The immune system is part of our body’s first-line defense, protecting us from nasty infections that can make us ill. However, just like humans, the immune system is susceptible to making mistakes. Those with autoimmune diseases experience such errors firsthand, as their immune system mistakenly targets and attacks the body's own tissues. Understanding the mechanisms behind these diseases is crucial for developing effective treatments – there are many different types, but among the few are lupus, rheumatoid arthritis, and multiple sclerosis. In this article, we will be delving into their pathophysiology, current research, and advancements in treatment.
Lupus (Systemic Lupus Erythematosus - SLE)
Lupus is an autoimmune disease characterized by widespread inflammation and tissue damage in organs like the skin, joints, kidneys, and brain. Whilst the exact cause of lupus is unknown, it is likely that it results from genetics and living environments.
Autoantibodies: The hallmark of lupus is the production of autoantibodies such as anti-Sm/RNP, anti-Ro/La, anti-dsDNA.
Immune Complexes: These autoantibodies form immune complexes that deposit in tissues, causing inflammation and damage.
T and B Cells: Abnormalities in T and B cell function contribute to production of such autoantibodies, and worsen inflammation.
Rheumatoid Arthritis (RA)
Rheumatoid arthritis is an autoimmune and inflammatory disease that mainly attacks the joints. Similar to lupus, the exact cause is unknown, but risk factors include smoking, obesity, and exposure to air pollution, as well as non-modifiable factors such as genetics and gender. The prevalence of RA is higher in industrialized countries where people are more susceptible to pollution and environmental toxins.
Autoantibodies: The most common antibodies found in RA patients are Rheumatoid factor (RF) and anti-citrullinated protein antibodies.
Cytokines: The pro-inflammatory cytokines that play a critical role in driving the inflammatory response are tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6).
Synovial Infiltration: Inflammatory cells infiltrate the joint’s synovial membrane, leading to pannus formation, which erodes cartilage and bone.
Multiple Sclerosis (MS)
Multiple sclerosis is a chronic disease of the central nervous system that can affect the brain and spinal cord. Symptoms between MS patients vary, from vision problems and walking difficulties, to fatigue and depression. With MS, the immune system mistakenly attacks myelin cells, which leads to disrupted nerve signal transmission. Causes involve genetic predispositions and environmental factors.
Demyelination: Immune cells attack the protective covering of nerve fibers (myelin), causing it to break down and damage the nerves.
Oligodendrocyte Damage: The cells that make myelin (oligodendrocytes) get damaged, making it hard to repair the protective covering.
Inflammation: Persistent CNS inflammation contributes to neurodegeneration and disease progression.
Conclusion
Autoimmune diseases like lupus, rheumatoid arthritis, and multiple sclerosis involve complex interactions between genetic, environmental, and immune factors. As of now, there are no known exact cures. Treatment focuses on managing symptoms with the use of anti-inflammatory medication and physical therapy etc. Ongoing research continues to uncover new insights, offering hope for potential cures.
Works Cited
Donvito, T. (2018). The 4 Stages of Rheumatoid Arthritis Progression. [online] CreakyJoints. Available at: https://creakyjoints.org/about-arthritis/rheumatoid-arthritis/ra-overview/rheumatoid-arthritis-stages-progression/ [Accessed 21 May 2024].
Laliberte, M. (2018). 17 Facts About Lupus You Might Not Know, But Should. [online] CreakyJoints. Available at: https://creakyjoints.org/about-arthritis/lupus/lupus-overview/lupus-facts [Accessed 21 May 2024].
National Multiple Sclerosis Society. (n.d.). Empowering people affected by MS to live their best lives. [online] Available at: https://www.nationalmssociety.org/understanding-ms/what-is-ms/how-ms-affects-the-brain [Accessed 21 May 2024].
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