Rheumatoid arthritis (RA) is both an inflammatory arthritis and an autoimmune disorder. Therefore, the function of the immune system and the inflammatory response are key concepts in understanding how RA works. And also in understanding how therapy is used to treat RA. In this article, we will examine the autoimmune response of the body and rheumatoid arthritis.

Body autoimmune response and rheumatoid arthritis

In the early stages, even before the appearance of articular inflammation, RA is believed to begin with a series of events in which the immune system loses its ability to distinguish between what belongs to the body (“I”) and what is foreign to the body (“not – I”). This process, which occurs systemically (throughout the body), begins with inadequate cell clearance when they die. As a rule, dying cells do not come into contact with the immune system and are not identified as a potential threat to the body.




As the cells reach the end of their life, they undergo citrullination. This is a process in which enzymes called peptidyl arginine – deiminases (PD) transform (citrullination) proteins in the cell. This is a normal part of cellular physiology.

However, in most patients who develop rheumatoid arthritis (and a common version of the gene of the immune system is associated with RA), citrullinated proteins flow from dying cells throughout the body. Leaked PDs convert (citrullination) proteins into extracellular fluid (outside the cell). These citrulline proteins and PDs are recognized as antigens by the immune system. In response to these antigens, the immune system generates Anti-citrullinated protein antibodies (ACPAs). The creation of ATPs indicates a loss of tolerance for the “I”. The presence of ACPA is an accurate predictor of RA, as well as a rheumatoid factor (RF) (accurate in about 80% of cases) and can even predict the disease 15 years before it becomes clinically apparent with joint symptoms.

see also:

 Diagnosis of rheumatology 

Rheumatoid Arthritis and Autoimmune Attack on the Joints

In patients with ADC or rheumatoid factor, autoantibodies and inflammation occur systemically (throughout the body) before they appear in the joints. Therefore, it is believed that some other factor or trigger (not yet known) is involved in the fact that the early systemic autoimmune response of the body goes to the synovial (articular), which leads to the symptoms characteristic of RA.

This unknown factor causes leukocyte migration and infiltration into synovia. When the immune system activates and the disease progresses, a cascade of inflammatory cell types and chemicals of the immune system arise. These cells of the immune system and the wide range of chemicals they produce play a role in the autoimmune process, which ultimately causes joint destruction.  Early signs of rheumatoid arthritis .

The main participants in the autoimmune response are white blood cells.

White blood cells are key cells in the immune system that play a central role in the autoimmune response that occurs during rheumatoid arthritis. White blood cells include a number of different types of white blood cells with different functions. Those with key roles in the autoimmune response of RA include neutrophils, lymphocytes (T and B cells), monocytes, macrophages and dendritic cells (these last two types of cells are derived from monocytes). In addition to white blood cells, another cell in the immune system called the mast cell plays an important role in the autoimmune process. It releases cytokines, chemokines, and enzymes called proteases.


Inflammatory Plectrum

A wide range of chemicals produced by the cells of the immune system performs many functions related to the autoimmune response. These chemicals, known as inflammatory mediators, include cytokines (eg, growth factors, interferon [IFN] -γ, TNF-α, interleukin 1 [IL-1]), enzymes, chemokines (small cytokines that serve as signaling proteins) (for example, interleukin 8 [IL-1]), signaling molecules (leukotrienes and prostaglandins) and antibodies, a type of protein, also called immunoglobulin (Ig).

In addition, another group of chemical reactions of the immune system, called the complement system, helps (complements) the ability of antibodies and phagocytic cells to clear antigens as part of the immune response. The complement system consists of more than 25 proteins and protein fragments, including cell membrane receptors.  Muscle and joint stretching exercises .

Autoimmune RA process and the evolution of joint damage

In rheumatoid arthritis, the immune system disrupts and attacks healthy joint tissue, as if it were a foreign invader. White blood cells move into the articular cavity, causing an inflammatory reaction. White blood cells, including B and T cells, neutrophils, dendritic cells, and macrophages. As well as other types of immune cells, including mast cells, multiply in the joint cavity.

These immune cells cause inflammatory mediators, including cytokines, leukotrienes, and prostaglandins. Some of these substances contribute to the growth of blood vessels, supplying nutrients to a growing mass of white blood cells, which leads to the formation of a pannus (this Latin word literally means a piece of tissue), a flap of fibrous tissue that forms above the synovial cartilage. The synovial pad inside the joint becomes inflamed and swollen. With prolonged exposure to inflammation, thickening of the synovial lining and the formation of the pannus, the joint space decreases over time, and the bone structure of the joint can be deformed. And in extreme cases, the joint may stop functioning. The autoimmune response of the body and rheumatoid arthritis see above.



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