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Chapter 33 : Phagocytosis in Immune Response

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Abstract:

Analysis of phagocytosis in has been greatly facilitated by the characterization of the phagocytic properties of S2 cells, an embryonic hemocyte-derived cell line that is readily amenable to RNA-mediated interference (RNAi), opening the field to systematic studies. Identification of new genes involved in phagocytosis relies either on genome-wide RNAi screens in S2 cell culture, proteomic analysis of the plasmatocyte phagosome, or in silico homology screening. An eater loss-of-function mutation has been generated, showing that Eater is required for phagocytosis of several types of bacteria in vivo. The second important conclusion from this brief overview of phagocytic receptors concerns the high redundancy in the receptors. Phagocytosis contributes to the natural defenses of insects against all microorganisms, including bacteria, yeast, and parasites, but has mainly been studied in the case of bacteria. The finding that many bacteria proliferate in the circulatory cavity of mutant flies lacking hemocytes demonstrated the role of phagocytosis. This chapter illustrates that in phagocytosis plays a major role in the removal of microorganisms following any type of infections. Understanding the resistance of intracellular bacteria to phagocytosis and identification of the receptors for their uptake will be of special interest. The major challenge is to decipher the relationships between cellular and humoral responses and the relative contribution of phagocytosis and AMP bacterial killing in various infection models.

Citation: Leclerc V, Caldelari I, Veresceaghina N, Reichhart J. 2009. Phagocytosis in Immune Response, p 513-521. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch33

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FIGURE 1

Model for the interactions between hemocytes and fat body. This model fits with most available data, but is still controversial on some aspects (see text for details). Two complementary signals would be required to activate AMP synthesis in the fat body. The first signal consists of the activation of the Toll and IMD pathways through direct recognition of microorganisms. After a septic injury, the second signal would be produced by the injury itself. The existence and the nature of this signal have not been demonstrated, but observations suggest that a clean injury results in a weak response by the fat body. After natural infections, the second signal would be generated by the hemocytes, activated by phagocytosis of microorganisms (or latex beads in experimental conditions). The nature of this signal is also unknown, but Upd3 or Spaetzle could be candidates.

Citation: Leclerc V, Caldelari I, Veresceaghina N, Reichhart J. 2009. Phagocytosis in Immune Response, p 513-521. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch33
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Tables

Generic image for table
TABLE 1

Phagocytic receptors and opsonizing molecules

Citation: Leclerc V, Caldelari I, Veresceaghina N, Reichhart J. 2009. Phagocytosis in Immune Response, p 513-521. In Russell D, Gordon S (ed), Phagocyte-Pathogen Interactions. ASM Press, Washington, DC. doi: 10.1128/9781555816650.ch33

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