE + si-NC, and LPS+KANK4-OE + si-TMEM260. The following analysis was conducted: (K) Western blot analysis was performed to measure CXCL16 protein expression in BV2 cells ( n = 3). For overexpression of TMEM260 and CXCL16 in LPS-treated BV2 cells, the groups included: Control, LPS, LPS + OE-NC, LPS+TMEM260-OE, LPS+TMEM260-OE + OE-NC, and LPS+TMEM260-OE+CXCL16-OE. The following analyses were carried out: (L) Western blot analysis was conducted to detect TMEM260 and CXCL16 protein levels in each group ( n = 3). (M) CCK-8 assay was applied to evaluate microglial cell viability across groups. (N) IF staining was performed to assess the expression of Iba-1 (green) and CD11b (red), indicating microglial activation status (Scale bar = 50 μm). * P < 0.05, ** P < 0.01, *** P < 0.001 vs. LPS/LPS + OE-NC/LPS+TMEM260-OE + OE-NC; ns, no significant difference vs. LPS/Control

Article Snippet: CXCL16 protein levels were measured by Western blot (antibody: Proteintech, 60123-1-Ig, 1:1000), and the band intensity was quantified using ImageJ.

Techniques: Glycoproteomics, Activation Assay, Isolation, Expressing, Western Blot, Co-Immunoprecipitation Assay, Control, Mutagenesis, Transfection, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Over Expression, Knockdown, CCK-8 Assay, Staining

Journal: bioRxiv

Article Title: CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis

doi: 10.1101/2025.04.10.647297

Figure Lengend Snippet: ( A ) Volcano plots of mouse synovial bulk RNAseq data comparing chemokine ligand expression in Sham vs 7d ACLR and Sham vs 28d ACLR. Genes with red datapoints were differentially expressed at P adj < 0.05 and |log 2 FC| > 0.585. ( B ) Bubble plot from a meta-analysis of human OA synovial transcriptomics datasets showing expression of CXCL16 , CXCR6 , and ADAM10 relative to healthy synovium. ( C ) CXCL16 ELISA of synovial fluid in contralateral and injured joints 3d post-ACLR (n=6 per group). Total number of ( D ) and percent positive ( E ) CXCL16+ and CXCR6+ cells in contralateral and injured synovium at 3d and 14d post-ACLR (n=3 per group. 1 sample = 1 male + 1 female synovia pooled). ( F ) Proportions plots showing the cell type breakdown of CXCL16+ and CXCR6+ cells. ( G ) Proportions plots further breaking down the CXCL16+ and CXCR6+ immune cell types. ( H ) Feature plots of mouse synovial single cell RNAseq data showing Cxcl16, Cxcr6, and Adam10 gene expression distribution across all cell types. All bars show mean ± SEM.

Article Snippet: To assess the disease-promoting effects of CXCL16 in healthy joints, CXCL16 (R&D Systems, Cat. #503-CX) (0.25 ng or 25 ng in 4 µL of sterile PBS) was injected for five consecutive days into one knee joint, and vehicle was injected in the contralateral joint (n=3 male, n=3 female per dose).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Gene Expression

Journal: bioRxiv

Article Title: CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis

doi: 10.1101/2025.04.10.647297

Figure Lengend Snippet: ( A ) Fibroblast like synoviocytes (FLS), bone marrow-derived macrophages (BMDM), and immortalized chondrogenic cells (ATDC5s) were treated with pro-inflammatory cytokines and perturbation of the CXCL16 signaling axis was evaluated via qPCR. ( B ) Gene expression of Cxcl16 , Cxcr6 , and Adam10 by qPCR in FLS (n=6 per group) and a CXCL16 ELISA of FLS conditioned media (n=6-7 per group). ( C ) Gene expression of Cxcl16 , Cxcr6 , and Adam10 by qPCR in BMDMs (n=6 per group). ( D ) Gene expression of Cxcl16 , Cxcr6 , and Adam10 by qPCR in ATDC5s. (n=4 per group). All bars show mean ± SEM.

