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> Solutions for Autoimmune Disease Drug Development The immune system's fundamental function depends on exquisitely regulated self-antigen recognition and tolerance mechanisms - the cornerstone of immunological homeostasis. This critical balance is maintained through complementary central tolerance (clonal deletion in thymus/bone marrow) and peripheral tolerance. However, when the immune system faces "immune warning signals", this balance may be threatened, increasing the risk of potential Autoimmune Disease (AIDs). According to statistics, about 10% of healthy individuals have detectable low levels of autoantibodies in their serum. These antibodies, though not causing noticeable symptoms, indicate a potential risk mechanism of immune imbalance.
Click to view ACROBiosystems Solutions for AIDs Drug Development
"Where Proteins and lnnovation Advance Biomedicine", ACROBiosystems collaborates with leading global pharmaceutical companies to provide comprehensive solutions for AIDs drug development. Our integrated portfolio encompasses high-quality biological reagents including recombinant proteins, antibodies, engineered cell lines, specialized assay kits and organoids, as well as one-stop services. We support the entire drug development process through integrated services spanning from drug discovery and development, manufacturing and quality control to preclinical and clinical studies.
| Discovery & Development | Manufacturing & Quality Control | Preclinical & Clinical Studies |
|---|---|---|
| Target Proteins 100+ AIDs-related targets covered Functional Cell Lines TR-FRET Kits Inhibitor Screening Kits Molecular Interaction Analysis Services (SPR & BLI) ... | GMP-grade Reagents Recombinant Factor C Endotoxin Detection Kit Residual Detection Kits ... | Organoid-related Solutions Anti-Idiotypic Antibody Development Service ClinMax™ Cytokine Detection ELISA Kits ... |
Inflammatory Bowel Disease (IBD)
Psoriasis (PsO)
Rheumatoid Arthritis (RA)
Atopic Dermatitis (AD)
Multiple Sclerosis (MS)
Systemic Lupus Erythematosus (SLE)
Ankylosing Spondylitis (AS)
Type 1 Diabetes Mellitus (T1DM)
Sjögren's Syndrome (SS)
Myasthenia Gravis (MG)
Key signaling pathways in IBD [1]
Inflammatory Bowel Disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract caused by immune dysregulation, encompassing both Crohn’s disease and ulcerative colitis. Its pathogenesis involves complex interactions among the immune system, gut microbiota, and environmental factors. Aberrantly activated T and B cells secrete inflammatory cytokines such as TNF-α, IL-17, and TL1A, leading to intestinal tissue damage. Key immune mechanisms include the Th17 pathway, JAK/STAT signaling, TL1A/DR3 axis, and integrin-mediated cell adhesion. Dysregulation of these pathways collectively drives the chronic intestinal inflammation and disease progression observed in IBD.
Overview of intracellular signaling pathways in PsO [2]
Psoriasis (PsO) is a chronic immune-mediated inflammatory skin disease primarily driven by aberrant activation of the IL-23/Th17 axis. This leads to the release of pro-inflammatory cytokines such as IL-17A and IL-22, causing excessive keratinocyte proliferation and inflammatory cell infiltration. Targeted therapies focus on key molecules in this pathway: IL-23 monoclonal antibodies (e.g., guselkumab) block upstream regulation, while IL-17A monoclonal antibodies (e.g., secukinumab) directly inhibit central inflammatory mediators. Additionally, IL-1Ra antagonists (e.g., anakinra) and LAG-3 inhibitors are under development, showing promising potential in the treatment of PsO.
Main signaling pathways and their inhibitors related to RA [3]
Rheumatoid Arthritis (RA) is a chronic autoimmune disease characterized by immune dysregulation leading to synovitis and joint destruction. Treatment strategies have evolved from traditional targets—such as TNF-α, IL-6R, and CD20—to novel targeted therapies. These include CTLA-4-IgG fusion proteins that modulate T cell activation, anti-IL-17A antibodies that block inflammatory pathways, FcRn inhibitors that accelerate the clearance of pathogenic antibodies, and complement C5 inhibitors that interfere with the inflammatory cascade. These therapies enable precise modulation of immune cell interactions, cytokine networks, and antibody metabolism, advancing RA treatment toward a personalized, multi-targeted therapeutic approach.
Pathogenesis of AD [4]
Atopic Dermatitis (AD) is a chronic inflammatory skin disorder driven by epidermal barrier dysfunction and overactivation of type 2 (Th2) immunity. Key cytokines such as IL-4, IL-13, and IL-31 contribute to pruritus and inflammation. Therapeutic strategies have shifted from traditional immunosuppressants to targeted biologics. IL-4Rα monoclonal antibodies (e.g., dupilumab) block signaling of both IL-4 and IL-13, while TSLP antibodies target upstream alarmins. Emerging therapies targeting IL-5, IL-17A, and IL-22 are also under development, marking a transition in AD treatment toward precision medicine that emphasizes both targeted immune blockade and restoration of the skin barrier.
