Immunotransmission is a complex pathological process, the core of which is the abnormal activation and reaction of the organism ‘ s immune system. When the organism is stimulied, such as infection, injury or self-immunological disease, the immune system mistakenly views its own organization as an external antigen, triggering a series of inflammatory reactions.
This process begins with the abnormal activation of immunocellular cells. Under normal circumstances, immunosuppressive cells such as T-cells, B-cells and megacormic cells play an important role in immune surveillance and defence in the machine. However, in the case of immunokinesis, these cells were erroneously activated, starting to produce and release a large number of inflammatory causes. These inflammatory factors, such as tumour cause of death (TNF-α), white cell meds (IL-1, IL-6, IL-17 and IL-22), are key media that trigger inflammation responses.
With the release of inflammatory factors, they can act on joints, skins, etc., leading to an increase in vascular expansion, permeability, proteins and other components of blood entering the inter-organizational gap, creating local oedema and edema. At the same time, immune cells are concentrated in damaged areas to devour and remove harmful substances. However, when the response is excessive or prolonged, it leads to increased tissue damage and inflammation.
In the case of silver crumb arthritis, specific mechanisms for immunokinitis are more complex. In addition to the above-mentioned emission factors for immunocellular abnormality and inflammation, there is also an abnormal increase in horny cell formation. Under normal conditions, an angular cell formation undergoes an orderly process of growth and decomposition to maintain skin health. However, in the case of silver crumb arthritis, due to the unusual reaction of the immune system, the horny form cell is over-activated, resulting in the cell being over-enactment, piled on the skin surface, and a typical silver crumb skin loss.
In addition, immunokinesis is associated with the generation of their own antibodies. These antibodies are the result of immune systems mistakenly viewing their own organizations as alien antigens. In silver crumb arthritis, self-antibodies attack the normal tissue of the joint and skin, further exacerbating inflammation and damage. Such attacks not only lead to the emergence and exacerbation of arthritis symptoms, but may also affect other systems, such as cardiovascular systems, metabolic systems, etc.
The strategy for the treatment of immunotransmissible inflammation is primarily to regulate the immune response. Inflammation and organizational damage can be effectively mitigated by inhibiting the abnormality of immunosuppressive cells, reducing the release of inflammatory factors, and neutral and self-antibodies. Common therapeutic drugs include immunosuppressants, biological agents, etc. These drugs can target and regulate the functioning of the immune system, thereby reducing the symptoms of patients and improving their quality of life.
In short, immunotransmissible inflammation is a complex pathological process that involves the abnormal activity of immunocellular cells, the release of inflammatory factors, the abnormal increase in horny cell formation and the generation of their own antibodies. A better understanding of this mechanism is important for developing more effective treatment strategies.