Article Snippet: To assess the disease-promoting effects of CXCL16 in healthy joints, CXCL16 (R&D Systems, Cat. #503-CX) (0.25 ng or 25 ng in 4 µL of sterile PBS) was injected for five consecutive days into one knee joint, and vehicle was injected in the contralateral joint (n=3 male, n=3 female per dose).

Techniques: Derivative Assay, Gene Expression, Enzyme-linked Immunosorbent Assay

Journal: bioRxiv

Article Title: CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis

doi: 10.1101/2025.04.10.647297

Figure Lengend Snippet: ( A ) In FLS, gene expression of the CXCL16 signaling axis, pro-inflammatory markers, and anti-inflammatory markers was measured by qPCR following stimulation with recombinant CXCL16 (n=6 per group). ( B ) In BMDMs, gene expression of the CXCL16 signaling axis and a macrophage score was measured by qPCR following stimulation with recombinant CXCL16 (n=6 per group). ( C ) In BMPCs, gene expression of the CXCL16 signaling axis, pro-inflammatory markers, and anti-inflammatory markers was measured by qPCR following stimulation with recombinant CXCL16 (n=6 per group). ( D ) Chemotaxis of BMDMs and BMPCs in response to CXCL16 was measured by migrated cell density (n=3 per group). All bars show mean ± SEM.

Article Snippet: To assess the disease-promoting effects of CXCL16 in healthy joints, CXCL16 (R&D Systems, Cat. #503-CX) (0.25 ng or 25 ng in 4 µL of sterile PBS) was injected for five consecutive days into one knee joint, and vehicle was injected in the contralateral joint (n=3 male, n=3 female per dose).

Techniques: Gene Expression, Recombinant, Chemotaxis Assay

Journal: bioRxiv

Article Title: CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis

doi: 10.1101/2025.04.10.647297

Figure Lengend Snippet: ( A ) Knee withdrawal threshold following repeated intra-articular injection of CXCL16 (either low dose or high dose) or vehicle in the contralateral side. Testing occurred at 7d and 14d post-first injection (n=6 per dose). ( B ) Histopathological scoring of limbs given repeated intra-articular injections of CXCL16 (either low or high dose) or vehicle in the contralateral side. Total PTOA score and total synovitis score are shown along with the synovitis subscores of anterior, inferior synovial lining hyperplasia and synovial fibrosis (n=5-6 mice per dose, n=3-12 images averaged together per limb). ( C ) Representative low dose CXCL16-injected limbs and vehicle-injected contralateral limbs. Yellow arrows – synovial lining hyperplasia. Green arrows – synovial fibrosis. ( D ) Knee withdrawal threshold and knee withdrawal threshold ratio (CXCL16/vehicle) following repeated intra-articular injection of CXCL16 (high dose only) or vehicle in the contralateral side (n=3 per sex). ( E ) Venn diagram of synovial bulk RNAseq showing differentially expressed genes (DEGs) between vehicle and CXCL16 injected joints in males compared to females (n=3 per group per sex, |log 2 FC| > .585, P adj < .05). Heatmap of male DEGs. Red indicates upregulated and blue indicates downregulated in CXCL16 injected joints relative to vehicle injected joints. ( F ) Gene set enrichment analysis of male synovia comparing vehicle vs CXCL16 injected joints. ( G ) Knee withdrawal threshold following repeated bilateral intra-articular injections of vehicle, CXCL16, or CXCL16 co-administered with ML339 (n=6 mice, i.e. n=12 limbs, per group). All bars show mean ± SEM.

Article Snippet: To assess the disease-promoting effects of CXCL16 in healthy joints, CXCL16 (R&D Systems, Cat. #503-CX) (0.25 ng or 25 ng in 4 µL of sterile PBS) was injected for five consecutive days into one knee joint, and vehicle was injected in the contralateral joint (n=3 male, n=3 female per dose).

