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mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. 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mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"UBERON-AE","denotations":[{"id":"T69","span":{"begin":667,"end":673},"obj":"http://purl.obolibrary.org/obo/UBERON_0002106"},{"id":"T70","span":{"begin":751,"end":762},"obj":"http://purl.obolibrary.org/obo/UBERON_0002371"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"GO-BP","denotations":[{"id":"T700","span":{"begin":1356,"end":1375},"obj":"http://purl.obolibrary.org/obo/GO_0001816"},{"id":"T701","span":{"begin":148,"end":160},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T702","span":{"begin":1547,"end":1559},"obj":"http://purl.obolibrary.org/obo/GO_0006954"},{"id":"T703","span":{"begin":236,"end":245},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T704","span":{"begin":983,"end":992},"obj":"http://purl.obolibrary.org/obo/GO_0046903"},{"id":"T705","span":{"begin":288,"end":296},"obj":"http://purl.obolibrary.org/obo/GO_0007349"},{"id":"T706","span":{"begin":965,"end":978},"obj":"http://purl.obolibrary.org/obo/GO_0006351"},{"id":"T707","span":{"begin":1088,"end":1107},"obj":"http://purl.obolibrary.org/obo/GO_0051092"},{"id":"T708","span":{"begin":1088,"end":1117},"obj":"http://purl.obolibrary.org/obo/GO_1901224"},{"id":"T709","span":{"begin":1102,"end":1117},"obj":"http://purl.obolibrary.org/obo/GO_0038061"},{"id":"T710","span":{"begin":1108,"end":1117},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T711","span":{"begin":1203,"end":1212},"obj":"http://purl.obolibrary.org/obo/GO_0023052"},{"id":"T712","span":{"begin":1140,"end":1144},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T713","span":{"begin":1169,"end":1172},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T714","span":{"begin":1198,"end":1202},"obj":"http://purl.obolibrary.org/obo/GO_0008384"},{"id":"T715","span":{"begin":1203,"end":1221},"obj":"http://purl.obolibrary.org/obo/GO_0007165"},{"id":"T716","span":{"begin":1307,"end":1326},"obj":"http://purl.obolibrary.org/obo/GO_0042088"},{"id":"T717","span":{"begin":1311,"end":1326},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T718","span":{"begin":1575,"end":1590},"obj":"http://purl.obolibrary.org/obo/GO_0006955"},{"id":"T719","span":{"begin":1311,"end":1341},"obj":"http://purl.obolibrary.org/obo/GO_0002922"},{"id":"T720","span":{"begin":1311,"end":1341},"obj":"http://purl.obolibrary.org/obo/GO_0045089"},{"id":"T721","span":{"begin":1311,"end":1341},"obj":"http://purl.obolibrary.org/obo/GO_0050778"},{"id":"T722","span":{"begin":1311,"end":1341},"obj":"http://purl.obolibrary.org/obo/GO_0002821"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"GO-MF","denotations":[{"id":"T724","span":{"begin":1140,"end":1144},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T725","span":{"begin":1169,"end":1172},"obj":"http://purl.obolibrary.org/obo/GO_0004707"},{"id":"T726","span":{"begin":1198,"end":1202},"obj":"http://purl.obolibrary.org/obo/GO_0008384"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"GO-CC","denotations":[{"id":"T727","span":{"begin":387,"end":392},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T728","span":{"begin":781,"end":786},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T729","span":{"begin":1405,"end":1410},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"sentences","denotations":[{"id":"T108","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"T109","span":{"begin":101,"end":283},"obj":"Sentence"},{"id":"T110","span":{"begin":284,"end":376},"obj":"Sentence"},{"id":"T111","span":{"begin":377,"end":547},"obj":"Sentence"},{"id":"T112","span":{"begin":548,"end":674},"obj":"Sentence"},{"id":"T113","span":{"begin":675,"end":909},"obj":"Sentence"},{"id":"T114","span":{"begin":910,"end":1061},"obj":"Sentence"},{"id":"T115","span":{"begin":1062,"end":1234},"obj":"Sentence"},{"id":"T116","span":{"begin":1235,"end":1411},"obj":"Sentence"},{"id":"T117","span":{"begin":1412,"end":1591},"obj":"Sentence"},{"id":"T3","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"T4","span":{"begin":101,"end":283},"obj":"Sentence"},{"id":"T5","span":{"begin":284,"end":376},"obj":"Sentence"},{"id":"T6","span":{"begin":377,"end":547},"obj":"Sentence"},{"id":"T7","span":{"begin":548,"end":674},"obj":"Sentence"},{"id":"T8","span":{"begin":675,"end":909},"obj":"Sentence"},{"id":"T9","span":{"begin":910,"end":1061},"obj":"Sentence"},{"id":"T10","span":{"begin":1062,"end":1234},"obj":"Sentence"},{"id":"T11","span":{"begin":1235,"end":1411},"obj":"Sentence"},{"id":"T12","span":{"begin":1412,"end":1591},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"ICD10","denotations":[{"id":"T723","span":{"begin":208,"end":218},"obj":"http://purl.bioontology.org/ontology/ICD10/L30.9"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

