Autoantibodies in Rheumatoid Arthritis and Type 1 Diabetes Quiz

Rheumatic heart disease, which occurs when the infection leads to damage to heart valves, either following the initial ARF or following repeated attacks of GAS infection with different M types.

Its high antigenicity and ability to cross-react with cardiac myofiber protein myosin and perivascular connective tissues, leading to autoimmune response.

50-60 years old.

Single amino acid substitutions.

M protein epitopes mimic those of mammalian muscle and connective tissue, leading to autoimmune response.

An increased risk of developing Rheumatic heart disease.

Presence of autoantibodies

Infection of Group A Streptococcus pyogenes (GAS)

Induce inflammation

About 10%

Autoantibodies contribute to the pathogenesis of Rheumatoid Arthritis

Autoimmune response leading to selective destruction of the insulin-secreting beta cells

Failure of tolerance, releasing sequestered antigens

Islet cell antibodies, antibodies to glutamic acid decarboxylase, insulin autoantibodies, and antibodies to tyrosine phosphatase

Genetic defect in the Aire gene

Antibody-antigen complexes inducing inflammation

Breakdown of self-tolerance

Genetic predisposition

Autoimmune diseases result from a breakdown in self-tolerance, leading to an immune response against self-antigens, as seen in rheumatoid arthritis and type 1 diabetes.

They are post-translational modifications that can trigger an autoimmune response, resulting in the production of autoantibodies such as ACPA and anti-CarP antibodies.

An autoimmune response leads to the destruction of beta cells, resulting in a lack of insulin production.

Tests for autoantibodies, such as islet cell antibodies and glutamic acid decarboxylase antibodies, can aid in the diagnosis of type 1 diabetes.

A breakdown in self-tolerance allows the immune system to recognize self-antigens as foreign, leading to an autoimmune response and the development of autoimmune diseases.

Autoantibodies against the Fc portion of IgG, such as rheumatoid factor, form antibody-antigen complexes that induce inflammation.

Genetic predisposition

Failures of tolerance

Antibody cross-reactions between streptococcal antigens and human proteins

Autoreactive T cells contribute to the pathogenesis of autoimmune diseases by recognizing and responding to self-antigens.

Loss of tolerance to self-antigens

Molecular mimicry due to immune response to infectious agents

The antigenic epitopes of M protein mimic those of mammalian muscle and connective tissue, leading to cross-reactivity and autoimmune responses.

M protein is a significant virulence factor of GAS, and its antigenic variation is primarily due to single amino acid substitutions, leading to the development of autoimmune responses.

Reinfections with different M types of GAS lead to repeated stimulation of the immune system, causing damage to heart valves and increasing the risk of Rheumatic Heart Disease.

ARF is a precursor to Rheumatic Heart Disease, and the inflammation and tissue damage caused by ARF can lead to the development of Rheumatic Heart Disease.

Rheumatoid Arthritis is a chronic disease that affects multiple joints, often starting in the small joints of the hands and feet, leading to deformities and inflammation of the synovium and supporting tissues.

The immune system responds to GAS infections by mounting an immune response, which can cross-react with host tissues, leading to autoimmune responses and diseases such as Rheumatic Fever and Rheumatoid Arthritis.