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Chapter 10 : Sarcoidosis

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Abstract:

This chapter reviews the available knowledge concerning mechanisms leading to inflammatory processes that occur at common sites of involvement in sarcoidosis. It provides a detailed description of cellular interactions that govern the dynamics of granuloma formation. Two theories, not mutually exclusive and both supported by several experimental findings, can been claimed to explain epidemiological and immunological features of sarcoidosis. The first postulates that the sarcoid inflammatory process is triggered by an infectious agent. The second hypothesis favors the concept that genetic factors alter the individual's susceptibility to sarcoidosis. Several epidemiological studies have reported differences in the occurrence and course of sarcoidosis among races and populations. The Kveim-Siltzbach (KS) skin test consists of the intradermal injection of a heat-sterilized extract obtained from splenic tissues of individuals with sarcoidosis. Data on the pattern of lymphokine production during sarcoidosis may be summarized in the context of the Th1/Th2 paradigm. Most chemokines are highly expressed during inflammatory responses taking place in sarcoidosis. Surprisingly, cyclosporine A (CyA) drug, which in theory could inhibit the production of cytokines in sarcoid Th1 cells, has no apparent benefits in sarcoidosis. A section on cytokines highlight that most cytokines set the stage for pathogenetic mechanisms involved in the granuloma formation and fibrosis development during sarcoidosis. This suggests the need to develop anticytokine approaches for the treatment of sarcoidosis which is refractory to the conventional therapy.

Citation: Agostini C, Semenzato G. 2003. Sarcoidosis, p 265-292. In Boros D (ed), Granulomatous Infections and Inflammations. ASM Press, Washington, DC. doi: 10.1128/9781555817879.ch10
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Figure 1

The natural history of sarcoidosis. Approximately 60% of patients spontaneously recover in a period of up to 3 years; over a period of 5 to 10 years, the disease progresses in one-third of patients. Genetic factors are likely to play a major role in disease progression (see text and Table 2 ).

Citation: Agostini C, Semenzato G. 2003. Sarcoidosis, p 265-292. In Boros D (ed), Granulomatous Infections and Inflammations. ASM Press, Washington, DC. doi: 10.1128/9781555817879.ch10
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Image of Figure 2
Figure 2

Following recognition of the unknown antigen(s) causing sarcoidosis, alveolar macrophages (AM) are triggered to produce IL-12 and IL-18. Both cytokines enable the activation of macrophages, which leads to the release of lymphotactic chemokines (CXC10/ IP-10) and cytokines (IL-15) involved in Th1 recruitment. Newly recruited Th1 cells release IFN-γ, which stimulates a further autocrine loop. The net effect is the development of the sarcoid granuloma.

Citation: Agostini C, Semenzato G. 2003. Sarcoidosis, p 265-292. In Boros D (ed), Granulomatous Infections and Inflammations. ASM Press, Washington, DC. doi: 10.1128/9781555817879.ch10
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Tables

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Table 1

Tentative list of infective agents that have been claimed as factors and/or cofactors for the pathogenesis of sarcoidosis

Citation: Agostini C, Semenzato G. 2003. Sarcoidosis, p 265-292. In Boros D (ed), Granulomatous Infections and Inflammations. ASM Press, Washington, DC. doi: 10.1128/9781555817879.ch10
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Table 2

Genetic determinants involved in the pathogenesis of sarcoidosis

Citation: Agostini C, Semenzato G. 2003. Sarcoidosis, p 265-292. In Boros D (ed), Granulomatous Infections and Inflammations. ASM Press, Washington, DC. doi: 10.1128/9781555817879.ch10
Generic image for table
Table 3

Immunologic features that have been observed in patients with sarcoidosis

Citation: Agostini C, Semenzato G. 2003. Sarcoidosis, p 265-292. In Boros D (ed), Granulomatous Infections and Inflammations. ASM Press, Washington, DC. doi: 10.1128/9781555817879.ch10

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