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Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
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Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
1
Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
1
Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
1
Of STING reduces the overproduction of IFN and chronic inflammation [90]. Supporting this idea, gain-of-function mutations in TMEM173, gene encoding STING, were recently reported in subjects with a monogenic condition characterized by high IFN levels and vascular and pulmonary inflammation [91, 92]. Loss-of-function polymorphisms for STING are also known, however they have not yet been linked to a
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Tinucleosomal antibodies were reported with a mutation in exon 2 of DNAse type 1 [79], however this mutation has not been confirmed in other patient populations. Recently, study of seven consanguineous families with multiple SLE affected children by linkage analysis and exome sequencing identified loss-of-function mutations in DNASE1L3 as a monogenic cause of an SLE-like syndrome [80]. A strict Me
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Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu
1
Poptotic cells. Interestingly, complement also plays a role in T and B cell activation and complement deficiency may disrupt the balance of lymphoid cell activation. Deficiencies of the classical complement component pathway are likely to affect SLE pathogenesis by decreasing clearance of apoptotic cell debris and immune complexes (IC), resulting in increased self-antigen availability, and dysregu