Essay
Multiple sclerosis is an autoimmune disease of the central nervous system that leads to demyelination of the nerves. Symptoms include tingling, numbness, muscle weakness, problems with coordination and balance, as well as other neurological problems. To understand more about this disease, a mouse model has been developed in which mice are experimentally induced to generate an autoimmune response to autoantigens expressed on the myelin sheaths of nerves in the central nervous system and spinal cord. To investigate the major immune system component responsible for the disease symptoms in EAE, lines of knockout mice were tested for the development of this autoimmune disease. To induce disease, mice are immunized with a peptide of murine myelin oligodendrocyte glycoprotein (MOG) in complete Freund's adjuvant (an adjuvant containing killed mycobacteria). Then disease symptoms are monitored on a scale of 1-5, where 1 is mild disease and 5 is moribundity and death. In comparison to wild-type mice, mice deficient in IFN- and mice deficient in IL-17 were each tested for development of EAE. The results are shown in Figure Q3)30)A. ![Multiple sclerosis is an autoimmune disease of the central nervous system that leads to demyelination of the nerves. Symptoms include tingling, numbness, muscle weakness, problems with coordination and balance, as well as other neurological problems. To understand more about this disease, a mouse model has been developed in which mice are experimentally induced to generate an autoimmune response to autoantigens expressed on the myelin sheaths of nerves in the central nervous system and spinal cord. To investigate the major immune system component responsible for the disease symptoms in EAE, lines of knockout mice were tested for the development of this autoimmune disease. To induce disease, mice are immunized with a peptide of murine myelin oligodendrocyte glycoprotein (MOG) in complete Freund's adjuvant (an adjuvant containing killed mycobacteria). Then disease symptoms are monitored on a scale of 1-5, where 1 is mild disease and 5 is moribundity and death. In comparison to wild-type mice, mice deficient in IFN- \gamma and mice deficient in IL-17 were each tested for development of EAE. The results are shown in Figure Q3)30)A. or IL-17-deficient mice were immunized with MOG peptide in CFA, and 10 days later, lymph node cells were isolated, and were stimulated for 3 days with MOG peptide. T cells were then isolated from the cultures of wild-type lymph node cells, as were the T cells from the Il17<sup>-/-</sup> cultures. Wild-type or Il17<sup>-/-</sup> T cells were then adoptively transferred into naive wild-type recipient mice, which were then monitored for EAE disease symptoms. The incidence of mice showing clinical disease is shown in Figure 3)30)B; the labels indicate the source of the transferred T cells. b) Do these data confirm or refute your answer to (a)? Explain your reasoning. c) What is a likely explanation for the results seen when EAE is induced in IFN- \gamma -deficient mice compared to wild-type and IL-17-deficient mice? Vitamin D and its metabolites have shown to provide partial protection against several autoimmune diseases in mice, including EAE. These findings correlate with the fact that multiple sclerosis incidence is reduced in areas of high sunlight exposure, and is also reduced in individuals on diets high in Vitamin D. To examine the mechanism of this protective effect of Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)<sub>2</sub>D<sub>3</sub>], the active form of vitamin D in the body, was administered to mice starting at 2 weeks post-immunization with MOG+CFA. As a control, a second group of mice are given the vehicle used to dissolve the 1,25(OH)<sub>2</sub>D<sub>3</sub> on its own (vehicle control). 1,25(OH)<sub>2</sub>D<sub>3</sub> is known to act by binding to the vitamin D receptor (VDR), a protein that functions in transcriptional regulation. 