Solved

Passage

Question 236

Multiple Choice

Passage
Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) .
Passage Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) . <strong>Figure 1</strong>  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) . <strong>Figure 2</strong>  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) . Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486. -Which graphic shows the expected results of Experiment 3? A) B) C) D) Figure 1  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) .
Passage Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) . <strong>Figure 1</strong>  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) . <strong>Figure 2</strong>  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) . Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486. -Which graphic shows the expected results of Experiment 3? A) B) C) D) Figure 2  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) .
Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486.
-Which graphic shows the expected results of Experiment 3?


A) Passage Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) . <strong>Figure 1</strong>  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) . <strong>Figure 2</strong>  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) . Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486. -Which graphic shows the expected results of Experiment 3? A) B) C) D)
B) Passage Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) . <strong>Figure 1</strong>  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) . <strong>Figure 2</strong>  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) . Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486. -Which graphic shows the expected results of Experiment 3? A) B) C) D)
C) Passage Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) . <strong>Figure 1</strong>  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) . <strong>Figure 2</strong>  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) . Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486. -Which graphic shows the expected results of Experiment 3? A) B) C) D)
D) Passage Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic synovial (joint) inflammation.  RA immunopathogenesis involves LFA-1, a surface receptor found on leukocytes that is composed of an α-chain (CD11a) and a β-chain (CD18) .  The binding of LFA-1 to ICAM-1, an adhesion protein on the surface of B cells and endothelial cells, stimulates the migration of leukocytes to specific areas of inflammation.  After successful LFA-1/ICAM-1 binding, CD18 is released into the plasma and synovial fluid (SF) , where it exists in soluble form (sCD18) .  The levels of sCD18 in SF can be used as a marker for inflammation in RA.CD18 release has been shown to increase in response to tumor necrosis factor (TNF) , a pro-inflammatory cytokine involved in the inflammatory response of RA.  In patients with newly diagnosed and untreated RA (eRA) , leukocytes produce adequate quantities of LFA-1 and plasma sCD18 levels are unchanged.  However, over time there is dysregulation of LFA-1 synthesis and an increase in competition for ICAM-1 by other ligands, leading to a reduction in CD18 shedding.  As a result, sCD18 is decreased in patients with chronic RA (cRA) .Experiment 1An immunofluorescence assay was used to measure plasma sCD18 levels in patients with eRA and cRA, and in age- and gender-matched healthy controls (HC) . <strong>Figure 1</strong>  Baseline sCD18 measurements (Note: 50% of data points are below the median value; median = line inside the box.) Experiment 2Clinical assessments were performed in eRA patients to establish a baseline disease status.  eRA patients were assigned DAS28CRP scores measured by RA-specific laboratory values.  This was followed by treatment with anti-inflammatory drugs.  DAS28CRP scores were calculated at 3-month intervals for 12 months, with lower scores indicating decreased RA severity (Figure 2) . <strong>Figure 2</strong>  DAS28CRP scores in eRA patientsExperiment 3Heterogeneous populations of mononuclear cells were cultured from the synovial fluid (SFMC) and peripheral blood (PBMC) of eRA patients during an acute exacerbation of their symptoms.  sCD18 levels were measured in SFMCs and PBMCs that were untreated, treated with TNF, or treated with monoclonal antibodies targeting TNF (anti-TNF) . Adapted from Kragstrup TW, Jalilian B, Keller KK, et al. Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response. PLoS ONE. 2016;11(2) :e0148486. -Which graphic shows the expected results of Experiment 3? A) B) C) D)

Correct Answer:

verifed

Verified

Unlock this answer now
Get Access to more Verified Answers free of charge

Related Questions

Q231: Passage<br>Mitochondria are thought to have been independent

Q232: Passage<br>Obstructive respiratory illnesses are characterized by an

Q233: One function of endothelial cells is to:<br>A)contract

Q234: Compared to the blood flowing into the

Q235: Passage<br>Lipopolysaccharides (LPS) found in gram-negative bacterial cells

Q237: Passage<br>Within the Actinopterygii (bony fish) lineage, marine

Q238: Which of the following cellular processes would

Q239: Passage<br>Each time a eukaryotic cell replicates its

Q240: Passage<br>A 6-day-old, genotypically normal (46,XX) female patient

Q241: Which of the following is generally true