Annual Review of Immunology Volume 22 2004 by Annual Reviews PDF

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Rev. Immunol. 22:33-54. org by HINARI on 09/01/07. For personal use only. ANTIGEN RECOGNITION BY C-TYPE LECTINS ON DC 43 At high concentrations, HIV-1 can infect DCs in cultures that coexpress CD4 and chemokine receptors (57, 101, 102). HIV-1 can replicate in immature as well as in mature DCs that interact with T cells (82, 103). In particular, the initial quantity of virus that enters the mucosal tissues may be decisive in whether DCs become infected by HIV-1 or whether the virus is captured for efficient transinfection of T cells (80).

Sgm LaTeX2e(2002/01/18) P1: IKH GEIJTENBEEK ET AL. steady-state conditions is continuously synthesized and degraded during the normal turnover of connective tissue (70). This process involves specific binding of collagen fibrils to the CLR, followed by the cellular uptake and degradation of the internalized collagen in the lysosomal compartment (71). Annu. Rev. Immunol. 22:33-54. org by HINARI on 09/01/07. For personal use only. CLR AND THE RECOGNITION OF SELF-GLYCOPROTEINS TO MEDIATE CELL ADHESION DC-SIGN functions as a cell-adhesion receptor that regulates DC migration (72) and DC-T cell interaction (21) through its interaction with the self-glycoproteins ICAM-2 and ICAM-3, respectively.

In summary, in vivo antigen targeting to DCs under steady-state conditions seems to induce deletional tolerance when immunity is induced in conditions where DC maturation is triggered. Tolerance can be achieved with small amounts of protein and is manifested as profound unresponsiveness, indicating that the mechanisms dictating tolerance and immune activation are strictly regulated. More than 50% of the proteins in the human body are glycosylated, and it can be envisaged that in the steady state, DCs define immunological self on the basis of sugar structures, thereby suppressing the self-reactivity of the T cell repertoire.

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Annual Review of Immunology Volume 22 2004 by Annual Reviews

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