1,25(OH)<sub>2</sub>D<sub>3</sub> enters cells, and binds to VDR. The activated VDR then migrates to the nucleus where it binds to DNA, functioning either as a transcriptional activator or as a repressor, depending on its binding partners. The results of 1,25(OH)<sub>2</sub>D<sub>3</sub> treatment on EAE induction are shown in Figure . In a second set of studies, naive CD4 T cells were isolated from wild-type mice, and were stimulated in vitro with anti-CD3/CD28 antibodies plus IL-6 and TGF- \beta for 3 days, and then expanded in IL-23 for an additional 4 days in the presence or absence of 1,25(OH)<sub>2</sub>D<sub>3</sub> or vehicle control. Following this, cells were restimulated with anti-CD3/CD28 antibodies, and 2 days later, supernatants were analyzed for IL-17 and IL-22, as shown in Figure. d) Given these data, propose a mechanism by which 1,25(OH)<sub>2</sub>D<sub>3</sub> is acting in the EAE disease model. Additional studies were performed in which mice were treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> (or vehicle control) starting at the time of immunization with MOG + CFA, and then analyzed two weeks later. CD4 T cells from the spleen or the spinal cord were stained with antibodies to CD25 and the transcription factor FoxP3, and the results are displayed in Figure. e) Based on the data shown above, what might be another role for 1,25(OH)<sub>2</sub>D<sub>3</sub> that contributes to the ability of this vitamin D metabolite to inhibit autoimmune diseases like EAE or multiple sclerosis?](https://d2lvgg3v3hfg70.cloudfront.net/TB1128/11eaa8f4_80d6_0e33_b44f_d551bfdbdeab_TB1128_00.jpg)
or IL-17-deficient mice were immunized with MOG peptide in CFA, and 10 days later, lymph node cells were isolated, and were stimulated for 3 days with MOG peptide. T cells were then isolated from the cultures of wild-type lymph node cells, as were the T cells from the Il17-/- cultures. Wild-type or Il17-/- T cells were then adoptively transferred into naive wild-type recipient mice, which were then monitored for EAE disease symptoms. The incidence of mice showing clinical disease is shown in Figure 3)30)B; the labels indicate the source of the transferred T cells. ![Multiple sclerosis is an autoimmune disease of the central nervous system that leads to demyelination of the nerves. Symptoms include tingling, numbness, muscle weakness, problems with coordination and balance, as well as other neurological problems. To understand more about this disease, a mouse model has been developed in which mice are experimentally induced to generate an autoimmune response to autoantigens expressed on the myelin sheaths of nerves in the central nervous system and spinal cord. To investigate the major immune system component responsible for the disease symptoms in EAE, lines of knockout mice were tested for the development of this autoimmune disease. To induce disease, mice are immunized with a peptide of murine myelin oligodendrocyte glycoprotein (MOG) in complete Freund's adjuvant (an adjuvant containing killed mycobacteria). Then disease symptoms are monitored on a scale of 1-5, where 1 is mild disease and 5 is moribundity and death. In comparison to wild-type mice, mice deficient in IFN- \gamma and mice deficient in IL-17 were each tested for development of EAE. The results are shown in Figure Q3)30)A. or IL-17-deficient mice were immunized with MOG peptide in CFA, and 10 days later, lymph node cells were isolated, and were stimulated for 3 days with MOG peptide. T cells were then isolated from the cultures of wild-type lymph node cells, as were the T cells from the Il17<sup>-/-</sup> cultures. Wild-type or Il17<sup>-/-</sup> T cells were then adoptively transferred into naive wild-type recipient mice, which were then monitored for EAE disease symptoms. The incidence of mice showing clinical disease is shown in Figure 3)30)B; the labels indicate the source of the transferred T cells. b) Do these data confirm or refute your answer to (a)? Explain your reasoning. c) What is a likely explanation for the results seen when EAE is induced in IFN- \gamma -deficient mice compared to wild-type and IL-17-deficient mice? Vitamin D and its metabolites have shown to provide partial protection against several autoimmune diseases in mice, including EAE. These findings correlate with the fact that multiple sclerosis incidence is reduced in areas of high sunlight exposure, and is also reduced in individuals on diets high in Vitamin D. To examine the mechanism of this protective effect of Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)<sub>2</sub>D<sub>3</sub>], the active form of vitamin D in the body, was administered to mice starting at 2 weeks post-immunization with MOG+CFA. As a control, a second group of mice are given the vehicle used to dissolve the 1,25(OH)<sub>2</sub>D<sub>3</sub> on its own (vehicle control). 