Autoimmune Disease Research: Key Targets & Therapeutic Insights

Autoimmune diseases are chronic conditions caused by the immune system mistakenly attacking the body's own tissues or organs, with complex etiologies involving genetic susceptibility, environmental factors (e.g., infections, stress, diet), and immune dysregulation. According to a 2025 study in The Lancet Rheumatology, over 800 million people globally were affected by autoimmune diseases in 2022, causing approximately 4 million deaths annually, making them a leading cause of chronic illness and disability. Women face a higher risk, with conditions like systemic lupus erythematosus showing a ninefold increased risk. At abinScience, we support global research efforts by providing rigorously validated antibodies and proteins against top immune targets.

Rheumatoid Arthritis (RA)

RA is a chronic systemic autoimmune disease primarily affecting joint synovium, leading to arthritis, cartilage destruction, and bone erosion. Clinical symptoms include morning stiffness, symmetrical joint swelling and pain, fatigue, and, in severe cases, joint deformities and loss of function. Immune activation involves T and B cell-mediated inflammation, overexpression of pro-inflammatory cytokines (e.g., TNF-α, IL-6), synovial hyperplasia, and production of autoantibodies (e.g., anti-CCP antibodies, rheumatoid factor).

Key Research Targets: TNF-α, IL-6, JAK, CD20, RANKL

Figure 1. Comparison of normal and RA joints

https://doi.org/10.3389/fbioe.2020.00652

Systemic Lupus Erythematosus (SLE)

SLE is a multisystem autoimmune disease characterized by the production of autoantibodies (e.g., anti-nuclear antibodies [ANA], anti-dsDNA antibodies). Symptoms vary, including rashes, joint pain, nephritis, neurological involvement, and hematological abnormalities. It involves B cell hyperactivity, immune complex deposition, complement system activation, and abnormal type I interferon signaling.

Key Research Targets: BAFF, IFN-α, CD20, BLyS, TLR7, TLR9

Figure 2. Pathophysiology of Systemic Lupus Erythematosus

https://www.wikidoc.org/index.php/Systemic_lupus_erythematosus_pathophysiology

Hyperthyroidism (Graves' Disease)

Graves' disease, a primary cause of hyperthyroidism, is triggered by anti-TSH receptor antibodies (TRAb) stimulating excessive thyroid hormone secretion. Symptoms include palpitations, anxiety, weight loss, exophthalmos, and goiter. B cells produce TRAb, activating TSH receptor signaling, leading to thyroid dysfunction, local inflammation, and tissue remodeling.

Key Research Targets: TSHR, TRAb, CD40, IL-1β

Figure 3. Pathogenesis of Graves' Hyperthyroidism

https://doi.org/10.1038/s41574-024-01016-5

Type 1 Diabetes (T1D)

T1D results from autoimmune destruction of pancreatic β cells, causing absolute insulin deficiency, commonly in children and adolescents. Symptoms include polyuria, thirst, weight loss, with long-term complications like cardiovascular disease and neuropathy. CD8+ T cells mediate β cell destruction, with anti-insulin antibodies (IAA) and anti-GAD65 antibodies. HLA-DR3/DR4 and viral infections (e.g., enteroviruses) are key risk factors.

Key Research Targets: GAD65, insulin, IL-1β, CTLA-4, PD-1

Figure 4. Pathogenesis of Type 1 and Type 2 Diabetes

Multiple Sclerosis (MS)

MS is a demyelinating disease of the central nervous system, presenting with visual disturbances, sensory issues, weakness, spasticity, and cognitive impairment. Lesions are multifocal and disseminated. T and B cell-mediated inflammation destroys myelin. Risk factors include Epstein-Barr virus, low vitamin D, and smoking. Anti-CD20 therapies (e.g., Ocrelizumab) are effective.

