Auto-immune disease Target

What is Auto-immune disease?

Autoimmune diseases occur when the immune system initiates an attack on the body tissues leading to inflammation and destruction of the tissues. Where and when these disorders occur is not completely understood, but genes, environment and sex hormones do play an important role. Common examples include:

• Rheumatoid arthritis: Antigen attacks the joints of our body.

• Systemic lupus erythematosus (SLE): it is a considerable impact on the skin, joints, kidneys, brain and, etc.

• Type 1 diabetes: Pancreatic cells which secrete insulin are attacked by the body’s immune system.

Exploring Therapeutic Strategies by Mechanism of Action (MOA)

Autoimmune diseases' MOAs classify how the immune system damages self-tissues, aiding diagnosis, treatment, and research: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 go straight for White Blood Cells of the human body. For example, Type 1 diabetes where T cells killing pancreatic beta cells and psoriasis where skin cells are the target of T cells.

   • Humoral Immunity: There is evidence on formation of autoantibodies by B cells that focus on the tissue. For example, Rheumatoid Arthritis – autoimmune complexes form in joints and Rheumatoid Arthritis – a broad number of autoantibodies cause generalized manifestations.

2. Organ-Specific vs. Systemic Autoimmune Diseases

   • Organ-Specific: It is an attack by the immune system requiring the targetting of special organelles like thyroid gland in Hashimotos thyroiditis or the neuromuscular junctions in Myasthenia Gravis.

   • Systemic: That is, systems like skin, joint, kidney, brain involve in SLE while in RA besides joint, lungs, and heart may also be involved.

3. Inflammatory vs. Non-Inflammatory

   • Inflammatory: As in chronic inflammation coupled with cytokine synthesis that leads to tissue injury such as; Crohn’s disease afflicting the gastrointestinal tract and Rheumatoid Arthritis affecting the joints.

   • Non-Inflammatory: While some people may exhibit no signs of inflammation but are affected functionally or experience degradation of their tissues, for example, autoimmune-mediated neuropathy in which the problem arises from interference with functioning rather than inflammation.

4. Pathway of Immune Activation

   • T-Cell Activation: These are T cells that become reactive with self-antigens, of very important in diabetes/AIDS 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: Th1 or Th17 associated diseases releasing cytokines resulting in inflammation as well as autoimmunity for type 1 diabetes driven by Th1 cells and psoriasis by Th17 cells.

   • Regulatory T Cell (Treg) Dysfunction: As Treg fail or reduce their function which is crucial to maintain immune tolerance to self antigens there is uncontrolled autoimmunity.

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

MOA Category	Target/Biomarker	Target ID	Therapeutic Use	Diagnostic Use
Cell-Mediated Immunity	CD4	GM-T10191	Monoclonal antibodies to modulate T cell responses	CD4+ T cell count in HIV/AIDS; indicates T cell involvement
CD8	P01732	Modulating CD8+ T cell activity	Assessing CD8+ T cell activation
Humoral Immunity	Autoantibodies	Varies	Plasma exchange, immunosuppressants, B cell depletion	Detection of specific autoantibodies for diagnosis
Organ-Specific Diseases	GAD2 (GAD65)	GM-T22128	-	Anti-GAD65 antibodies as markers for type 1 diabetes, Stiff-Person Syndrome
Systemic Diseases	Anti-nuclear antibodies (ANAs)	Varies	-	Broad diagnostic tool for diseases like SLE
Inflammatory	TNF	GM-T20178	Anti-TNF therapies (e.g., Infliximab, Adalimumab)	Elevated TNF-伪 levels indicate active inflammation
Pathway of Immune Activation	IL-17	GM-T22095	IL-17 inhibitors (e.g., Secukinumab)	Elevated IL-17 levels suggest Th17 involvement