1,25(OH)<sub>2</sub>D<sub>3</sub> is known to act by binding to the vitamin D receptor (VDR), a protein that functions in transcriptional regulation. 1,25(OH)<sub>2</sub>D<sub>3</sub> enters cells, and binds to VDR. The activated VDR then migrates to the nucleus where it binds to DNA, functioning either as a transcriptional activator or as a repressor, depending on its binding partners. The results of 1,25(OH)<sub>2</sub>D<sub>3</sub> treatment on EAE induction are shown in Figure . In a second set of studies, naive CD4 T cells were isolated from wild-type mice, and were stimulated in vitro with anti-CD3/CD28 antibodies plus IL-6 and TGF- \beta for 3 days, and then expanded in IL-23 for an additional 4 days in the presence or absence of 1,25(OH)<sub>2</sub>D<sub>3</sub> or vehicle control. Following this, cells were restimulated with anti-CD3/CD28 antibodies, and 2 days later, supernatants were analyzed for IL-17 and IL-22, as shown in Figure. d) Given these data, propose a mechanism by which 1,25(OH)<sub>2</sub>D<sub>3</sub> is acting in the EAE disease model. Additional studies were performed in which mice were treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> (or vehicle control) starting at the time of immunization with MOG + CFA, and then analyzed two weeks later. CD4 T cells from the spleen or the spinal cord were stained with antibodies to CD25 and the transcription factor FoxP3, and the results are displayed in Figure. e) Based on the data shown above, what might be another role for 1,25(OH)<sub>2</sub>D<sub>3</sub> that contributes to the ability of this vitamin D metabolite to inhibit autoimmune diseases like EAE or multiple sclerosis?](https://d2lvgg3v3hfg70.cloudfront.net/TB1128/11eaa8f4_80d6_0e34_b44f_35a869a3a7d1_TB1128_00.jpg)
b) Do these data confirm or refute your answer to (a)? Explain your reasoning.
c) What is a likely explanation for the results seen when EAE is induced in IFN- -deficient mice compared to wild-type and IL-17-deficient mice?
Vitamin D and its metabolites have shown to provide partial protection against several autoimmune diseases in mice, including EAE. These findings correlate with the fact that multiple sclerosis incidence is reduced in areas of high sunlight exposure, and is also reduced in individuals on diets high in Vitamin
D. To examine the mechanism of this protective effect of Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], the active form of vitamin D in the body, was administered to mice starting at 2 weeks post-immunization with MOG+CFA. As a control, a second group of mice are given the vehicle used to dissolve the 1,25(OH)2D3 on its own (vehicle control). 1,25(OH)2D3 is known to act by binding to the vitamin D receptor (VDR), a protein that functions in transcriptional regulation. 1,25(OH)2D3 enters cells, and binds to VDR. The activated VDR then migrates to the nucleus where it binds to DNA, functioning either as a transcriptional activator or as a repressor, depending on its binding partners. The results of 1,25(OH)2D3 treatment on EAE induction are shown in Figure .
![Multiple sclerosis is an autoimmune disease of the central nervous system that leads to demyelination of the nerves. Symptoms include tingling, numbness, muscle weakness, problems with coordination and balance, as well as other neurological problems. To understand more about this disease, a mouse model has been developed in which mice are experimentally induced to generate an autoimmune response to autoantigens expressed on the myelin sheaths of nerves in the central nervous system and spinal cord. To investigate the major immune system component responsible for the disease symptoms in EAE, lines of knockout mice were tested for the development of this autoimmune disease. To induce