When you get injured, in addition to the blood clotting reaction, the body too quickly to protect the openings on the wound from bacterial infection and other microorganisms. The existence of direct injury has damaged the external nonspecific immune system.
When there is injury, histamine released by mast cells (mastosit), and basofil cells scattered throughout the network. Received histamine receptors on smooth muscle and endothelium of blood capillary walls causes the blood capillaries through vasodilation (increase in diameter), while venous narrowing. This causes the blood capillaries become more permeable.
These areas will look red and swell. In addition to histamine release, also produced a factor mastosit kemotaksis for 'interesting' and activate eosinophils, neutrophils, and
monocytes (phagocytic cells), as well as activating factor chips will be involved in blood clotting process. Tues phagocytes, will be seen around the wound area after about 30 to 90 minutes later.
Eosinophils play a role in inhibiting and reducing the concentration of histamine released mastosit, in order to avoid an overreaction. If there is infection by bacteria, the neutrophils activates lysosome. Lysosomes release enzymes that will degrade lysozim selsel of bacteria and damaged tissue around the wound.
Monocytes and macrophages also produce endogenous pyrogen. These substances give signals to the thermostat in the hypothalamus, to raise body temperature several degrees. We call this situation as a fever. This happens especially if the infection suffered quite heavy. Rising temperature
body to inhibit growth of pathogenic bacteria or organisms, so that more can be easily overpowered. This body's response can be described as nonspecific immune system response and not involve the lymphocyte cells.
Macrophages, which amounts to only a few percent of the total leukocytes plays an important role. Macrophages have the MHC protein (macrophage's histocompatibility complex), which then bind to the antigen on the microbe. MHC-antigen complex is then migrated to the cell membrane of macrophages.
Lymphocytes also participate in the crippling of microbes that enter the body, only with different mechanisms. Tues B lymphocytes with complement receptors bind to the antigens from pathogenic bacteria or organisms. This is to recognize those antigens. B lymphocytes will divide and differentiate into memory cells and plasma cells. Menyekresikan plasma cell antibodies that can cripple the microbes that enter the body fluids (humor). Operating targets B lymphocytes are bacteria, viruses outside of cells, fungi and protists. T lymphocytes form the cellular immune system. Tues Cytotoxic will stick to the cells already infected
viruses, cancer cells or foreign cells are transplanted into the body.
Receptor on helper T cells bind to MHC-antigen complexes macrophages. These bonds cause helper T cells produce interleukin hormone that induces helper T cells to divide and differentiate into memory cells. Helper T cells can also bind
with cells and induces B lymphocytes (with the help of hormone interleukin) B lymphocyte cells to divide and differentiate into memory cells and plasma cells. Plasma cells will menyekresikan antibodies.
Plasma cells secreted antibodies that will bind to the microbial antigen, then it can be recognized by macrophages and digested. This phenomenon is called opsonic adherence (Opsin is a term that means "ready to eat ') or opsonisasi. This process is basically the mechanism of microbial cell labeling with antibody antigen paralytic.
Cytotoxic T cell can also divide and differentiate actively with the help of interleukin hormone secreted from helper T cells. Tues cytotoxic cells recognize foreign or virus-infected cells in the body, and then outlines the cell membranes with the proteins they produce.
This is very important, because antibodies can not attack pathogens that have infected cells.