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Review
. 2001 Feb;102(2):115-22.
doi: 10.1046/j.1365-2567.2001.01193.x.

Specificity, restriction and effector mechanisms of immunoregulatory CD8 T cells

M Vukmanovic-Stejic  1 , M J Thomas, A Noble, D M Kemeny
Affiliations
Review

Specificity, restriction and effector mechanisms of immunoregulatory CD8 T cells

M Vukmanovic-Stejic et al. Immunology. 2001 Feb.
No abstract available

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Figures

Figure 1
Figure 1
Model of activation and function of Qa-1-restricted regulatory CD8 T cells. CD8 T cells can interact with antigen-activated CD4 T cells in a T-cell receptor (TCR)-specific, Qa-1-restricted manner. CD4 T cells recognize antigen–major histocompatibility complex (Ag–MHC) complex on antigen-presenting cells (APCs), and become activated. Antigen-activated CD4 T cells start to express Qa-1 molecules in association with TCR-Vβ-derived peptides. CD8 T cells recognize Qa-1/Vβ complex on the CD4 T cells, and differentiate into regulatory CD8 T cells. Regulatory CD8 T cells downregulate ‘inducer’ CD4 cells.
Figure 2
Figure 2
Novel mechanism by which CD8 T cells regulate immunoglobulin (IgE) responses. Ovalbumin is taken up by dendritic cells in the periphery which then migrate to lymphoid organs (a). Once there, ovalbumin (OVA) is processed and peptides presented in the context of both major histocompatibility complex (MHC) class I and class II molecules (b). Presentation of peptide to OVA-specific CD8 T cells facilitates further activation and the expression of costimulatory molecules such as CD40L and CD28 or survival factors such as TRANCE. IFN-γ production is not required (c). Interaction with the CD8 T cell induces the production of IL-12 by the dendritic cell (d). The IL-12-produced influences the differentiation of the OVA-specific CD4 T cell bound to the dendritic cell (DC), thus generating a T helper type 1 (Th1)-dominant response (e). The interferon-γ (IFN-γ) produced by the dominant Th1 cell population is sufficient to suppress the activity of any Th2 cells generated by OVA priming (f). The resulting suppression of Th2 cell activity reduces the degree of help available to B cells and prevents isotype switching to IgE (g).
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