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Chapter 10 : Innate Immunity and Fungal Infections

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Abstract:

Innate immunity is central to host defense against fungi. For many types of fungal infections, innate immunity is solely responsible for host defense. However, even for fungal infections that require an adaptive immune response for clearance, innate immunity plays a key role in the effective development of adaptive immunity. Several broad effector mechanisms are induced early to combat a fungal infection. Complement, mannose binding protein (MBP), and surfactant proteins promote initial recognition (opsonization) of fungi. The complement pathways are an essential part of the innate response to fungi. Opsonization can also be mediated by MBP via recognition and binding to complex carbohydrates (e.g., D-mannose and N-acetylglucosamine) on fungal surfaces. During pulmonary infections, surfactant proteins may also opsonize fungi and participate in host defense. The cells of the innate immune system possess many immunoregulatory functions, along with potent antifungal effector mechanisms that can be activated by adaptive immunity. The cells of the innate immune system rapidly release cytokines in response to fungal products and binding of opsonized fungi. Fungal infections induce the production of both C-C and C-X-C chemokines. Dendritic cells are the most effective antigen-presenting cells (APC) for stimulating naive T cells and are probably key APC in initiating Th1-type cellmediated immunity against fungi. Fungal virulence factors and secreted or shed fungal products can interfere with a number of innate mechanisms, resulting in a dynamic interaction between microbe and host.

Citation: Herring A, Huffnagle G. 2002. Innate Immunity and Fungal Infections, p 127-137. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch10

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Figure 1.

Functions and interplay of innate and adaptive immunity.

Citation: Herring A, Huffnagle G. 2002. Innate Immunity and Fungal Infections, p 127-137. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch10
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Image of Figure 2.
Figure 2.

Cytokine networks in the innate response to that promote adaptive T1-cell-mediated immunity. This is a working model of early signal generation in response to pulmonary infection. The solid arrows represent information proven experimentally, whereas the dashed arrows represent hypothesized interactions. IL-18, IL-1, and MIP-1α, which also drive Th1 responses to , are not included here.

Citation: Herring A, Huffnagle G. 2002. Innate Immunity and Fungal Infections, p 127-137. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch10
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Tables

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Table 1.

Cells of the innate and adaptive immune response that are sources of signal molecules

Citation: Herring A, Huffnagle G. 2002. Innate Immunity and Fungal Infections, p 127-137. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch10
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Table 2.

Effect of signals from innate immunity on the development of adaptive immunity

Citation: Herring A, Huffnagle G. 2002. Innate Immunity and Fungal Infections, p 127-137. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch10
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Table 3.

Fungal virulence factors

Citation: Herring A, Huffnagle G. 2002. Innate Immunity and Fungal Infections, p 127-137. In Kaufmann S, Sher A, Ahmed R (ed), Immunology of Infectious Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817978.ch10

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