Techniques: Injection

Journal: bioRxiv

Article Title: CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis

doi: 10.1101/2025.04.10.647297

Figure Lengend Snippet: ( A ) Experimental design for intra-articular CXCL16 injection followed by acute knee hyperalgesia. Knee withdrawal threshold ( B ) and knee withdrawal threshold ratio ( C ) at acute timepoints following intra-articular injection of CXCL16 or vehicle in the contralateral joint (n=3 per sex). ( D ) Experimental design for intra-articular CXCL16 +/− ML339 injection followed by acute knee hyperalgesia. Knee withdrawal threshold ( E ) and knee withdrawal threshold ratio ( F ) at acute timepoints following intra-articular injection of CXCL16 or CXCL16 + ML339, and vehicle in the contralateral joint (n=9 per group). ( G ) Experimental design for intra-peritoneal ML339 injections and acute knee hyperalgesia post-ACLR. Knee withdrawal threshold ( H ) and knee withdrawal threshold ratio ( I ) pre- and post-intraperitoneal injection of vehicle or ML339 at 7d post-ACLR (n=8-9 per group). ( J ) Complete blood count analysis showing total number of circulating white blood cells and neutrophils from naïve mice and mice treated with vehicle or ML339 7d post-ACLR (n=10-13 per group). All bars show mean ± SEM.

Article Snippet: To assess the disease-promoting effects of CXCL16 in healthy joints, CXCL16 (R&D Systems, Cat. #503-CX) (0.25 ng or 25 ng in 4 µL of sterile PBS) was injected for five consecutive days into one knee joint, and vehicle was injected in the contralateral joint (n=3 male, n=3 female per dose).

Techniques: Injection

Journal: bioRxiv

Article Title: CXCL16 mediates nociception and inflammation in murine post-traumatic osteoarthritis

doi: 10.1101/2025.04.10.647297

Figure Lengend Snippet: ( A ) Experimental design: Murine DRG cultures were pre-treated with either vehicle or ML339, treated with CXCL16 or CXCL16 + ML339, and then followed by a positive control stimulus, KCl. ( B ) Quantification of percent responsive cells to CXCL16 stimulation in the presence and absence of CXCR6 antagonist, ML339. Total number of responsive cells is detailed for each sex. ( C ) Representative images of each stage of the experiment – pretreatment, treatment, positive control. ( D ) Representative line plots showing ΔF/Fo of a single responsive cell (responds to KCl) for each condition.

Article Snippet: To assess the disease-promoting effects of CXCL16 in healthy joints, CXCL16 (R&D Systems, Cat. #503-CX) (0.25 ng or 25 ng in 4 µL of sterile PBS) was injected for five consecutive days into one knee joint, and vehicle was injected in the contralateral joint (n=3 male, n=3 female per dose).

Techniques: Positive Control

Journal: PLOS Pathogens

Article Title: The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney

doi: 10.1371/journal.ppat.1012969

Figure Lengend Snippet: (A) CXCL16 mRNA expression in the kidney during MuPyV infection. Expression is shown as fold change relative to sham infected samples. Data are from three independent experiments (n = 10-11). (B) Expression of NKCC2 [marks the ascending loop of Henle ], CD8, and CXCL16 in epithelia in sham-infected and 8 dpi kidneys; bottom right photomicrographs are merged images. Representative of two independent experiments. (C) CXCL16 expression in sham-infected, 4 dpi, and 8 dpi kidney lysates (left). Western blot image is representative of two independent experiments with each lane indicating protein lysate from kidneys of individual mice. Protein band intensity quantification for sCXCL16 was normalized to β-actin and analyzed by ImageLab and normalized to the loading control (right). Data are combined from two independent experiments (n = 3-5). (D) Experimental design of in vivo CXCL16 mAb administration. Mice were administered 250 µg of CXCL16 mAb or control rat IgG every two days from days 4-14 post infection and euthanized at 15 dpi. Numbers of CD45 mAb i.v.-negative, CD8 + CD44 + D b -LT359 tetramer + T cells and CD4 + CD44 + T cells in kidneys and spleens of infected mice given anti-CXCL16 or control rat IgG. Data were analyzed by one-way ANOVA (A and C) and by multiple Mann-Whitney tests (D).

