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ifn λ3 il 28b  (R&D Systems)


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    R&D Systems ifn λ3 il 28b
    Ifn λ3 Il 28b, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 9 article reviews
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    Activity levels of <t>IFN-I,</t> IFN-II, and IFN-III in patients from the SPARE cohort (A‒C) HEK-Blue IFN-α/β (A), HEK-Blue IFN-γ (B), and HEK-Blue IFN-λ (C) cells were incubated with increasing amounts of IFN-α6, IFN-γ, and <t>IFN-λ3.</t> The cells only detected their specific IFN with a range of 1.0–2,000 IU/mL for IFN-I and IFN-III and from 1 to 160 IU/mL for IFN-II. Experiments were performed in duplicate. Error bars represent the lower and upper values. (D‒F) Activity levels of IFN-I, IFN-II, and IFN-III in SLE ( n = 191), and healthy controls (HCs) ( n = 56). Whiskers indicate the lower and upper IFN values up to 1.5 times the interquartile range of the box. Samples with elevated levels of IFN-I, IFN-II, or IFN-III are colored in red. Cutoff was determined by ROC curve analysis with a 95% specificity vs. HCs. Elevated levels of IFN were set at 5.17, 2.9, and 5.0 IU/mL for IFN-I, IFN-II, and IFN-III, respectively. In patients with serial samples, only the first sample was included in the analysis. p values were obtained using Student’s t test. ∗∗∗∗ p < 0.0001. (G) Venn diagram showing the intersection between elevated IFN types in patients with SLE. (H‒J) Correlation between increased activity levels of IFN-I, IFN-II, and IFN-III. The relationship between the IFN types was evaluated using linear regression.
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    Activity levels of <t>IFN-I,</t> IFN-II, and IFN-III in patients from the SPARE cohort (A‒C) HEK-Blue IFN-α/β (A), HEK-Blue IFN-γ (B), and HEK-Blue IFN-λ (C) cells were incubated with increasing amounts of IFN-α6, IFN-γ, and <t>IFN-λ3.</t> The cells only detected their specific IFN with a range of 1.0–2,000 IU/mL for IFN-I and IFN-III and from 1 to 160 IU/mL for IFN-II. Experiments were performed in duplicate. Error bars represent the lower and upper values. (D‒F) Activity levels of IFN-I, IFN-II, and IFN-III in SLE ( n = 191), and healthy controls (HCs) ( n = 56). Whiskers indicate the lower and upper IFN values up to 1.5 times the interquartile range of the box. Samples with elevated levels of IFN-I, IFN-II, or IFN-III are colored in red. Cutoff was determined by ROC curve analysis with a 95% specificity vs. HCs. Elevated levels of IFN were set at 5.17, 2.9, and 5.0 IU/mL for IFN-I, IFN-II, and IFN-III, respectively. In patients with serial samples, only the first sample was included in the analysis. p values were obtained using Student’s t test. ∗∗∗∗ p < 0.0001. (G) Venn diagram showing the intersection between elevated IFN types in patients with SLE. (H‒J) Correlation between increased activity levels of IFN-I, IFN-II, and IFN-III. The relationship between the IFN types was evaluated using linear regression.
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    Activity levels of IFN-I, IFN-II, and IFN-III in patients from the SPARE cohort (A‒C) HEK-Blue IFN-α/β (A), HEK-Blue IFN-γ (B), and HEK-Blue IFN-λ (C) cells were incubated with increasing amounts of IFN-α6, IFN-γ, and IFN-λ3. The cells only detected their specific IFN with a range of 1.0–2,000 IU/mL for IFN-I and IFN-III and from 1 to 160 IU/mL for IFN-II. Experiments were performed in duplicate. Error bars represent the lower and upper values. (D‒F) Activity levels of IFN-I, IFN-II, and IFN-III in SLE ( n = 191), and healthy controls (HCs) ( n = 56). Whiskers indicate the lower and upper IFN values up to 1.5 times the interquartile range of the box. Samples with elevated levels of IFN-I, IFN-II, or IFN-III are colored in red. Cutoff was determined by ROC curve analysis with a 95% specificity vs. HCs. Elevated levels of IFN were set at 5.17, 2.9, and 5.0 IU/mL for IFN-I, IFN-II, and IFN-III, respectively. In patients with serial samples, only the first sample was included in the analysis. p values were obtained using Student’s t test. ∗∗∗∗ p < 0.0001. (G) Venn diagram showing the intersection between elevated IFN types in patients with SLE. (H‒J) Correlation between increased activity levels of IFN-I, IFN-II, and IFN-III. The relationship between the IFN types was evaluated using linear regression.

