Creative Biolabs providing a full range of complement therapeutic services for our customer. Based on extensive knowledge, we are fully equipped to reach out to our clients who may have problem or difficulty dealing with rheumatoid arthritis (RA) drug development.
Rheumatoid Arthritis (RA)
RA is a long-term autoimmune disorder that can cause joints pain and damage a wide variety of body systems. In RA patients, typical characteristics can be diagnosed, including warm, swollen, and painful in the joints. Notably, pain and stiffness even worsen after rest. As a joint inflammation disease which begins slowly and progresses over time, early symptoms of RA usually occurs on the fingers and toes and they are often subtle and imperceptible. As the disease progresses, symptoms often extend to other joints (wrists, knees, ankles, elbows, hips, and shoulders) and nonjoint structures (including the skin, eyes, lungs, heart, kidneys, salivary glands, nerve tissue, bone marrow and blood vessels). The people suffering from RA may increase the risk of osteoporosis, rheumatoid nodules, dry eyes and mouth, infections, carpal tunnel syndrome, heart problems, lung disease, and lymphoma.
Symptoms of Rheumatoid Arthritis
RA primarily affects joints, but it also affects other body systems in about 15-25% of individuals.
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Joints Symptoms: pain, stiffness, swelling, warmth, and redness of the joints.
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Physical Symptoms: fatigue, morning stiffness, minor fever, loss of appetite, skin rash, muscle aches, neck pain (if the RA is in the cervical spine), weight loss.
Fig. 1 Rheumatoid arthritis.1
Factors in the Pathogenesis of Rheumatoid Arthritis
The initiation of RA is a combination of genes and environment, leading to a breakdown of immune tolerance and synovial inflammation in a characteristic autoimmune disorder.
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Genetic and Immunologic Factors
Genome-wide association studies revealed that RA is strongly associated with genes of leukocyte antigen (HLA) system, encoding the major histocompatibility complex (MHC) proteins in humans. HLA-DR4 and HLA-DRB1 are the major genetic factors. The abnormalities of immune system also contribute to disease propagation. Various immune-associated cells (CD4 T cells, T helper cells, mononuclear phagocytes, fibroblasts, and neutrophils) play major roles in the pathophysiology of RA, whereas B cells produce autoantibodies (i.e., rheumatoid factors). Abnormal generation of numerous cytokines, chemokines, and inflammatory mediators has been demonstrated in RA, including TNF-α, IL-1, IL-6, IL-8, TGF-ß, FGF, and PDGF. Notably, strong evidence has been discovered that both the classical and the alternative pathways of complement are pathologically activated during RA, especially C5aR, C3 and factor D contribute to RA pathogenesis.
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Environmental Factors
There are a variety of environmental factors involved in RA pathogenesis, including cigarette smoke, industrial pollutants like silica crystals, disturbances of intestinal, lung, oral microbiota, as well as some specific bacterial and viral infection. Smoking is a widely accepted risk factor for RA in Caucasian populations, increasing the risk three times compared to non-smokers, particularly in men indulged in heavy smoking.
Fig. 2 Pathogenesis of rheumatoid arthritis.2
Creative Biolabs has established advanced Complement Therapeutics platform including antibody engineering platform, protease inhibitor platform, and drug discovery platform, and is equipped to offer a full range of biotherapeutics development services regarding drug discovery and validation for RA. Please contact us for detailed information.
References
1. De Souza, S., R. K. Bansal, and J. Galloway. "Managing patients with rheumatoid arthritis." BdJ Team 4.4 (2017): 17064.
Mueller, Anna-Lena, et al. "Recent advances in understanding the pathogenesis of rheumatoid arthritis: new treatment strategies." Cells 10.11 (2021): 3017.
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Questions & Answer
A: Several experimental approaches are being explored to target the complement system in RA treatment. These include inhibiting specific complement proteins, blocking complement receptors, and developing complement-specific antibodies. Additionally, there is ongoing research into the use of complement-modulating drugs to regulate complement activity in RA patients.
A: Preclinical models used for studying complement therapeutics in RA include murine models of RA, such as the collagen-induced arthritis model. These models mimic various aspects of human RA and provide a platform for testing the efficacy and safety of complement-targeted therapies.
A: Challenges include identifying the right target, understanding the complex complement system, and optimizing drug delivery. Experimental research focuses on target validation, biomarker discovery, and developing novel drug delivery systems to overcome these challenges.
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