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Since the discovery of aquaporin-4 (AQP4) antibody a decade ago, neuromyelitis optica (NMO) has been distinguished from multiple sclerosis (MS). MS mainly features T lymphocyte-oriented autoimmune responses while NMO is more precisely influenced by humoral immunity, among which the complement activation has always been reckoned as an important mechanism. The AQP4 antibody, namely NMO-IgG, adds to new evidence of how complement affects the severity of NMO. We compared the levels of complement (C3, C4, CH50) and immunoglobulins (IgG, IgM, IgA) between NMO patients and controls. Groups with AQP4 antibody positive and negative NMO patients were also compared with controls, respectively, aiming to elaborate on the relationship between complement activation and immunoglobulins. We also compared these indexes together with expanded disability status scale (EDSS) between two different groups in NMO patients and endeavored to figure out their correlations with each other. Complement and immunoglobulins were compared between NMO patients in acute phase and non-acute phase of the disease to find out the level fluctuation of CH50 and other indexes during different stages of NMO. We analyzed NMO patients (n = 88) and controls (n = 44) for IgG, IgM, IgA, other indexes like CH50, C3, C4 have also been explored between the two groups. Furthermore, we investigated whether these antibodies could mediate complement-dependent cytotoxicity. Thus, the NMO patients were split into two groups with or without AQP4 antibody to find out the status of NMO-IgG in the development and severity of the disease. EDSS was used as criteria for the evaluating the seriousness of NMO. Comparison between NMO patients in acute stage and non-acute stage of the disease was also made for a better understanding of the disease. Compared with controls, NMO patients had much higher IgG (13.984 ± 5.981 mg/ml, 11.430 ± 3.254 mg/ml, P < 0.01) but lower CH50 (respectively, 43.55 ± 12.172 U/L, 50.66 ± 12.523 U/L, P < 0.01). While IgG increased in Anti-AQP4 antibody-positive NMO patients, CH50 dropped in this group when compared with AQP4-negative patients. When compared with controls, both of the NMO groups had enhanced IgG and decreased CH50 though only AQP4-positive NMO patients showed significance (IgG 15.004 ± 6.613 mg/ml, 11.430 ± 3.254 mg/ml, P < 0.01) (CH50, respectively, 41.12 ± 12.581U/L, 50.66 ± 12.523 U/L, P < 0.01). C4 was also decreased though without evident significance (0.215 ± 0.118 mg/ml, 0.260 ± 0.133 mg/ml, P = 0.069). Those NMO patients in acute phase (with the course of newly attack of less than 1 month) had increased immunoglobulin (IgG 14.991 ± 6.639 mg/ml, 12.460 ± 4.490 mg/ml) but decreased complement (CH50 42.755 ± 12.403 U/L, 44.743 ± 11.890 U/L) than those who passed the acute phase. There was correlation between IgG and CH50 (R = -0.402, P < 0.01) in NMO patients. Relationship was also found between IgG and EDSS (R = 0.609, P < 0.001), CH50 and EDSS (R = -0.333, P < 0.01). These results indicate that NMO patients had enhanced immunoglobulin in acute phase but decreased complement. The complement was correlated with immunoglobulin. Among the two NMO groups, the complement system was only activated in NMO-IgG positive patients, which might indicate a potential different pathogenetic mechanism in NMO-IgG negative patients. Also, patients' disability of the former group was more serious than their counterparts. Those patients in acute phase obviously had increased immunoglobulin but decreased complement. Thus, we have come to the conclusion that in AQP4-positive NMO patients, immunoglobulin activates complement system, which influences the functions of NMO patients.
Department of Neurology, Third Affiliated Hospital of Sun-Yat-Sen University, 600#, Tianhe Road, Guangzhou, Guangdong, China, email@example.com.
This article was published in the following journal.
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A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.
A rare, X-linked immunodeficiency syndrome characterized by ECZEMA; LYMPHOPENIA; and, recurrent pyogenic infection. It is seen exclusively in young boys. Typically, IMMUNOGLOBULIN M levels are low and IMMUNOGLOBULIN A and IMMUNOGLOBULIN E levels are elevated. Lymphoreticular malignancies are common.
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
Serine proteases that cleave COMPLEMENT C3 into COMPLEMENT C3A and COMPLEMENT C3B, or cleave COMPLEMENT C5 into COMPLEMENT C5A and COMPLEMENT C5B. These include the different forms of C3/C5 convertases in the classical and the alternative pathways of COMPLEMENT ACTIVATION. Both cleavages take place at the C-terminal of an ARGININE residue.
Complement activation initiated by the binding of COMPLEMENT C1 to ANTIGEN-ANTIBODY COMPLEXES at the COMPLEMENT C1Q subunit. This leads to the sequential activation of COMPLEMENT C1R and COMPLEMENT C1S subunits. Activated C1s cleaves COMPLEMENT C4 and COMPLEMENT C2 forming the membrane-bound classical C3 CONVERTASE (C4B2A) and the subsequent C5 CONVERTASE (C4B2A3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
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Multiple Sclerosis MS
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