disease, mice are immunized with a peptide of murine myelin oligodendrocyte glycoprotein (MOG) in complete Freund's adjuvant (an adjuvant containing killed mycobacteria). Then disease symptoms are monitored on a scale of 1-5, where 1 is mild disease and 5 is moribundity and death. In comparison to wild-type mice, mice deficient in IFN- \gamma and mice deficient in IL-17 were each tested for development of EAE. The results are shown in Figure Q3)30)A. or IL-17-deficient mice were immunized with MOG peptide in CFA, and 10 days later, lymph node cells were isolated, and were stimulated for 3 days with MOG peptide. T cells were then isolated from the cultures of wild-type lymph node cells, as were the T cells from the Il17<sup>-/-</sup> cultures. Wild-type or Il17<sup>-/-</sup> T cells were then adoptively transferred into naive wild-type recipient mice, which were then monitored for EAE disease symptoms. The incidence of mice showing clinical disease is shown in Figure 3)30)B; the labels indicate the source of the transferred T cells. b) Do these data confirm or refute your answer to (a)? Explain your reasoning. c) What is a likely explanation for the results seen when EAE is induced in IFN- \gamma -deficient mice compared to wild-type and IL-17-deficient mice? Vitamin D and its metabolites have shown to provide partial protection against several autoimmune diseases in mice, including EAE. These findings correlate with the fact that multiple sclerosis incidence is reduced in areas of high sunlight exposure, and is also reduced in individuals on diets high in Vitamin D. To examine the mechanism of this protective effect of Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)<sub>2</sub>D<sub>3</sub>], the active form of vitamin D in the body, was administered to mice starting at 2 weeks post-immunization with MOG+CFA. As a control, a second group of mice are given the vehicle used to dissolve the 1,25(OH)<sub>2</sub>D<sub>3</sub> on its own (vehicle control). 1,25(OH)<sub>2</sub>D<sub>3</sub> is known to act by binding to the vitamin D receptor (VDR), a protein that functions in transcriptional regulation. 1,25(OH)<sub>2</sub>D<sub>3</sub> enters cells, and binds to VDR. The activated VDR then migrates to the nucleus where it binds to DNA, functioning either as a transcriptional activator or as a repressor, depending on its binding partners. The results of 1,25(OH)<sub>2</sub>D<sub>3</sub> treatment on EAE induction are shown in Figure . In a second set of studies, naive CD4 T cells were isolated from wild-type mice, and were stimulated in vitro with anti-CD3/CD28 antibodies plus IL-6 and TGF- \beta for 3 days, and then expanded in IL-23 for an additional 4 days in the presence or absence of 1,25(OH)<sub>2</sub>D<sub>3</sub> or vehicle control. Following this, cells were restimulated with anti-CD3/CD28 antibodies, and 2 days later, supernatants were analyzed for IL-17 and IL-22, as shown in Figure. d) Given these data, propose a mechanism by which 1,25(OH)<sub>2</sub>D<sub>3</sub> is acting in the EAE disease model. Additional studies were performed in which mice were treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> (or vehicle control) starting at the time of immunization with MOG + CFA, and then analyzed two weeks later. CD4 T cells from the spleen or the spinal cord were stained with antibodies to CD25 and the transcription factor FoxP3, and the results are displayed in Figure. e) Based on the data shown above, what might be another role for 1,25(OH)<sub>2</sub>D<sub>3</sub> that contributes to the ability of this vitamin D metabolite to inhibit autoimmune diseases like EAE or multiple sclerosis?](https://d2lvgg3v3hfg70.cloudfront.net/TB1128/11eaa8f4_80d6_3545_b44f_99b12fc2a040_TB1128_00.jpg)
In a second set of studies, naive CD4 T cells were isolated from wild-type mice, and were stimulated in vitro with anti-CD3/CD28 antibodies plus IL-6 and TGF- for 3 days, and then expanded in IL-23 for an additional 4 days in the presence or absence of 1,25(OH)2D3 or vehicle control. Following this, cells were restimulated with anti-CD3/CD28 antibodies, and 2 days later, supernatants were analyzed for IL-17 and IL-22, as shown in Figure.
