Chapter 28 : Dendritic Cells in Host Immunity to

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Since their identification by Steinman and Cohn over 30 years ago, dendritic cells (DCs) have been shown to play a central role in the initiation and control of the protective host immune response to pathogens. Recent advances in the understanding of the interactions between DCs and and how these interactions affect the course of immune activation and induction of protection against infection are reviewed. Phagocytosis of particulate material and intact organisms occurs by receptor-mediated endocytosis. Engagement of costimulatory molecules by CD28 expressed on the surface of the T cells leads to recruitment of membrane rafts containing kinases and adapters to the immunological synapse, thus amplifying by up to 100-fold the signaling process started by T-cell receptor engagement. The importance of this cytokine in regulating the immune response is highlighted by the observation that individuals with germ line mutations in genes of the interleukin-12 (IL-12) receptor and signaling pathway (that result in defective activity) have an increased risk of contracting mycobacterial diseases, including tuberculosis. Despite increasing knowledge about the interaction between and DCs in vitro, relatively little is known about the sequence of events during infection with in vivo. Researchers have recently initiated studies to compare the number and function of blood DCs in human immunodeficiency virus-seronegative adults with various clinical presentations of tuberculosis (TB).

Citation: Mendelson M, Kaplan G, Hanekom W. 2005. Dendritic Cells in Host Immunity to , p 451-462. In Cole S, Eisenach K, McMurray D, Jacobs, Jr. W (ed), Tuberculosis and the Tubercle Bacillus. ASM Press, Washington, DC. doi: 10.1128/9781555817657.ch28

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Immune Systems
Tumor Necrosis Factor alpha
Plasmacytoid Dendritic Cells
Major Histocompatibility Complex
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Figure 1

(A) Electron micrograph of an in vitro-matured monocyte- derived DC showing the characteristic dendritic processes (arrows). (B) Monocyte-derived DC infected with (arrow), with a higher-magnification view (insert) showing replicating bacilli (arrows).

Citation: Mendelson M, Kaplan G, Hanekom W. 2005. Dendritic Cells in Host Immunity to , p 451-462. In Cole S, Eisenach K, McMurray D, Jacobs, Jr. W (ed), Tuberculosis and the Tubercle Bacillus. ASM Press, Washington, DC. doi: 10.1128/9781555817657.ch28
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Image of Figure 2
Figure 2

The outcome of infection of DCs by may depend on the capacity of the infecting strain to induce DC maturation. In the figure, infection with strain A induces suboptimal DC maturation, thereby inducing a weak Th1 response. The immature state of the infected DC augments the action of Tr cells, allowing active disease and subsequent persistence. Strain B, in contrast, induces optimal DC maturation and a strong Th1 response, leading to control of the infection and reducing the chance of active disease.

Citation: Mendelson M, Kaplan G, Hanekom W. 2005. Dendritic Cells in Host Immunity to , p 451-462. In Cole S, Eisenach K, McMurray D, Jacobs, Jr. W (ed), Tuberculosis and the Tubercle Bacillus. ASM Press, Washington, DC. doi: 10.1128/9781555817657.ch28
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