Article Snippet: For CXCL16 neutralization, mice were infected with MuPyV and received 250 μg of anti-mouse CXCL16 mAb (clone 12-81, BioXCell) i.p. on alternate days from days 4-14 post infection or control rat IgG (Jackson ImmunoResearch Laboratories).

Techniques: Expressing, Infection, Western Blot, Control, In Vivo, MANN-WHITNEY

Journal: PLOS Pathogens

Article Title: The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney

doi: 10.1371/journal.ppat.1012969

Figure Lengend Snippet: (A) Dense lymphoplasmacytic infiltrate surrounding and infiltrating cortical tubules (H&E, x400). (B) Immunohistochemical staining for Large T antigen in nuclei of tubular epithelium (x250). (C) Expression of CXCR6 on infiltrating CD8 + cells. Photomicrographs (right) are enlarged images in the white squares (left); bottom right are merged images. No 1 o , no primary antibody. (D) Log-fold change of CXCL16 and CXCR6 across four independent studies, each comparing KTx biopsies from patients with PVAN and stable graft function. The error bars indicate the 95% confidence interval of log-fold change, with horizontal dashed grey line indicating log-fold change = 0, or no difference. GSE120495 is an RNA-seq study, while remaining studies are microarray based. Given the heterogeneity of the data, a Cauchy combination method with uniform weights was employed to integrate the p-values across these studies. The combined p-values for CXCL16 = 0.000337 and CXCR6 = 2.72x10 -05 . ns, non-significant at adjusted p-value > 0.05; *, statistical significance at adjusted p-value ≤ 0.05; **, statistical significance at adjusted p-value ≤ 0.01; ***, statistical significance at adjusted p-value ≤ 0.001.

Article Snippet: For CXCL16 neutralization, mice were infected with MuPyV and received 250 μg of anti-mouse CXCL16 mAb (clone 12-81, BioXCell) i.p. on alternate days from days 4-14 post infection or control rat IgG (Jackson ImmunoResearch Laboratories).

Techniques: Immunohistochemical staining, Staining, Expressing, RNA Sequencing, Microarray

Journal: PLOS Pathogens

Article Title: The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney

doi: 10.1371/journal.ppat.1012969

Figure Lengend Snippet: Summary of differential gene expression of CXCL16 and CXCR6 in four studies of KTx biopsies with PVAN. Because of the heterogeneity of the data (i.e., one RNA-seq, three microarray), a Cauchy combination method with uniform weights was employed to integrate the p-values across these studies. P-values significant after false discover rate (FDR) correction are bolded and italicized in the Adj. P-value column. Cauchy combined p-values < 0.05 are bolded and italicized.

Article Snippet: For CXCL16 neutralization, mice were infected with MuPyV and received 250 μg of anti-mouse CXCL16 mAb (clone 12-81, BioXCell) i.p. on alternate days from days 4-14 post infection or control rat IgG (Jackson ImmunoResearch Laboratories).