![Multiple sclerosis is an autoimmune disease of the central nervous system that leads to demyelination of the nerves. Symptoms include tingling, numbness, muscle weakness, problems with coordination and balance, as well as other neurological problems. To understand more about this disease, a mouse model has been developed in which mice are experimentally induced to generate an autoimmune response to autoantigens expressed on the myelin sheaths of nerves in the central nervous system and spinal cord. To investigate the major immune system component responsible for the disease symptoms in EAE, lines of knockout mice were tested for the development of this autoimmune disease. To induce disease, mice are immunized with a peptide of murine myelin oligodendrocyte glycoprotein (MOG) in complete Freund's adjuvant (an adjuvant containing killed mycobacteria). Then disease symptoms are monitored on a scale of 1-5, where 1 is mild disease and 5 is moribundity and death. In comparison to wild-type mice, mice deficient in IFN- \gamma and mice deficient in IL-17 were each tested for development of EAE. The results are shown in Figure Q3)30)A. or IL-17-deficient mice were immunized with MOG peptide in CFA, and 10 days later, lymph node cells were isolated, and were stimulated for 3 days with MOG peptide. T cells were then isolated from the cultures of wild-type lymph node cells, as were the T cells from the Il17<sup>-/-</sup> cultures. Wild-type or Il17<sup>-/-</sup> T cells were then adoptively transferred into naive wild-type recipient mice, which were then monitored for EAE disease symptoms. The incidence of mice showing clinical disease is shown in Figure 3)30)B; the labels indicate the source of the transferred T cells. b) Do these data confirm or refute your answer to (a)? Explain your reasoning. c) What is a likely explanation for the results seen when EAE is induced in IFN- \gamma -deficient mice compared to wild-type and IL-17-deficient mice? Vitamin D and its metabolites have shown to provide partial protection against several autoimmune diseases in mice, including EAE. These findings correlate with the fact that multiple sclerosis incidence is reduced in areas of high sunlight exposure, and is also reduced in individuals on diets high in Vitamin D. To examine the mechanism of this protective effect of Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)<sub>2</sub>D<sub>3</sub>], the active form of vitamin D in the body, was administered to mice starting at 2 weeks post-immunization with MOG+CFA. As a control, a second group of mice are given the vehicle used to dissolve the 1,25(OH)<sub>2</sub>D<sub>3</sub> on its own (vehicle control). 1,25(OH)<sub>2</sub>D<sub>3</sub> is known to act by binding to the vitamin D receptor (VDR), a protein that functions in transcriptional regulation. 1,25(OH)<sub>2</sub>D<sub>3</sub> enters cells, and binds to VDR. The activated VDR then migrates to the nucleus where it binds to DNA, functioning either as a transcriptional activator or as a repressor, depending on its binding partners. The results of 1,25(OH)<sub>2</sub>D<sub>3</sub> treatment on EAE induction are shown in Figure . In a second set of studies, naive CD4 T cells were isolated from wild-type mice, and were stimulated in vitro with anti-CD3/CD28 antibodies plus IL-6 and TGF- \beta for 3 days, and then expanded in IL-23 for an additional 4 days in the presence or absence of 1,25(OH)<sub>2</sub>D<sub>3</sub> or vehicle control. Following this, cells were restimulated with anti-CD3/CD28 antibodies, and 2 days later, supernatants were analyzed for IL-17 and IL-22, as shown in Figure. d) Given these data, propose a mechanism by which 1,25(OH)<sub>2</sub>D<sub>3</sub> is acting in the EAE disease model. Additional studies were performed in which mice were treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> (or vehicle control) starting at the time of immunization with MOG + CFA, and then analyzed two weeks later. CD4 T cells from the spleen or the spinal cord were stained with antibodies to CD25 and the transcription factor FoxP3, and the results are displayed in Figure. e) Based on the data shown above, what might be another role for 1,25(OH)<sub>2</sub>D<sub>3</sub> that contributes to the ability of this vitamin D metabolite to inhibit autoimmune diseases like EAE or multiple sclerosis?](https://d2lvgg3v3hfg70.cloudfront.net/TB1128/11eaa8f4_80d6_3546_b44f_839d05512cde_TB1128_00.jpg)
d) Given these data, propose a mechanism by which 1,25(OH)2D3 is acting in the EAE disease model.
Additional studies were performed in which mice were treated with 1,25(OH)2D3 (or vehicle control) starting at the time of immunization with MOG + CFA, and then analyzed two weeks later. CD4 T cells from the spleen or the spinal cord were stained with antibodies to CD25 and the transcription factor FoxP3, and the results are displayed in Figure.