Pathogenesis of MS [5]
Multiple Sclerosis (MS) is a chronic, inflammatory, demyelinating disease primarily affecting the central nervous system. Its core mechanism involves abnormal immune responses that result in damage to nerve fibers. Advances in immune regulation and neurorepair strategies have driven therapeutic innovation. Emerging treatments targeting B cells, BAFF inhibitors, and TGF-β modulators have shown promise. Additionally, novel agents such as TL1A blockers and Neuropilin-2 antibodies are opening new avenues for neuroprotection in MS therapy.
Immunobiological mechanisms of SLE [6]
Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease caused by the immune system mistakenly attacking the body's own tissues. Its pathogenesis involves aberrant activation of multiple immune cell types, immune complex deposition, and cytokine dysregulation. Abnormal expression of cytokines such as IFN-α and BAFF plays a pivotal role in the onset and progression of SLE. Targeted therapies against B cells and T cells, as well as emerging strategies involving BCMA, are paving the way for more precise and personalized treatment approaches in SLE.
Summary figure of molecular and cellular mechanisms in AS pathogenesis [7]
Ankylosing Spondylitis (AS) is characterized by immune dysregulation, in which the immune system mistakenly attacks the body’s own tissues, ultimately leading to the formation of bone spurs and joint ankylosis. Targeted therapies have evolved from traditional TNF-α inhibitors to novel treatments. Dual IL-17A/F inhibitors (e.g., bimekizumab) precisely suppress the IL-17 inflammatory axis, significantly improving axial symptoms of AS. IL-12/IL-23 p40 inhibitors (e.g., ustekinumab) show potential by blocking the Th17 differentiation pathway. Dual-targeted strategies that address both inflammation and bone metabolism may represent a promising future direction in AS management.
Mechanisms of Immune Tolerance and Therapeutics in T1DM [8]
Type 1 Diabetes Mellitus (T1DM), also known as insulin-dependent diabetes, is a chronic autoimmune disease primarily driven by pathological activation of T cells, leading to an immune attack against pancreatic β-cell antigens. Immunotherapeutic strategies focus on restoring immune tolerance, targeting molecules such as CD3, CD20, and CD40L. Currently, teplizumab, a CD3-targeting monoclonal antibody, is the only approved drug for this indication. The future of T1DM drug development lies in multi-target interventions and integration with artificial pancreas technologies.
Pathogenesis of SS [9]
Sjögren's Syndrome (SS) is characterized by aberrant lymphocyte activation leading to damage of exocrine glands. Common symptoms include dry mouth and dry eyes, and the disease may involve multiple organ systems such as the kidneys and lungs, with a subset of patients at risk for lymphoma transformation. Recent advances in targeted drug development include FcRn inhibitors, CD3/BCMA bispecific antibodies, CD40 antagonists, and IFNAR monoclonal antibodies. These therapies aim to precisely modulate dysregulated immune responses and preserve glandular function, offering promising new directions for clinical treatment.
Immunopathogenesis of AChR-MG and MuSK-MG, and therapeutic targets [10]
Myasthenia Gravis (MG) is an autoimmune disease characterized by skeletal muscle fatigue and weakness, with symptoms typically worsening after activity. The pathogenesis involves autoantibodies attacking acetylcholine receptors at the neuromuscular junction, leading to impaired signal transmission. Therapeutic advances include inhibitors targeting CD20, CD19, and JAK, as well as agents that modulate co-stimulatory molecules. In addition, strategies targeting the complement C1s pathway and Fcγ receptor signaling have shown promising potential for clinical application.
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2. Guo J, Zhang H, Lin W, et al. Signaling pathways and targeted therapies for psoriasis[J]. Signal transduction and targeted therapy, 2023, 8(1): 437. https://doi.org/10.1038/s41392-023-01655-6
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7. Zhang Y, Liu W, Lai J, et al. Genetic associations in ankylosing spondylitis: circulating proteins as drug targets and biomarkers[J]. Frontiers in Immunology, 2024, 15: 1394438. https://doi.org/10.3389/fimmu.2024.1394438
8. Warshauer J T, Bluestone J A, Anderson M S. New frontiers in the treatment of type 1 diabetes[J]. Cell metabolism, 2020, 31(1): 46-61. https://doi.org/10.1016/j.cmet.2019.11.017
9. Srivastava A, Makarenkova H P. Innate immunity and biological therapies for the treatment of Sjögren’s syndrome[J]. International journal of molecular sciences, 2020, 21(23): 9172. https: //doi.org/10.3390/ijms21239172
10. Iorio R. Myasthenia gravis: the changing treatment landscape in the era of molecular therapies[J]. Nature Reviews Neurology, 2024, 20(2): 84-98. https://doi.org/10.1038/s41582-023-00916-w
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