According to the provided information, autoantibodies work by binding to the body's own components, often initiating specific immune responses.
The Mechanism Explained (Based on Reference A)
Autoantibodies are a type of antibody produced by the immune system's B lymphocytes. Unlike typical antibodies that target foreign invaders like bacteria or viruses, autoantibodies mistakenly target self-antigens – molecules that are part of the body's own tissues and cells.
The specific process described in Reference A involves the following steps:
- Production: Autoantibodies are produced by B lymphocytes.
- Binding: These autoantibodies bind to self-antigens. These self-antigens are released from damaged or dying cells, specifically those undergoing apoptotic or necrotic processes.
- Complex Formation: When the autoantibodies bind to these self-antigens, they form antigen–antibody (immune) complexes.
- Cell Activation (Conditional): When these immune complexes contain nucleic acids (like DNA or RNA, often released from the nucleus of dead cells) and are taken up (endocytosed) by specific immune cells called pDCs (plasmacytoid dendritic cells), a further reaction occurs.
- Receptor Activation: Inside the pDCs, the nucleic acid-containing immune complexes activate Toll-like receptors (TLRs). These receptors are part of the innate immune system and recognize specific molecular patterns.
- Signal Secretion: Upon activation of the Toll-like receptors, the pDCs are prompted to secrete interferon-α. Interferon-α is a powerful signaling molecule (cytokine) that plays a role in immune responses, including inflammation and antiviral defense.
Essentially, this specific mechanism highlights how autoantibodies can turn components of dead cells into triggers for immune cell activation, particularly in the presence of self-nucleic acids, leading to the release of inflammatory signals like interferon-α.
