Mechanisms and classification
Normally, immunity destroys foreign antigens or altered self-cells (e.g., tumor cells). In autoimmune diseases, this process fails. Autoreactive clones of lymphocytes are formed, and autoantibodies and cytotoxic T cells directed against healthy tissues are produced.
Diseases are divided into two main groups:
- Organ-specific. The attack targets a specific organ. Examples: autoimmune thyroiditis, type 1 diabetes mellitus, atrophic gastritis, autoimmune hemolytic anemia.
- Systemic. The targets are autoantigens present in many tissues of the body. Examples: systemic lupus erythematosus (SLE), rheumatoid arthritis, multiple sclerosis.
It is not uncommon for a single person to have multiple autoimmune conditions at once.
Causes of development (etiology)
Autoimmune diseases are multifactorial in nature. They are triggered by a combination of external and internal factors.
Exogenous (external) factors:
- Infections, vaccination.
- Ultraviolet radiation (excessive sun exposure), hypothermia.
- Use of certain medications.
Endogenous (internal) factors:
- Genetics. Predisposition is associated with major histocompatibility complex (HLA) genes and immunoglobulin genes.
- Hormonal background. Female sex hormones (estrogens) can provoke exacerbations. For example, SLE is 10 times more common in women, and patients' condition often worsens during pregnancy or after childbirth.
- Complement system defects. Clearance of immune complexes is impaired, and serum complement reserves are depleted.
- Cytokine dysregulation. Imbalance between pro- and anti-inflammatory cytokines.
Role of infections and immune-privileged organs
Infectious agents can trigger pathology in two ways. The first is molecular mimicry, where microbial proteins structurally resemble human proteins, and antibodies mistakenly strike "home." The second way is that the pathogen alters the structure of the body's own antigens, making them foreign to the immune system.
A special mechanism of development is associated with immune-privileged organs. Normally, certain tissues (brain, eye, thyroid gland, testes) are separated from the immune system by blood-tissue barriers. Lymphocytes do not contact them. If the barrier is destroyed due to trauma or inflammation, the immune system "sees" these antigens for the first time and perceives them as foreign, triggering an autoimmune reaction.
Principles of treatment
The basic strategy is aimed at suppressing the pathological immune response.
- Anti-inflammatory and cytostatic drugs are the mainstay of therapy.
- Glucocorticosteroids (GCS). Used during exacerbations. Pulse therapy is possible (ultra-high doses of GCS with cytostatics), but it has severe side effects.
- Targeted (biological) therapy. Includes anti-cytokine drugs (blocking inflammatory mediators) and suppression of cellular receptors.
- Aminoquinoline derivatives (plaquenil, delagil). Possess anti-inflammatory, antioxidant, and photoprotective effects. Prescribed in the absence of severe organ damage.
Briefly: answers to topical questions
Which diseases belong to systemic autoimmune conditions?
Systemic autoimmune conditions include diseases in which aggression is directed against autoantigens present in many tissues of the body. The source provides the following examples:
- Systemic lupus erythematosus.
- Rheumatoid arthritis.
- Multiple sclerosis.
What mechanisms lead to the breakdown of natural immunological tolerance?
The breakdown of natural immunological tolerance occurs under the action of various triggers through several pathogenetic mechanisms. The main mechanisms include:
- Molecular mimicry — structural similarity between proteins of an infectious agent and the body's own autoantigens.
- Alteration of the structure of self-antigens under the action of microorganisms.
- Production of anti-idiotypic antibodies.
- Activation of polyclonal lymphocytes — nonspecific stimulation of B lymphocytes by infectious agents.
- Increased immunogenicity of self-structures, inducing an immune response.
- Disruption of natural barriers of immunologically privileged sites during trauma or inflammation, resulting in antigens coming into contact with immune factors.
Which specific anti-cytokine drugs are used in targeted therapy for autoimmune diseases?
Targeted anti-cytokine therapy utilizes:
- Infliximab — a monoclonal antibody inhibiting tumor necrosis factor alpha (TNF-alpha).
- Anakinra — a recombinant antagonist that competitively blocks interleukin-1 (IL-1) receptors.
- Etanercept — a soluble TNF receptor acting as a decoy protein.
Class and exam questions
What is the difference between a systemic and an organ-specific autoimmune disease?
In an organ-specific disease, the immune system attacks only one specific organ (e.g., the thyroid gland). In a systemic disease, autoantibodies target antigens found in many tissues throughout the body (as in systemic lupus erythematosus).
Why can eye trauma cause an autoimmune disease?
The eye is an immune-privileged organ. Its tissues are normally isolated from the immune system. During trauma, the barrier is breached, eye antigens enter the bloodstream, and the immune system attacks them as foreign.
How does an infection trigger an autoimmune process?
Infection can act via molecular mimicry (where microbial proteins resemble human tissues) or alter the body's own antigens so that they are no longer recognized as "self."
What else to study on this topic
- The mechanism of molecular mimicry in specific infections
- Pathogenesis features of systemic lupus erythematosus (SLE)
- Complement system dysregulation and the role of C1q
- Cytokine profile in autoimmune conditions
- Pulse therapy: protocols and complications
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