Mechanism's _ general knowledge of pathogenic factor and having illness coming on of tubercle

Mechanism's _ general knowledge of pathogenic factor and having illness coming on of tubercle
First, pathogenic factor
The cause of disease of tubercle has not been bright so far, it may be one kind and infects factor, immune factor, one's own immune system disease associating with inherent cause at the same time. The pathological hypothesis of the immunity thinks, tubercle is under the function of some unknown antigen, mainly started the cell immunity of tubercle to reply by macrophages; Macrophages release many kinds of factors, such as IL-1, cause T to assist cell gathering and hyperplasia; T assists cells to secrete the cell factor, hastens and melts and gathers other inflammatory cells. In addition, are produced immunoglobulin (Ig) to increase by B lymphocytes after stimulating, begin hyperplasia too as fibrous cells. The above-mentioned immunology changes interaction to lead to the fact it is being swollen that the inflammatory cell is being given much trouble the hyperplasia of organ and formed the granulation.
Second, have illness coming on in the mechanism
It is the important amynologic characteristic of tubercle that the cell immunological function is low, are shown as peripheral blood lymphocytes are reduced, to many kinds of late person who send the intersection of skin and test react, subside or disappear, irritate lotion (BALF) to patient of tubercle disease the intersection of bronchus and alveolus Finding,increase macrophage at BALF and lymphocyte absolute number obviously, but the proportion that macrophages account for drops but the lymphocyte proportion rises, indicate the position of disease T cell function is obviously strengthened, drop and form the contrast with peripheral blood T lymphocytes, the two present and separate the phenomenon. Until the intersection of T and the intersection of cell and inferior group analyze, find activity issues of patient of tubercle disease T assist and induce cells (CD4) further in the BALF Obviously increase, and T inhibiting malicious cells (CD8) of cell It is normal to be lower than. Make CD4/CD8 ratio obviously rise.
Tubercle disease granulation is swollen from at there make up is skin kinds of cell, macrophage and some effect cell. Its mechanism is under the function of the outside antigen, T cell and macrophages in the alveolus are activated, release a series of lymphocytic factor, the ones that include T cells to emerge are lain between in vain plainly - 2 (IL-2)s , the factor (MCF) of hastening and melting of the monocyte , the monocyte moves the conduct and inhibits the factor (MIF) The ones that produce with macrophages are lain between in vain plainly - l (IL-1) . IL-1 can impel T lymphocytes to move the conduct to the intersection of pathological change and activity department, and impel its hyperplasia and division, form alveolus inflammation finishing a disease and relying mainly on the fact that inflammation cells or immune effect cells such as T cells, the monocyte and alveolus macrophage,etc. are soaked in early days, IL-1 can also make IL-2 receptor in surface of T cell expose, and impel T cells to release IL-2, IL-2 stimulates B cells, produce immunoglobulin (Ig) in the form of cloning more, can be seen high 's globulin blood disease at being clinical, as pathological change continues progress, the cell composition of alveolus inflammation is reducing constantly, have one kind of cells of skin and increase gradually, and it is not that the cheese granulation is swollen to form a typical one under the swollen function of stimulating the factor of granulation that it secretes gradually. On tubercle later stage, the fibrous conjugated proteln that release macrophages absorbs a large number of fibrous master cells, meanwhile, inflammation and immune effect cell around so that disappear while further reducing, cause the extensive fiber finally.
Organize pathology, the early pathology of tubercle displays mainly T lymphocyte, monocyte and macrophage soak alveolus inflammation caused in the alveolus; Until pathological change develop, the intersection of cell and composition, alveolus of inflammation reduce constantly, and upper the intersection of peel and kinds of cell that macrophage derive and become increase and preponderate gradually, under formating and secreting swollen function which stimulate the factor of the granulation, it is not that a kind of tubercle granulation of cheese is swollen to form a typical one gradually; Pathological change later stage, the connection that alveolus macrophages release is plain can be attracted and become fibrous cells in a large amount, make it and ground substance stick outside the cell, in addition what macrophage secrete become fibrous the intersection of cell and growth factor impel fibrous the intersection of cell and hyperplasia, cause the extensive fiber of lung. Acute the intersection of tubercle and the intersection of disease and arthritis and the intersection of patient and the intersection of joint and slippery membrane and tendon sheath of tenosynovitis examine pathology, show cheese swollen kind of granulation changes while being living, and there are T lymphocytes that are soaked; Chronic the intersection of tubercle and the intersection of joint and slippery membrane, disease of arthritis become extensive hyperplasia, tubercle joint, disease of arthritis accumulate liquid, ooze out liquid for inflammation nature; Patient's slippery membrane of inflammation is organized normally around the tubercle joint.
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