Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity
Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multip...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yeremenko, Nataliya [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2021transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle - 2011transfer abstract, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:20 ; year:2021 ; number:6 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.autrev.2021.102833 |
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| 520 | |a Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. | ||
| 520 | |a Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. | ||
| 700 | 1 | |a Danger, Richard |4 oth | |
| 700 | 1 | |a Baeten, Dominique |4 oth | |
| 700 | 1 | |a Tomilin, Alexey |4 oth | |
| 700 | 1 | |a Brouard, Sophie |4 oth | |
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10.1016/j.autrev.2021.102833 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001431.pica (DE-627)ELV053986369 (ELSEVIER)S1568-9972(21)00105-1 DE-627 ger DE-627 rakwb eng 540 VZ 660 VZ 540 VZ BIODIV DE-30 fid 42.13 bkl Yeremenko, Nataliya verfasserin aut Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Danger, Richard oth Baeten, Dominique oth Tomilin, Alexey oth Brouard, Sophie oth Enthalten in Elsevier Science Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle 2011transfer abstract Amsterdam [u.a.] (DE-627)ELV020724853 volume:20 year:2021 number:6 pages:0 https://doi.org/10.1016/j.autrev.2021.102833 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 42.13 Molekularbiologie VZ AR 20 2021 6 0 |
| spelling |
10.1016/j.autrev.2021.102833 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001431.pica (DE-627)ELV053986369 (ELSEVIER)S1568-9972(21)00105-1 DE-627 ger DE-627 rakwb eng 540 VZ 660 VZ 540 VZ BIODIV DE-30 fid 42.13 bkl Yeremenko, Nataliya verfasserin aut Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Danger, Richard oth Baeten, Dominique oth Tomilin, Alexey oth Brouard, Sophie oth Enthalten in Elsevier Science Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle 2011transfer abstract Amsterdam [u.a.] (DE-627)ELV020724853 volume:20 year:2021 number:6 pages:0 https://doi.org/10.1016/j.autrev.2021.102833 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 42.13 Molekularbiologie VZ AR 20 2021 6 0 |
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10.1016/j.autrev.2021.102833 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001431.pica (DE-627)ELV053986369 (ELSEVIER)S1568-9972(21)00105-1 DE-627 ger DE-627 rakwb eng 540 VZ 660 VZ 540 VZ BIODIV DE-30 fid 42.13 bkl Yeremenko, Nataliya verfasserin aut Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Danger, Richard oth Baeten, Dominique oth Tomilin, Alexey oth Brouard, Sophie oth Enthalten in Elsevier Science Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle 2011transfer abstract Amsterdam [u.a.] (DE-627)ELV020724853 volume:20 year:2021 number:6 pages:0 https://doi.org/10.1016/j.autrev.2021.102833 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 42.13 Molekularbiologie VZ AR 20 2021 6 0 |
| allfieldsGer |
10.1016/j.autrev.2021.102833 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001431.pica (DE-627)ELV053986369 (ELSEVIER)S1568-9972(21)00105-1 DE-627 ger DE-627 rakwb eng 540 VZ 660 VZ 540 VZ BIODIV DE-30 fid 42.13 bkl Yeremenko, Nataliya verfasserin aut Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Danger, Richard oth Baeten, Dominique oth Tomilin, Alexey oth Brouard, Sophie oth Enthalten in Elsevier Science Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle 2011transfer abstract Amsterdam [u.a.] (DE-627)ELV020724853 volume:20 year:2021 number:6 pages:0 https://doi.org/10.1016/j.autrev.2021.102833 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 42.13 Molekularbiologie VZ AR 20 2021 6 0 |
| allfieldsSound |
10.1016/j.autrev.2021.102833 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001431.pica (DE-627)ELV053986369 (ELSEVIER)S1568-9972(21)00105-1 DE-627 ger DE-627 rakwb eng 540 VZ 660 VZ 540 VZ BIODIV DE-30 fid 42.13 bkl Yeremenko, Nataliya verfasserin aut Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. Danger, Richard oth Baeten, Dominique oth Tomilin, Alexey oth Brouard, Sophie oth Enthalten in Elsevier Science Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle 2011transfer abstract Amsterdam [u.a.] (DE-627)ELV020724853 volume:20 year:2021 number:6 pages:0 https://doi.org/10.1016/j.autrev.2021.102833 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 42.13 Molekularbiologie VZ AR 20 2021 6 0 |
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Enthalten in Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle Amsterdam [u.a.] volume:20 year:2021 number:6 pages:0 |
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Enthalten in Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle Amsterdam [u.a.] volume:20 year:2021 number:6 pages:0 |
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Synthesis and anti-hepatitis B virus activity of acyclovir conjugated stearic acid-g-chitosan oligosaccharide micelle |
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Yeremenko, Nataliya @@aut@@ Danger, Richard @@oth@@ Baeten, Dominique @@oth@@ Tomilin, Alexey @@oth@@ Brouard, Sophie @@oth@@ |
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Transcriptional regulator BOB.1: Molecular mechanisms and emerging role in chronic inflammation and autoimmunity |
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Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. |
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Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. |
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Lymphocytes constitute an essential and potent effector compartment of the immune system. Therefore, their development and functions must be strictly regulated to avoid inappropriate immune responses, such as autoimmune reactions. Several lines of evidence from genetics (e.g. association with multiple sclerosis and primary biliary cirrhosis), human expression studies (e.g. increased expression in target tissues and draining lymph nodes of patients with autoimmune diseases), animal models (e.g. loss of functional protein protects animals from the development of collagen-induced arthritis, experimental autoimmune encephalomyelitis, type 1 diabetes, bleomycin-induced fibrosis) strongly support a causal link between the aberrant expression of the lymphocyte-restricted transcriptional regulator BOB.1 and the development of autoimmune diseases. In this review, we summarize the current knowledge of unusual structural and functional plasticity of BOB.1, stringent regulation of its expression, and the pivotal role that BOB.1 plays in shaping B- and T-cell responses. We discuss recent developments highlighting the significant contribution of BOB.1 to the pathogenesis of autoimmune diseases and how to leverage our knowledge to target this regulator to treat autoimmune tissue inflammation. |
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