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The document summarizes the human immune system's defenses against fungal infections. It describes how both humoral and cellular immune mechanisms fight fungal infections. Protective mechanisms involve chemokines and cytokines activating neutrophils, monocytes, macrophages, and epithelial cells to fight infections. Different T cell types also respond - TH1 and TH17 cells aid inflammation while TH2 and regulatory T cells inhibit inflammation but can also downregulate antifungal immunity.
The document summarizes the human immune system's defenses against fungal infections. It describes how both humoral and cellular immune mechanisms fight fungal infections. Protective mechanisms involve chemokines and cytokines activating neutrophils, monocytes, macrophages, and epithelial cells to fight infections. Different T cell types also respond - TH1 and TH17 cells aid inflammation while TH2 and regulatory T cells inhibit inflammation but can also downregulate antifungal immunity.
The document summarizes the human immune system's defenses against fungal infections. It describes how both humoral and cellular immune mechanisms fight fungal infections. Protective mechanisms involve chemokines and cytokines activating neutrophils, monocytes, macrophages, and epithelial cells to fight infections. Different T cell types also respond - TH1 and TH17 cells aid inflammation while TH2 and regulatory T cells inhibit inflammation but can also downregulate antifungal immunity.
Developed as part of the RCSB Collaborative Curriculum Development Program 2014
Developed as part of the RCSB Collaborative Curriculum Development Program 2014 Developed as part of the RCSB Collaborative Curriculum Development Program 2014 (atas, dari kiri ke kanan) Chronic mucocutaneous candidiasis, chromoblastomycosis, and mucicarmine-stained histological section of the cerebellum of an AIDS patient who died from cryptococcal meningoencephalitis (demonstrating an abundance of pink-stained fungi). (bawah) Computed tomography (CT) scan of the lungs of a patient showing a large fungal ball (aspergilloma, black box), which was surgically removed (kanan). Three smaller cavities are also visible in the CT scan (red arrows), which is typical of chronic pulmonary aspergillosis.
Developed as part of the RCSB Collaborative Curriculum Development Program 2014
Developed as part of the RCSB Collaborative Curriculum Development Program 2014 Developed as part of the RCSB Collaborative Curriculum Development Program 2014 Host defense mechanisms. In the human host, fungal infections are fought by both humoral (complement, antibodies) and cellular (phagocytes, T cells) immune mechanisms. Protective mechanisms in both systemic and mucosal antifungal immunity are based on chemotaxis and activation of neutrophils, monocytes/macrophages, and, in the case of mucosal immunity, epithelial cells, by chemokines and cytokines released by macrophages and proinflammatory TH1 and TH17 cells. In contrast, TH2 and some other regulatory T lymphocytes (under the control of modulatory mechanisms such as indoleamine 2,3-dioxygenase) release anti-inflammatory cytokines that provide the tolerance mechanisms necessary to balance inflammation and tissue damage. However, when activated inappropriately or too strongly, the anti-inflammatory TH2 and other regulatory T cell responses can down-regulate antifungal immunity and increase susceptibility to infection. CREDIT: C. BICKEL/SCIENCE TRANSLATIONAL MEDICINE
Developed as part of the RCSB Collaborative Curriculum Development Program 2014
Developed as part of the RCSB Collaborative Curriculum Development Program 2014 Developed as part of the RCSB Collaborative Curriculum Development Program 2014 • Flow of the immune response against fungi in healthy individuals. The first line of defence consisting of the mucus barrier and alveolar macrophages is generally sufficient for the efficient elimination of fungal spores. Breaching of the first line of defence may result in an increased exposure to fungal antigens eliciting a T-helper (Th)1-type response in normal individuals and in a Th2- type response in atopic individuals. sIgA: secretory immunoglobulin-A; IL: interleukin; Developed as part of the RCSB Collaborative Curriculum Development Program 2014