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Related Concept Videos

Complement System01:27

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
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Rheumatic heart disease or RHD is a chronic condition that results from rheumatic fever, causing permanent damage to the heart valves.Etiology and Risk FactorsIt primarily arises from rheumatic fever, an inflammatory disease that can develop after untreated or inadequately treated group A streptococcal (GAS) pharyngitis. Streptococcus spreads through direct contact with oral or respiratory secretions. While the bacteria are the causative agents, factors like malnutrition, overcrowding, poor...
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The key clinical manifestations of Rheumatic heart disease (RHD) include several distinct cardiac symptoms.Carditis, a hallmark of acute rheumatic fever, involves inflammation of the heart's endocardium, myocardium, and pericardium. Chronic RHD often results from recurrent episodes of carditis. Its symptoms include the following:Murmurs are caused by valvular damage, especially to the mitral and aortic valves. Mitral stenosis or regurgitation is common, with characteristic heart murmurs...
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Antibodies, or immunoglobulins, are critical players in the immune system's arsenal against invading pathogens. Produced by B cells and plasma cells, their primary role is to detect and bind to specific antigens, molecules found on the surface of pathogens like bacteria or viruses. Beyond antigen recognition, antibodies perform several vital functions that contribute to immune defense.
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Generation of Two-color Antigen Microarrays for the Simultaneous Detection of IgG and IgM Autoantibodies
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Autoantibodies against complement factor B in rheumatoid arthritis.

Alexandra T Matola1,2, Angéla Fülöp3, Bernadette Rojkovich3

  • 1Department of Immunology, ELTE Eötvös Loránd University, Budapest, Hungary.

Frontiers in Immunology
|March 9, 2023
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Researchers identified autoantibodies against factor B (FB) in rheumatoid arthritis (RA) patients. These autoantibodies inhibited complement activation, suggesting a potential protective role in RA pathogenesis.

Keywords:
C3 convertasealternative pathwayautoantibodycomplementfactor B (FB)rheumatoid arthritis

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Area of Science:

  • Immunology
  • Rheumatology
  • Biochemistry

Background:

  • Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint inflammation.
  • The complement system's overactivation is implicated in RA pathogenesis.
  • Previous studies reported autoantibodies against complement components like C1q, MBL, and factor H (FH) in RA.

Purpose of the Study:

  • To investigate the presence and role of autoantibodies against complement proteins in a Hungarian RA cohort.
  • To characterize autoantibodies against factor B (FB), a complement regulator, in ACPA-positive RA patients.

Main Methods:

  • Serum samples from 97 ACPA-positive RA patients and 117 healthy controls were analyzed for autoantibodies against complement proteins.
  • Western blot was used to detect in vivo formed FB-autoanti-FB complexes.
  • Complement assays (hemolysis, fluid phase activation, solid phase convertase) were performed to assess the functional impact of FB autoantibodies.

Main Results:

  • Autoantibodies against C1q, MBL, and FB were detected in a subset of RA patients.
  • FB autoantibodies, primarily IgG isotypes binding to the Bb region, were identified in five RA patients.
  • These FB autoantibodies demonstrated inhibitory effects on complement-mediated hemolysis and C3-convertase activity, and reduced C3 and C5b-9 deposition.

Conclusions:

  • The study identified FB autoantibodies in ACPA-positive RA patients.
  • These autoantibodies appear to inhibit, rather than enhance, complement activation.
  • The findings suggest a potential protective role for these autoantibodies against complement overactivation in RA, warranting further investigation.