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Chapter 33 : Pulmonary Innate and Adaptive Defenses against

Authors: Kristi L. Williams1, Floyd L. Wormley, Jr.2, Scarlett Geunes-Boyer3, Jo Rae Wright4, Gary B. Huffnagle5
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Affiliations: 1: Department of Cell Biology, Duke University Medical Center, Durham, NC 27710; 2: The University of Texas at San Antonio, Department of Biology, San Antonio, TX 78249; 3: Department of Cell Biology, Duke University Medical Center, Durham, NC 27710; 4: Department of Cell Biology, Duke University Medical Center, Durham, NC 27710; 5: Internal Medicine - Pulmonary Division, University of Michigan Med Center, Ann Arbor, MI 48109–5642
Content Type: Monograph
Publication Year: 2011

Category: Clinical Microbiology; Fungi and Fungal Pathogenesis

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Pulmonary Innate and Adaptive Defenses against , Page 1 of 2

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Abstract:

Clinical and experimental studies clearly substantiate the role of acquired cell-mediated immunity in the establishment of long-term protection against pulmonary cryptococcosis. However, the innate immune system is also centrally involved in both immediate antifungal immune responses as well as promoting adaptive immunity. Surfactant is secreted by type II cells in the alveolar space of the lung, and it is composed of a complex mixture of phospholipids and proteins, including surfactant proteins A and D (SP-A, SP-D), which play a role in innate host defense. Complement plays an important role during innate immune responses to cells in extrapulmonary sites as a consequence of its ability to bind to encapsulated yeast cells and function as an opsonin. Toll-like receptors (TLRs) have been implicated in airway inflammation, and recent evidence suggests the involvement of certain TLRs in mediating a protective response by promoting a Th1-type T-cell adaptive immune response. enters the pulmonary system in both a spore and yeast form and has the ability to remain dormant for many years within the phagosomal compartment before infection is activated. The immune response to this organism is flexible and involves both cellular and humoral factors. However, environmental, genetic, or cryptococcal factors can exert pressures on this flexible program of host defense, leading to chronic and/or progressive infections, including disseminated disease.

Citation: Williams K, Wormley, Jr. F, Geunes-Boyer S, Wright J, Huffnagle G. 2011. Pulmonary Innate and Adaptive Defenses against , p 451-464. In Heitman J, Kozel T, Kwon-Chung K, Perfect J, Casadevall A (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555816858.ch33
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