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Một cơ chế có thể cho tolerisation (desensitisation) của các tế bào T đặc biệt phản ứng lưu hành bởi kháng nguyên là như sau. Khi họ đang lưu thông trong cơ thể, tế bào T không làm cho liên kết thân mật thông thường của họ với các tế bào đuôi gai, các tế bào B, vv Thay vào đó, phản ứng tế bào T trở nên pha loãng trong các mô khác | 7 Microbial Strategies in Relation to the Immune Response 187 sary enabling sensitised lymphocytes to destroy host cells infected with Leishmania microorganisms. A possible mechanism for tolerisa-tion desensitisation of specifically reactive circulating T cells by antigen is as follows. When they are circulating through the body T cells fail to make their usual intimate association with dendritic cells B cells etc. Instead the T-cell response becomes diluted among various tissues leading to a reduction in the critical cell mass required for activation. In this environment T cells may encounter antigen on nonprofessional antigen-presenting cells that lack the necessary costimulator molecules for activating T cells and instead may deliver a tolerogenic signal. Under these circumstances CD4 and CD8 T cells although not damaged lose their ability to respond to the specific antigen. They are defused or anergised. In a similar way developing B cells can be rendered immunologically impotent by direct exposure to circulating antigen. After infection with Treponema pallidum immobilising and other antibodies see Ch. 6 are formed and there is an initial T-cell response as detected by lymphocyte transformation in vitro in the presence of treponemes. This initial response disappears as the bacteria multiply and spread through the body and lymphocytes from patients with early secondary syphilis fail to respond in vitro to Treponema pallidum. Later in the secondary stage weeks or months after infection lymphocyte reactivity reappears delayed skin reactions are demonstrable granulomata appear in lymph nodes and the infectious process is finally brought under control. It is not known why lymphocytes from patients with early secondary syphilis fail to respond to the infecting bacteria. Antigen-specific suppression see pp. 192-193 is a possibility or T cells become anergised due to high levels of circulating antigen or alternatively T cells become sequestered in particular tissues .