    Journal: Cell Reports Medicine

    Article Title: Uncoupling interferons and the interferon signature explains clinical and transcriptional subsets in SLE

    doi: 10.1016/j.xcrm.2024.101569

    Figure Lengend Snippet: Activity levels of IFN-I, IFN-II, and IFN-III in patients from the SPARE cohort (A‒C) HEK-Blue IFN-α/β (A), HEK-Blue IFN-γ (B), and HEK-Blue IFN-λ (C) cells were incubated with increasing amounts of IFN-α6, IFN-γ, and IFN-λ3. The cells only detected their specific IFN with a range of 1.0–2,000 IU/mL for IFN-I and IFN-III and from 1 to 160 IU/mL for IFN-II. Experiments were performed in duplicate. Error bars represent the lower and upper values. (D‒F) Activity levels of IFN-I, IFN-II, and IFN-III in SLE ( n = 191), and healthy controls (HCs) ( n = 56). Whiskers indicate the lower and upper IFN values up to 1.5 times the interquartile range of the box. Samples with elevated levels of IFN-I, IFN-II, or IFN-III are colored in red. Cutoff was determined by ROC curve analysis with a 95% specificity vs. HCs. Elevated levels of IFN were set at 5.17, 2.9, and 5.0 IU/mL for IFN-I, IFN-II, and IFN-III, respectively. In patients with serial samples, only the first sample was included in the analysis. p values were obtained using Student’s t test. ∗∗∗∗ p < 0.0001. (G) Venn diagram showing the intersection between elevated IFN types in patients with SLE. (H‒J) Correlation between increased activity levels of IFN-I, IFN-II, and IFN-III. The relationship between the IFN types was evaluated using linear regression.

    Article Snippet: IFN-λ3 (IL-28B) , Gibco , Cat# PHC0894.

    Techniques: Activity Assay, Incubation

    Longitudinal patterns of IFN type and their association with markers of disease activity and treatment in SLE (A) Intraclass correlation coefficient (ICC) of increased IFN activity levels in patients with SLE ( n = 77) with more than 1 longitudinal sample. (B) Sankey diagram showing the flow of normal and increased IFN levels in patients with SLE ( n = 42) with three longitudinal samples. Normal = normal IFN; I = high IFN-I; I+ = high IFN-I plus high IFN-II or IFN-III; II = high IFN-II; III = high IFN-III; II + III = high IFN-II + IFN-III; I + II + III = elevation of the three IFN types. Node height represents the proportion of patients with SLE with the indicated elevation of IFNs at the time of visit. Visit 1: normal, 17% ( n = 7); I, 10% ( n = 4); I+, 5% ( n = 2); II, 12% ( n = 5); II + III, 31% ( n = 13); and I + II + III, 26% ( n = 11). Visit 2: normal, 18% ( n = 8); I, 7% ( n = 3); I+, 2% ( n = 1); II, 21% ( n = 9); II + III, 19% ( n = 8); I + II + III, 26% ( n = 11); and III, 5% ( n = 2). Visit 3: normal, 14% ( n = 6); I, 7% ( n = 3); I+, 3% ( n = 7); II, 7% ( n = 17); II + III, 31% ( n = 13); I + II + III, 21% ( n = 9); and III, 2% ( n = 1). Each flow or link between the nodes represents a single patient. (C) Trajectory of elevated IFN types along with SLEDAI, C3, C4, and anti-dsDNA in patients with SLE. To represent grouped trajectories, Z scores of elevated IFN type and disease activity markers (SLEDAI, C3, and dsDNA) were projected over disease duration using loess-fitted curves. (D) Correlation between disease activity markers and elevated IFN type obtained by a Bayesian mixed-effects model in patients with SLE adjusted by disease duration. (E) Mixed-effects multinomial regression model examining the association between treatment and elevated IFN groups at the time of visit. (F) Mixed-effects multinomial regression model analyzing the relationship between normal and elevated IFN groups with SLE disease activity. Mild (SLEDAI = 1–2), moderate (SLEDAI = 2–9), severe (SLEDAI ≥10). In (C) and (D), the data are from 322 visits from 184 patients. In (E) and (F), the data are from the visits of 177 patients. Other elevated IFN groups (i.e., IFN-I + IFN-II, IFN-I + III, and IFN-III alone) were excluded in (E) and (F) due to the small number of patients in each group. MMF, mofetil mycophenolate; AZA, azathioprine; MTX, methotrexate; HCQ, hydroxychloroquine; PDN, prednisone.

    Journal: Cell Reports Medicine

    Article Title: Uncoupling interferons and the interferon signature explains clinical and transcriptional subsets in SLE

