Human T helper cells reactive with somatic bacterial antigens belong to the Th1 subset

Schlaak, J. F.; Nieder, P.; Büschenfelde, K H Meyer zum; Fleischer, Bernhard

doi:10.1007/bf00196051

Cited by 13 publications

(10 citation statements)

References 27 publications

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“…Human T-cell clones raised against E. coli secrete IFN-g, but not IL-4 and only a little IL-10 [33]. This complies with the cytokine pro®le detected here.…”

Section: Discussionsupporting

confidence: 88%

Interleukin‐10 Produced by the Innate Immune System Masks In Vitro Evidence of Acquired T‐Cell Immunity to E. coli

2000

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Hessle C, Hanson LA Ê , Wold AE. Interleukin-10 Produced by the Innate Immune System Masks In Vitro Ecidence of Acquired T-Cell Immunity. Scand J Immunol 2000;52:13±20 Bacteria trigger stimulation of antigen-speci®c, as well as innate, immune responses. Cytokines and other products of cells belonging to the innate immune system may interfere with the detection of acquired immunity to whole bacteria in vitro. Proliferation and cytokine production by human blood mononuclear cells in response to a whole UV-killed Escherichia coli was compared with the response to commonly used antigen preparations: puri®ed protein derivative (PPD), Candida albicans and in¯uenza proteins. E. coli induced a weaker proliferative response with later onset than did the other antigens, and production of interferon (IFN)-g comparable with that in response to C. albicans and in¯uenza vaccine, but lower than that induced by PPD. Both proliferation and IFN-g production were abolished by removal of CD4 cells or blocking of HLA-D, but not CD1 antigen-presenting molecules. Puri®ed lipopolysaccharide (LPS) induced neither proliferation nor IFN-g production. None of the antigen preparations stimulated interleukin (IL)-4 production but, in contrast to the other antigens, whole E. coli, as well as puri®ed O6 LPS, induced large quantities of IL-10. IL-10 production was independent of CD4 cells or HLA-D molecules. Blocking of IL-10 by neutralizing antibodies increased both E. coli-induced proliferation and IFN-g production markedly. Conversely, the addition of whole E. coli or LPS to cultures stimulated with other antigens (C. albicans or Staphylococcus aureus) downregulated proliferative and IFN-g responses, an effect which was at least partly IL-10 dependent. The results indicate a substantial T-cell memory to commensal E. coli, but suggest that the evidence of such memory, e.g. proliferation and IFN-g production, is effectively prevented by IL-10 and perhaps other factors produced by monocytes in response to bacteria. Thus, the innate immune responses must be taken into account when acquired immune responses to microbes are measured.

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“…Human T-cell clones raised against E. coli secrete IFN-g, but not IL-4 and only a little IL-10 [33]. This complies with the cytokine pro®le detected here.…”

Section: Discussionsupporting

confidence: 88%

Interleukin‐10 Produced by the Innate Immune System Masks In Vitro Evidence of Acquired T‐Cell Immunity to E. coli

2000

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“…The lifelong adaptation of H. pylori, which is noninvasive or minimally invasive (17,18,32,38) with the host inflammatory and immune response (6,7,14,38) is distinctly different from invasive enteric pathogens, such as Salmonella and Shigella species, that are usually associated with self-limited infection and generation of protective immunity (42,47). Interestingly, both invasive enteric pathogens and H. pylori generate innate immune responses characterized by intense inflammation and immunity (6,7,14,38,42,47) dominated by Th1 cytokine (such as IFN-␥ and IL-12) production (2,11,20,36,37,42). This raises the question as to whether the persistence of H. pylori is primarily due to inaccessibility of the intraluminal bacteria to mucosal immune effector mechanisms or is due to other qualitative or quantitative differences in the inflammatory and immune response that favor persistent bacterial colonization.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Innate Cytokine Responses by Products ofHelicobacter pylori