Key Research Targets: CD20/MS4A1, CD52, GPC4, MBP, MOG

Figure 5. Cellular Key Players in MS Pathology

https://doi.org/10.3389/fncel.2024.1488691

Alopecia Areata

Alopecia areata is an autoimmune disorder characterized by the immune system mistakenly attacking hair follicles, leading to sudden, unpredictable hair loss, typically in round or oval patches on the scalp or other areas of the body. In severe cases, it can progress to total scalp hair loss (alopecia totalis) or complete body hair loss (alopecia universalis). The condition affects approximately 2% of the global population, with onset often occurring in childhood or young adulthood, though it can develop at any age. Symptoms include well-defined bald patches, sometimes accompanied by tingling or mild discomfort in affected areas. The exact cause remains unclear, but genetic predisposition (e.g., family history of autoimmune diseases), environmental triggers (e.g., stress, viral infections), and immune dysregulation play significant roles. T cells, particularly CD8+ T cells, infiltrate hair follicles, releasing pro-inflammatory cytokines like IL-15 and IFN-γ, which disrupt the hair growth cycle and induce follicle regression. The disease is associated with other autoimmune conditions, such as thyroid disease or vitiligo, and can significantly impact quality of life due to its visible nature and psychological effects. While no cure exists, treatments like JAK inhibitors, corticosteroids, and immunotherapy show promise in managing symptoms and promoting hair regrowth. abinScience supports research into alopecia areata by providing high-quality proteins and antibodies targeting key molecules like IL-15, IFN-γ, and JAK to advance understanding and therapeutic development.

Key Research Targets: IL-15, IFN-γ, JAK

Figure 6. Pathophysiology of Alopecia Areata

Psoriasis

Psoriasis is a chronic skin disease characterized by erythema, scaling, and itching, often with psoriatic arthritis. It impacts quality of life. Overactive T cells (especially Th17) and cytokines (IL-17, IL-23) drive inflammation. Genetic (HLA-Cw6) and environmental factors (e.g., infections, stress) are associated. Some patients develop psoriatic arthritis (PsA), causing joint pain and dysfunction.

Key Research Targets: IL-17, IL-23, TNF-α, HLA-Cw6, PDE4

Figure 7. Molecular Mechanisms of Psoriasis

https://www.embopress.org/doi/full/10.15252/emmm.202114455

Myasthenia Gravis (MG)

MG is a neuromuscular junction disorder characterized by muscle weakness and fatigability (e.g., ptosis, diplopia). Anti-acetylcholine receptor antibodies (AChR-Ab) are the primary marker. AChR-Ab block neuromuscular signaling, and complement activation causes junction damage. Thymic abnormalities (e.g., thymoma) are common.

Key Research Targets: AChR, MuSK, LRP4, FcRn

Figure 8. Pathophysiology of Myasthenia Gravis

https://doi.org/10.1038/s41572-019-0085-0

Vitiligo

Vitiligo results from immune-mediated destruction of melanocytes, causing depigmented skin patches, often in exposed areas, sometimes with white hair. It is frequently associated with other autoimmune diseases like thyroid disorders. Melanocyte damage involves T cell-mediated attacks, oxidative stress, and inflammatory cytokines (e.g., IL-2, IL-17), leading to loss of melanocyte function.

Key Research Targets: IL-2, IL-17, JAK

Figure 9. Pathophysiology of Vitiligo

https://doi.org/10.1038/s41586-021-04221-8

Inflammatory Bowel Disease (IBD)

IBD, including Crohn's disease (CD) and ulcerative colitis (UC), presents with abdominal pain, diarrhea, bloody stools, and intestinal inflammation. Dysregulated gut immunity, Th17 cells, and cytokines (e.g., IL-23, TNF-α) are involved. Gut microbiota dysbiosis and genetics (e.g., NOD2) are associated.

Key Research Targets: TNF-α, IL-23, IL-12, NOD2, ATG16L1

Figure 10. Strategies for Targeting Cytokines in IBD

https://doi.org/10.1038/s41577-024-01008-6

Why Choose abinScience?

abinScience is committed to advancing autoimmune disease research by offering:

• Validated antibodies for ELISA, flow cytometry, WB, and in vivo applications
• High-purity recombinant proteins and cytokines
• Scientific support backed by peer-reviewed references
• Dedicated autoimmune disease collections covering RA, SLE, MS, and more