Auto-immune disease Target

What is Auto-immune disease?

Autoimmune diseases arise when the immune system mistakenly targets the body's tissues, causing inflammation and damage. Their precise triggers are unclear, but genetics, environment, and hormones are influential. Common examples include:

• Rheumatoid arthritis: Immune system targets joints.

• Systemic lupus erythematosus (SLE): Affects skin, joints, kidneys, brain, etc.

• Type 1 diabetes: Immune system attacks insulin-producing pancreatic cells.

Exploring Therapeutic Strategies by Mechanism of Action (MOA)

Autoimmune diseases' MOAs classify how the immune system damages self-tissues, aiding diagnosis, treatment, and research:

1. Cell-Mediated Immunity vs. Humoral Immunity

   • Cell-Mediated Immunity: T cells directly attack the body's cells. E.g., Type 1 diabetes (T cells destroy pancreatic beta cells), and psoriasis (T cells target skin cells).

   • Humoral Immunity: B cells produce autoantibodies targeting tissues. E.g., Rheumatoid Arthritis (autoantibodies form immune complexes in joints), and SLE (broad autoantibody range causes systemic symptoms).

2. Organ-Specific vs. Systemic Autoimmune Diseases

   • Organ-Specific: Immune response targets specific organs/tissues, such as the thyroid gland in Hashimoto's thyroiditis, or the neuromuscular junction in Myasthenia Gravis.

   • Systemic: Multiple organs/systems affected, as with SLE impacting skin, joints, kidneys, brain, and Rheumatoid Arthritis potentially affecting lungs and heart as well.

3. Inflammatory vs. Non-Inflammatory

   • Inflammatory: Chronic inflammation, often with cytokine production causing tissue damage, as in Crohn's disease (gastrointestinal tract inflammation) and Rheumatoid Arthritis (joint inflammation).

   • Non-Inflammatory: Some lack overt inflammation but cause functional impairment or tissue damage, such as certain autoimmune-mediated neuropathies, where the issue is functional interference, not inflammation.

4. Pathway of Immune Activation

   • T-Cell Activation: Autoreactive T cells are activated against self-antigens, significant in Type 1 diabetes and Multiple Sclerosis.

   • B-Cell Activation and Autoantibody Production: E.g., SLE and Rheumatoid Arthritis, where autoantibodies are pathogenic or form damaging immune complexes.

5. Cytokine Profile

   • Th1/Th17 Dominance: Diseases characterized by Th1 or Th17 cells, producing cytokines leading to inflammation and autoimmunity, observed in Type 1 diabetes (Th1) and psoriasis (Th17).

   • Regulatory T Cell (Treg) Dysfunction: Failure/reduction in Treg function, essential for immune tolerance to self-antigens, leads to uncontrolled autoimmunity.

Detailed Insights into Therapeutic and Diagnostic Targets of MOA-Based Strategies