2000

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The gastric inflammatory and immune response in Helicobacter pylori infection may be due to the effect of different H. pylori products on innate immune mechanisms. The aim of this study was to determine whether bacterial components could modulate cytokine production in vitro and thus contribute to Th1 polarization of the gastric immune response observed in vivo. The effect of H. pylori recombinant urease, bacterial lysate, intact bacteria, and bacterial DNA on proliferation and cytokine production by peripheral blood mononuclear cells (PBMCs) from H. pylori-negative donors was examined as a model for innate cytokine responses. Each of the different H. pylori preparations induced gamma interferon (IFN-γ) and interleukin-12p40 (IL-12p40), but not IL-2 or IL-5, production, and all but H. pylori DNA stimulated release of IL-10. Addition of anti-IL-12 antibody to cultures partially inhibited IFN-γ production. In addition, each bacterial product inhibited mitogen-stimulated IL-2 production by PBMCs and Jurkat T cells. The inhibitory effect of bacterial products on IL-2 production correlated with inhibition of mitogen-stimulated lymphocyte proliferation, although urease inhibited IL-2 production without inhibiting proliferation, suggesting that inhibition of IL-2 production alone is not sufficient to inhibit lymphocyte proliferation. The results of these studies demonstrate that Th1 polarization of the gastric immune response may be due in part to the direct effects of multiple different H. pylori components that enhance IFN-γ and IL-12 production while inhibiting both IL-2 production and cell proliferation that may be necessary for Th2 responses.

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“…Bacterial infections with, for example, Bordetella pertussis, Listeria monozytogenes, Mycobacterium bovis, leishmania and many others are associated with increased production of IFN-c, reflecting the requirement of Th-1 immunity for defence and protection [79][80][81][82]. Cytokines produced by the cells of the innate immune system including macrophages and NK cells in response to Mycobacterium tuberculosis and/or its components, were able to shift, at least in vitro, the development of allergen-specific T-cells from a Th-2/ Th-0 to a Th-1 profile.…”

Section: The Issue Of Mycobacterial Infection and Bacillusmentioning

confidence: 99%

The bidirectional capacity of bacterial antigens to modulate allergy and asthma

Renz

Herz²

2002

Eur Respir J

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In recent decades, the prevalence of allergic diseases including bronchial asthma, hay fever and atopic dermatitis, has risen steadily in high-income countries. The underlying mechanisms for this phenomenon remain largely unknown. Since the natural mutation rate is low, altered environmental and lifestyle conditions are thought to play an important role.Epidemiological and clinical studies have provided indirect evidence that infections may prevent the development of atopy and atopic disease. This is referred to as the "hygiene hypothesis". According to the hygiene hypothesis, viral and/or bacterial infections could inhibit the T-helper (Th)-2 immune response associated with atopic reactions by stimulating a Th-1 response involved in defence of bacterial infections and delayed-type hypersensitivity reactions.In particular, the prenatal period and early childhood are considered to be critical for the establishment and maintenance of a normal Th-1/Th-2 balance. On the other hand, several studies suggested that infections exacerbate established allergic diseases, e.g. bronchial asthma, airway hyperresponsiveness and atopic dermatitis. Therefore, viral and/or microbial infections and/or their products may have bidirectional effects on the development of allergy and asthma.This review will focus on recent findings related to the interaction between allergic disorders and infectious diseases, with the main emphasis on bacterial infections.

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Human T helper cells reactive with somatic bacterial antigens belong to the Th1 subset

Cited by 13 publications

References 27 publications

Interleukin‐10 Produced by the Innate Immune System Masks In Vitro Evidence of Acquired T‐Cell Immunity to E. coli

Interleukin‐10 Produced by the Innate Immune System Masks In Vitro Evidence of Acquired T‐Cell Immunity to E. coli

Modulation of Innate Cytokine Responses by Products ofHelicobacter pylori

The bidirectional capacity of bacterial antigens to modulate allergy and asthma

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