Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation of the joints. It is sometimes confused with osteoarthritis, but they are different inflammatory diseases.
It affects women to a greater extent, possibly due to the influence of estrogens in the generation of inflammation. In addition, women are more susceptible to autoimmune diseases due to methylation of the X chromosome. There is also a certain heredity with regard to connective tissue diseases, so having a mother with a history of the disease is a risk factor.
Rheumatoid arthritis causes pain, stiffness, swelling, and can even cause joint deformity and loss of normal joint movement. It can also be accompanied by fatigue, occasional episodes of fever, or other symptoms such as heart complications, osteoporosis, or lung complications.
The exact causes of this disease are still not fully understood, although it has been shown that the immune system plays a key role in its development and progression. A combination of genetic and environmental factors triggers an abnormal immune response that results in the production of autoantibodies and chronic activation of the immune system. Let's see what happens to the immune system.
The Adaptive Immune Response in Arthritis
The adaptive response plays a crucial role in this joint disease. Both B cells and T cells, specialized lymphocytes, are altered and are key in the development of the pathology.
Specifically, an increase in CD4+ T cells and a decrease in Regulatory T cells, responsible for maintaining tolerance and preventing immune reactivity to structures and tissues, have been observed in the affected joints. CD4+ T cells produce proinflammatory cytokines such as interleukin 6, tumor necrosis factor alpha (TNF-α), and interferon gamma. All contribute to chronic inflammation and joint destruction.
B cells also play an important role. Immune complexes consisting of autoantibodies and antigens have been found in the joints of people with this disease. Especially B cells producing anti-citrullinated peptide antibodies (ACPA), are closely associated with disease severity and joint destruction in RA.
In addition, B cells can activate T cells and give rise to a vicious circle that perpetuates the inflammatory response.
Proinflammatory environment and cytokines in arthritis
Chronic inflammation is a hallmark symptom of rheumatoid arthritis. The synovial inflammation typical of arthritis has been shown to be mediated by excessive production of proinflammatory cytokines. These cytokines include IL-1β, IL-6, TNF-α, and IL-17, among others.
They promote the migration of inflammatory cells to the joints and stimulate the production of enzymes that degrade cartilage and bone. TNF-α is one of the most studied cytokines in this disease and has been identified as an important therapeutic target to reduce inflammation and disease progression in these patients.
Solving the Immunological Puzzle
Rheumatoid arthritis is a complex autoimmune disease that involves a dysfunctional adaptive immune response and chronic inflammation of the joints. It must be treated by specialists to prevent it from progressing to other locations and to maintain joint functionality.
Many of the available treatments usually help to relieve symptoms, although they do not always treat the root of the problem. In this regard, it is also worth considering approaches that allow the mediators involved to be modulated simultaneously, trying to redirect the immune response both locally and systemically, so that it works optimally, depending on each person's situation.
Immunomodulatory treatments are an option to consider in this case, since they can offer complementary support to symptomatic relief, helping to rebalance inflammatory signaling.
This is precisely the goal of microimmunotherapy. Doctors who use it in patients with rheumatoid arthritis seek to counteract the deregulation that exists in the inflammatory response and its persistence, in order to limit the deterioration of the affected tissue.
It should be noted that microimmunotherapy is based on the use of the same type of molecules and immunological mediators that the immune system uses, in low and very low doses, to work from a physiological point of view, coming as close as possible to the natural functioning of the body.
For example, it can be aimed at down-regulating the action of cytokines such as IL-1 or IL-6, involved in the inflammatory reaction.
In the end, in rheumatoid arthritis as in other autoimmune diseases, it is not just a matter of slowing down immunity, but of returning it to a state of balance.
Bibliography
- Miguel-Lavariega D, Elizararrás-Rivas J, Villarreal-Ríos E, Baltiérrez-Hoyos R, Velasco-Tobón U, Vargas-Daza ER, Galicia-Rodríguez L. Epidemiological profile of rheumatoid arthritis. Rev Med Inst Mex Seguro Soc. 2023 Sep 4;61(5):574-582. Spanish. doi: 10.5281/zenodo.8316427.
- van Delft MAM, Huizinga TWJ. An overview of autoantibodies in rheumatoid arthritis. J Autoimmun. 2020 Jun;110:102392. doi: 10.1016/j.jaut.2019.102392. Epub 2020 Jan 3.
- Radu AF, Bungau SG. Management of Rheumatoid Arthritis: An Overview. Cells. 2021 Oct 23;10(11):2857. doi:10.3390/cells10112857.
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