    doi: 10.1016/j.xcrm.2024.101569

    Figure Lengend Snippet: Longitudinal patterns of IFN type and their association with markers of disease activity and treatment in SLE (A) Intraclass correlation coefficient (ICC) of increased IFN activity levels in patients with SLE ( n = 77) with more than 1 longitudinal sample. (B) Sankey diagram showing the flow of normal and increased IFN levels in patients with SLE ( n = 42) with three longitudinal samples. Normal = normal IFN; I = high IFN-I; I+ = high IFN-I plus high IFN-II or IFN-III; II = high IFN-II; III = high IFN-III; II + III = high IFN-II + IFN-III; I + II + III = elevation of the three IFN types. Node height represents the proportion of patients with SLE with the indicated elevation of IFNs at the time of visit. Visit 1: normal, 17% ( n = 7); I, 10% ( n = 4); I+, 5% ( n = 2); II, 12% ( n = 5); II + III, 31% ( n = 13); and I + II + III, 26% ( n = 11). Visit 2: normal, 18% ( n = 8); I, 7% ( n = 3); I+, 2% ( n = 1); II, 21% ( n = 9); II + III, 19% ( n = 8); I + II + III, 26% ( n = 11); and III, 5% ( n = 2). Visit 3: normal, 14% ( n = 6); I, 7% ( n = 3); I+, 3% ( n = 7); II, 7% ( n = 17); II + III, 31% ( n = 13); I + II + III, 21% ( n = 9); and III, 2% ( n = 1). Each flow or link between the nodes represents a single patient. (C) Trajectory of elevated IFN types along with SLEDAI, C3, C4, and anti-dsDNA in patients with SLE. To represent grouped trajectories, Z scores of elevated IFN type and disease activity markers (SLEDAI, C3, and dsDNA) were projected over disease duration using loess-fitted curves. (D) Correlation between disease activity markers and elevated IFN type obtained by a Bayesian mixed-effects model in patients with SLE adjusted by disease duration. (E) Mixed-effects multinomial regression model examining the association between treatment and elevated IFN groups at the time of visit. (F) Mixed-effects multinomial regression model analyzing the relationship between normal and elevated IFN groups with SLE disease activity. Mild (SLEDAI = 1–2), moderate (SLEDAI = 2–9), severe (SLEDAI ≥10). In (C) and (D), the data are from 322 visits from 184 patients. In (E) and (F), the data are from the visits of 177 patients. Other elevated IFN groups (i.e., IFN-I + IFN-II, IFN-I + III, and IFN-III alone) were excluded in (E) and (F) due to the small number of patients in each group. MMF, mofetil mycophenolate; AZA, azathioprine; MTX, methotrexate; HCQ, hydroxychloroquine; PDN, prednisone.

    Article Snippet: IFN-λ3 (IL-28B) , Gibco , Cat# PHC0894.

    Techniques: Activity Assay

    SLE disease subsets are predictive of increased activity levels of IFN types (A‒C) Effect of SLE activity features at time of visit on increased levels of IFN-I (A), IFN-II (B), and IFN-III (C). (D) Predictive value of normal and elevated IFN groups for specific SLEDAI items at the time of visit. (E) Increased activity levels of IFN-I, IFN-II, or IFN-III according to autoantibody positivity in SLE. (F) Predictive value of SLE autoantibodies for elevated IFN groups at the time of visit. In (D)–(F), other elevated IFN groups (i.e., IFN-I + IFN-II, IFN-I + IFN-III, and IFN-III alone) were excluded due to the small number of patients in each group. In (A)–(C) and (E), associations were evaluated using a mixed-effects linear regression model adjusted by disease duration. Data analysis included 322 visits from 184 patients. In (D) and (F), associations were evaluated using a mixed-effects multinomial logistic regression adjusted by disease duration. Data analysis included 300 visits from 177 patients. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

    Journal: Cell Reports Medicine

    Article Title: Uncoupling interferons and the interferon signature explains clinical and transcriptional subsets in SLE

    doi: 10.1016/j.xcrm.2024.101569

    Figure Lengend Snippet: SLE disease subsets are predictive of increased activity levels of IFN types (A‒C) Effect of SLE activity features at time of visit on increased levels of IFN-I (A), IFN-II (B), and IFN-III (C). (D) Predictive value of normal and elevated IFN groups for specific SLEDAI items at the time of visit. (E) Increased activity levels of IFN-I, IFN-II, or IFN-III according to autoantibody positivity in SLE. (F) Predictive value of SLE autoantibodies for elevated IFN groups at the time of visit. In (D)–(F), other elevated IFN groups (i.e., IFN-I + IFN-II, IFN-I + IFN-III, and IFN-III alone) were excluded due to the small number of patients in each group. In (A)–(C) and (E), associations were evaluated using a mixed-effects linear regression model adjusted by disease duration. Data analysis included 322 visits from 184 patients. In (D) and (F), associations were evaluated using a mixed-effects multinomial logistic regression adjusted by disease duration. Data analysis included 300 visits from 177 patients. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

    Article Snippet: IFN-λ3 (IL-28B) , Gibco , Cat# PHC0894.

    Techniques: Activity Assay

    Journal: Cell Reports Medicine

    Article Title: Uncoupling interferons and the interferon signature explains clinical and transcriptional subsets in SLE

    doi: 10.1016/j.xcrm.2024.101569

    Figure Lengend Snippet:

    Article Snippet: IFN-λ3 (IL-28B) , Gibco , Cat# PHC0894.

    Techniques: Expressing, Microarray, Software