Techniques: Gene Expression, Microarray

Journal: PLOS Pathogens

Article Title: The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney

doi: 10.1371/journal.ppat.1012969

Figure Lengend Snippet: (A) CXCL16 mRNA expression in the kidney during MuPyV infection. Expression is shown as fold change relative to sham infected samples. Data are from three independent experiments (n = 10-11). (B) Expression of NKCC2 [marks the ascending loop of Henle ], CD8, and CXCL16 in epithelia in sham-infected and 8 dpi kidneys; bottom right photomicrographs are merged images. Representative of two independent experiments. (C) CXCL16 expression in sham-infected, 4 dpi, and 8 dpi kidney lysates (left). Western blot image is representative of two independent experiments with each lane indicating protein lysate from kidneys of individual mice. Protein band intensity quantification for sCXCL16 was normalized to β-actin and analyzed by ImageLab and normalized to the loading control (right). Data are combined from two independent experiments (n = 3-5). (D) Experimental design of in vivo CXCL16 mAb administration. Mice were administered 250 µg of CXCL16 mAb or control rat IgG every two days from days 4-14 post infection and euthanized at 15 dpi. Numbers of CD45 mAb i.v.-negative, CD8 + CD44 + D b -LT359 tetramer + T cells and CD4 + CD44 + T cells in kidneys and spleens of infected mice given anti-CXCL16 or control rat IgG. Data were analyzed by one-way ANOVA (A and C) and by multiple Mann-Whitney tests (D).

Article Snippet: For CXCL16 neutralization, mice were infected with MuPyV and received 250 μg of anti-mouse CXCL16 mAb (clone 12-81, BioXCell) i.p. on alternate days from days 4-14 post infection or control rat IgG (Jackson ImmunoResearch Laboratories).

Techniques: Expressing, Infection, Western Blot, Control, In Vivo, MANN-WHITNEY

Journal: PLOS Pathogens

Article Title: The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney

doi: 10.1371/journal.ppat.1012969

Figure Lengend Snippet: (A) Dense lymphoplasmacytic infiltrate surrounding and infiltrating cortical tubules (H&E, x400). (B) Immunohistochemical staining for Large T antigen in nuclei of tubular epithelium (x250). (C) Expression of CXCR6 on infiltrating CD8 + cells. Photomicrographs (right) are enlarged images in the white squares (left); bottom right are merged images. No 1 o , no primary antibody. (D) Log-fold change of CXCL16 and CXCR6 across four independent studies, each comparing KTx biopsies from patients with PVAN and stable graft function. The error bars indicate the 95% confidence interval of log-fold change, with horizontal dashed grey line indicating log-fold change = 0, or no difference. GSE120495 is an RNA-seq study, while remaining studies are microarray based. Given the heterogeneity of the data, a Cauchy combination method with uniform weights was employed to integrate the p-values across these studies. The combined p-values for CXCL16 = 0.000337 and CXCR6 = 2.72x10 -05 . ns, non-significant at adjusted p-value > 0.05; *, statistical significance at adjusted p-value ≤ 0.05; **, statistical significance at adjusted p-value ≤ 0.01; ***, statistical significance at adjusted p-value ≤ 0.001.

Article Snippet: For CXCL16 neutralization, mice were infected with MuPyV and received 250 μg of anti-mouse CXCL16 mAb (clone 12-81, BioXCell) i.p. on alternate days from days 4-14 post infection or control rat IgG (Jackson ImmunoResearch Laboratories).

Techniques: Immunohistochemical staining, Staining, Expressing, RNA Sequencing, Microarray

Journal: PLOS Pathogens

Article Title: The CXCR6-CXCL16 axis mediates T cell control of polyomavirus infection in the kidney

doi: 10.1371/journal.ppat.1012969

Figure Lengend Snippet: Summary of differential gene expression of CXCL16 and CXCR6 in four studies of KTx biopsies with PVAN. Because of the heterogeneity of the data (i.e., one RNA-seq, three microarray), a Cauchy combination method with uniform weights was employed to integrate the p-values across these studies. P-values significant after false discover rate (FDR) correction are bolded and italicized in the Adj. P-value column. Cauchy combined p-values < 0.05 are bolded and italicized.

Article Snippet: For CXCL16 neutralization, mice were infected with MuPyV and received 250 μg of anti-mouse CXCL16 mAb (clone 12-81, BioXCell) i.p. on alternate days from days 4-14 post infection or control rat IgG (Jackson ImmunoResearch Laboratories).

Techniques: Gene Expression, Microarray