Thelansis

 Complement Deficiencies (CD) cause susceptibility not only to bacterial infection but also to autoimmune disease. Genetically determined MBL deficiencies are observed in autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Observation of the low concentrations of MBL and other complement proteins (e.g. C1q, C1r, C4) and poor activation of the complement system are also characteristic findings of inactive SLE. Complement activation almost inevitably results in some degree of tissue destruction, as seen in rheumatic diseases such as SLE, RA, vasculitis, and antiphospholipid antibody syndrome. Interest in complement in inflammatory disease has led to the development of pharmacologic complement inhibitors such as eculizumab, a humanized monoclonal anti-C5 antibody approved for paroxysmal nocturnal hemoglobinuria. Inflammatory conditions also result from hereditary or acquired deficiencies of complement regulatory proteins. For example, deficien...

 Complement Deficiencies (CD) cause susceptibility not only to bacterial infection but also to autoimmune disease. Genetically determined MBL deficiencies are observed in autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Observation of the low concentrations of MBL and other complement proteins (e.g. C1q, C1r, C4) and poor activation of the complement system are also characteristic findings of inactive SLE. Complement activation almost inevitably results in some degree of tissue destruction, as seen in rheumatic diseases such as SLE, RA, vasculitis, and antiphospholipid antibody syndrome. Interest in complement in inflammatory disease has led to the development of pharmacologic complement inhibitors such as eculizumab, a humanized monoclonal anti-C5 antibody approved for paroxysmal nocturnal hemoglobinuria. Inflammatory conditions also result from hereditary or acquired deficiencies of complement regulatory proteins. For example, deficien...

  Complement deficiencies cause susceptibility not only to bacterial infection but also to autoimmune disease. Genetically determined MBL deficiencies are observed in autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Observation of the low concentrations of MBL and other complement proteins (e.g., C1q, C1r, C4) and poor complement system activation are also characteristic of inactive SLE. Complement activation almost inevitably results in tissue destruction, as seen in rheumatic diseases such as SLE, RA, vasculitis, and antiphospholipid antibody syndrome. Interest in complement in inflammatory disease has led to the development of pharmacologic complement inhibitors such as eculizumab, a humanized monoclonal anti-C5 antibody approved for paroxysmal nocturnal hemoglobinuria. Inflammatory conditions also result from hereditary or acquired deficiencies of complement regulatory proteins. For example, lack of the C1q inhibitor protein leads to...