![Multiple sclerosis is an autoimmune disease of the central nervous system that leads to demyelination of the nerves. Symptoms include tingling, numbness, muscle weakness, problems with coordination and balance, as well as other neurological problems. To understand more about this disease, a mouse model has been developed in which mice are experimentally induced to generate an autoimmune response to autoantigens expressed on the myelin sheaths of nerves in the central nervous system and spinal cord. To investigate the major immune system component responsible for the disease symptoms in EAE, lines of knockout mice were tested for the development of this autoimmune disease. To induce disease, mice are immunized with a peptide of murine myelin oligodendrocyte glycoprotein (MOG) in complete Freund's adjuvant (an adjuvant containing killed mycobacteria). Then disease symptoms are monitored on a scale of 1-5, where 1 is mild disease and 5 is moribundity and death. In comparison to wild-type mice, mice deficient in IFN- \gamma and mice deficient in IL-17 were each tested for development of EAE. The results are shown in Figure Q3)30)A. or IL-17-deficient mice were immunized with MOG peptide in CFA, and 10 days later, lymph node cells were isolated, and were stimulated for 3 days with MOG peptide. T cells were then isolated from the cultures of wild-type lymph node cells, as were the T cells from the Il17<sup>-/-</sup> cultures. Wild-type or Il17<sup>-/-</sup> T cells were then adoptively transferred into naive wild-type recipient mice, which were then monitored for EAE disease symptoms. The incidence of mice showing clinical disease is shown in Figure 3)30)B; the labels indicate the source of the transferred T cells. b) Do these data confirm or refute your answer to (a)? Explain your reasoning. c) What is a likely explanation for the results seen when EAE is induced in IFN- \gamma -deficient mice compared to wild-type and IL-17-deficient mice? Vitamin D and its metabolites have shown to provide partial protection against several autoimmune diseases in mice, including EAE. These findings correlate with the fact that multiple sclerosis incidence is reduced in areas of high sunlight exposure, and is also reduced in individuals on diets high in Vitamin D. To examine the mechanism of this protective effect of Vitamin D, 1,25-dihydroxyvitamin D3 [1,25(OH)<sub>2</sub>D<sub>3</sub>], the active form of vitamin D in the body, was administered to mice starting at 2 weeks post-immunization with MOG+CFA. As a control, a second group of mice are given the vehicle used to dissolve the 1,25(OH)<sub>2</sub>D<sub>3</sub> on its own (vehicle control). 1,25(OH)<sub>2</sub>D<sub>3</sub> is known to act by binding to the vitamin D receptor (VDR), a protein that functions in transcriptional regulation. 1,25(OH)<sub>2</sub>D<sub>3</sub> enters cells, and binds to VDR. The activated VDR then migrates to the nucleus where it binds to DNA, functioning either as a transcriptional activator or as a repressor, depending on its binding partners. The results of 1,25(OH)<sub>2</sub>D<sub>3</sub> treatment on EAE induction are shown in Figure . In a second set of studies, naive CD4 T cells were isolated from wild-type mice, and were stimulated in vitro with anti-CD3/CD28 antibodies plus IL-6 and TGF- \beta for 3 days, and then expanded in IL-23 for an additional 4 days in the presence or absence of 1,25(OH)<sub>2</sub>D<sub>3</sub> or vehicle control. Following this, cells were restimulated with anti-CD3/CD28 antibodies, and 2 days later, supernatants were analyzed for IL-17 and IL-22, as shown in Figure. d) Given these data, propose a mechanism by which 1,25(OH)<sub>2</sub>D<sub>3</sub> is acting in the EAE disease model. Additional studies were performed in which mice were treated with 1,25(OH)<sub>2</sub>D<sub>3</sub> (or vehicle control) starting at the time of immunization with MOG + CFA, and then analyzed two weeks later. CD4 T cells from the spleen or the spinal cord were stained with antibodies to CD25 and the transcription factor FoxP3, and the results are displayed in Figure. e) Based on the data shown above, what might be another role for 1,25(OH)<sub>2</sub>D<sub>3</sub> that contributes to the ability of this vitamin D metabolite to inhibit autoimmune diseases like EAE or multiple sclerosis?](https://d2lvgg3v3hfg70.cloudfront.net/TB1128/11eaa8f4_80d6_3547_b44f_257e3eff8e57_TB1128_00.jpg)
e) Based on the data shown above, what might be another role for 1,25(OH)2D3 that contributes to the ability of this vitamin D metabolite to inhibit autoimmune diseases like EAE or multiple sclerosis?
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a) TH17 effector cells. Since...View Answer
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