Interferon-gamma (IFN-γ) production by human T lymphocytes upon<i>Legionella pneumophila</i>stimulation<i>in vitro</i>

Kitsukawa, Keizo; Nakamoto, Atsushi; Koito, Hisami; Matsuda, Yasushi; Saitô, Atsushi; Yamamoto, Hiroshi

doi:10.1111/j.1365-2249.1995.tb03475.x

Cited by 7 publications

(2 citation statements)

References 28 publications

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“…L. pneumophila infections are uncommon in patients with AIDS (122), although some reports suggested that the disease is more severe (261). The nature of the effector cells controlling L. pneumophila infection in humans is not clear, but in vitro studies show that Th1-type CD4 T cells respond to L. pneumophila by secreting IFN-␥ (193).…”

Section: Interactions With the Adaptive Immune Systemmentioning

confidence: 99%

Molecular Pathogenesis of Infections Caused byLegionella pneumophila

Newton¹,

et al. 2010

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SUMMARY The genus Legionella contains more than 50 species, of which at least 24 have been associated with human infection. The best-characterized member of the genus, Legionella pneumophila, is the major causative agent of Legionnaires' disease, a severe form of acute pneumonia. L. pneumophila is an intracellular pathogen, and as part of its pathogenesis, the bacteria avoid phagolysosome fusion and replicate within alveolar macrophages and epithelial cells in a vacuole that exhibits many characteristics of the endoplasmic reticulum (ER). The formation of the unusual L. pneumophila vacuole is a feature of its interaction with the host, yet the mechanisms by which the bacteria avoid classical endosome fusion and recruit markers of the ER are incompletely understood. Here we review the factors that contribute to the ability of L. pneumophila to infect and replicate in human cells and amoebae with an emphasis on proteins that are secreted by the bacteria into the Legionella vacuole and/or the host cell. Many of these factors undermine eukaryotic trafficking and signaling pathways by acting as functional and, in some cases, structural mimics of eukaryotic proteins. We discuss the consequences of this mimicry for the biology of the infected cell and also for immune responses to L. pneumophila infection.

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Section: Interactions With the Adaptive Immune Systemmentioning

confidence: 99%

Molecular Pathogenesis of Infections Caused byLegionella pneumophila

Newton¹,

et al. 2010

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“…Kitsukawa et al found that mRNA for IFN-␥ but not IL-4 was produced by in vitro stimulation of human PBMCs with live or formalin-killed Legionella pneumophila (195). CD4 ϩ T-cell clones specific for L. pneumophila also expressed mRNA for IFN-␥ but not IL-4.…”

Section: Mycobacterial and Other Bacterial Diseasesmentioning

confidence: 99%

Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases

1996

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In the mid-1980s, Mosmann, Coffman, and their colleagues discovered that murine CD4+ helper T-cell clones could be distinguished by the cytokines they synthesized. The isolation of human Th1 and Th2 clones by Romagnani and coworkers in the early 1990s has led to a large number of reports on the effects of Th1 and Th2 on the human immune system. More recently, cells other than CD4+ T cells, including CD8+ T cells, monocytes, NK cells, B cells, eosinophils, mast cells, basophils, and other cells, have been shown to be capable of producing "Th1" and "Th2" cytokines. In this review, we examine the literature on human diseases, using the nomenclature of type 1 (Th1-like) and type 2 (Th2-like) cytokines, which includes all cell types producing these cytokines rather than only CD4+ T cells. Type 1 cytokines include interleukin-2 (IL-2), gamma interferon, IL-12 and tumor necrosis factor beta, while type 2 cytokines include IL-4, IL-5, IL-6, IL-10, and IL-13. In general, type 1 cytokines favor the development of a strong cellular immune response whereas type 2 cytokines favor a strong humoral immune response. Some of these type 1 and type 2 cytokines are cross-regulatory. For example, gamma interferon and IL-12 decrease the levels of type 2 cytokines whereas IL-4 and IL-10 decrease the levels of type 1 cytokines. We use this cytokine perspective to examine human diseases including infections due to viruses, bacteria, parasites, and fungi, as well as selected neoplastic, atopic, rheumatologic, autoimmune, and idiopathic-inflammatory conditions. Clinically, type 1 cytokine-predominant responses should be suspected in any delayed-type hypersensitivity-like granulomatous reactions and in infections with intracellular pathogens, whereas conditions involving hypergammaglobulinemia, increased immunoglobulin E levels, and/or eosinophilia are suggestive of type 2 cytokine-predominant conditions. If this immunologic concept is relevant to human diseases, the potential exists for novel cytokine-based therapies and novel cytokine-directed preventive vaccines for such diseases.

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