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The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

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mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

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The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

{"project":"bionlp-st-ge-2016-uniprot","denotations":[{"id":"T668","span":{"begin":29,"end":36},"obj":"Q9H0F6"},{"id":"T669","span":{"begin":109,"end":114},"obj":"Q9H0F6"},{"id":"T670","span":{"begin":462,"end":469},"obj":"Q9H0F6"},{"id":"T671","span":{"begin":584,"end":591},"obj":"Q9H0F6"},{"id":"T672","span":{"begin":888,"end":892},"obj":"P25942"},{"id":"T673","span":{"begin":894,"end":898},"obj":"P33681"},{"id":"T674","span":{"begin":904,"end":908},"obj":"P42081"},{"id":"T675","span":{"begin":930,"end":937},"obj":"Q9H0F6"},{"id":"T676","span":{"begin":1023,"end":1026},"obj":"P05231"},{"id":"T677","span":{"begin":1037,"end":1042},"obj":"P04141"},{"id":"T678","span":{"begin":1131,"end":1136},"obj":"P28482"},{"id":"T679","span":{"begin":1140,"end":1144},"obj":"P27361"},{"id":"T680","span":{"begin":1152,"end":1158},"obj":"Q15759"},{"id":"T681","span":{"begin":1169,"end":1172},"obj":"P53778"},{"id":"T682","span":{"begin":1169,"end":1172},"obj":"Q16539"},{"id":"T683","span":{"begin":1169,"end":1172},"obj":"Q15759"},{"id":"T684","span":{"begin":1169,"end":1172},"obj":"O15264"},{"id":"T685","span":{"begin":1198,"end":1202},"obj":"Q9UHD2"},{"id":"T686","span":{"begin":1398,"end":1401},"obj":"P01730"},{"id":"T687","span":{"begin":1435,"end":1442},"obj":"Q9H0F6"}],"namespaces":[{"prefix":"_base","uri":"http://www.uniprot.org/uniprot/"}],"text":"Spontaneous mutations of the Sharpin (SHANK-associated RH domain-interacting protein, other aliases: Rbckl1, Sipl1) gene in mice result in systemic inflammation that is characterized by chronic proliferative dermatitis and dysregulated secretion of T helper1 (Th1) and Th2 cytokines. The cellular and molecular mechanisms underlying this inflammatory phenotype remain elusive. Dendritic cells may contribute to the initiation and progression of the phenotype of SHARPIN-deficient mice because of their pivotal role in innate and adaptive immunity. Here we show by flow cytometry that SHARPIN- deficiency did not alter the distribution of different DC subtypes in the spleen. In response to TOLL-like receptor (TLR) agonists LPS and poly I:C, cultured bone marrow-derived dendritic cells (BMDC) from WT and mutant mice exhibited similar increases in expression of co-stimulatory molecules CD40, CD80, and CD86. However, stimulated SHARPIN-deficient BMDC had reduced transcription and secretion of pro-inflammatory mediators IL6, IL12P70, GMCSF, and nitric oxide. Mutant BMDC had defective activation of NF-κB signaling, whereas the MAPK1/3 (ERK1/2) and MAPK11/12/13/14 (p38 MAP kinase isoforms) and TBK1 signaling pathways were intact. A mixed lymphocyte reaction showed that mutant BMDC only induced a weak Th1 immune response but stimulated increased Th2 cytokine production from allogeneic naïve CD4+ T cells. In conclusion, loss of Sharpin in mice significantly affects the immune function of DC and this may partially account for the systemic inflammation and Th2-biased immune response.\n"}

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