The tubercle bacilli are removed by the cilia so they do not come to their cells after inhalation. No immediate reaction on the part of a healthy organism is caused by tubercle bacilli that arrive in the alveoli of the healthy organism. Resident macrophages and circulating monocytes begin to phagocytose the bacilli are transported to the nearest lymph through the lymphatic channels, while others remain bacilli instead of falling.
The multiplication of tubercle bacilli phagocytosed or not continues and this is when the defense mechanisms of the body come into play.
The appearance of an exudate and a sérofirineux afflut neutrophils are the first signs of response, after two days and two weeks during the growing number of monocytes and macrophages is evident, this period corresponds to the first degradation process phagocytosed bacilli.
The early development of cell-mediated hypersensitivity is signed by the presentation of macrophages and bacillary antigenic components from the BK degraded to T cells on one side, and by the release of interleukin-cell else side. The appearance of epithelioid cell metaplasia by macrophages in which métaplaisent Langhans giant cells around the outbreak and a crown is formed by affluée cells by releasing interleukines2 interfering gamma and stimulates macrophages and lymphocytes. The installation of the mechanisms of hypersensibiliretardée and specific immunity of the organism reached.
The early development of cell-mediated hypersensitivity is signed by the presentation of macrophages and bacillary antigenic components from the BK degraded to T cells on one side, and by the release of interleukin-lymphocytes by other side. The appearance of epithelioid cell metaplasia by macrophages in which métaplaisent Langhans giant cells around the outbreak and a crown is formed by affluée cells by releasing interleukines2 interfering gamma and stimulates macrophages and lymphocytes. The installation of the mechanisms of delayed hypersensitivity and specific immunity of the organism reached.
In 1891 Koch described the new capabilities of the organization under the name of the Koch phenomenon. The subcutaneous injection of BK channel in guinea pig virulent healthy, no immediate reaction occurs at the point of inoculation a nodule appears 10 to 14 days later which subsequently ulcerated, the persistence of the ulcer until the death of the animal. In case of injection of BK virulent guinea pig infected within 24 to 72 appears a necrotic lesion that progresses to regression and cure tuberculosis [url=http://www.medecinesami.com]tuberculose[/url] without underlying being affected. Reactive cells (monocytes and lymphocytes) requires 24 to 72 hours to flow instead of inoculation and causes hypersensitivity tuberculin or TB which is a delayed hypersensitivity reaction.
The sign of immunity is the character Benin and transient lesion is a superinfection immunity because it occurs during the re-inoculation and we have no way of assessing the quantitative tuberculin tests despite current for the measurement of allergy including its existence and its degrees are not correlated with immunity.
For the diagnosis of latent tuberculosis [url=http://www.medecinesami.com]tuberculose[/url] in a child is currently using blood tests that are based on the demonstration in vitro secretion of interferon gamma by T cells sensitized specifically to BK after stimulation by antigens specific BK.
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