From the Th1/Th2 Paradigm towards a Toll-Like Receptor/T-Helper Bias

Netea, Mihai G.; Meer, J.W.M. van der; Sutmuller, Roger P.M.; Adema, Gosse J.; Kullberg, Bart‐Jan

doi:10.1128/aac.49.10.3991-3996.2005

Cited by 160 publications

(129 citation statements)

References 60 publications

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“…We therefore predict that the secretion levels we observe in IFNAR-intact bone marrow cultures and animals results from repeated cycles of amplification via a mechanism of positive-feedback signaling through IFNAR (43). In addition to type I IFNs, proinflammatory cytokines are likewise critically important contributors to effective innate immunity, as well as playing a role in determining how the adaptive response will be biased (38). Interleukin-6 secretion has a profound impact on inflammation through its ability to direct leukocyte recruitment, activation, and eventually apoptosis and also through its contribution to the differentiation of B cells into antibody-producing plasma cells, in conjunction with type I IFNs (26).…”

Section: Discussionmentioning

confidence: 99%

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

Lousberg

Fraser

Tovey

et al. 2010

J Virol

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Section: Discussionmentioning

confidence: 99%

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

Lousberg

Fraser

Tovey

et al. 2010

J Virol

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“…Several studies have highlighted the distinct roles of TLR2 and TLR4 agonists to modulate T cell immune responses by regulating expression of anti-inflammatory and pro-inflammatory cytokines (11,16,19,21,77,78).…”

Section: Discussionmentioning

confidence: 99%

Endocytosis of Mycobacterium tuberculosis Heat Shock Protein 60 Is Required to Induce Interleukin-10 Production in Macrophages*

Parveen

Varman

Nair

et al. 2013

Journal of Biological Chemistry

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Background: Mtbhsp60 induces TLR2-mediated anti-inflammatory response in macrophages, but the mechanisms are not well understood. Results: Clathrin-dependent TLR2-mediated endocytosis of Mtbhsp60 is required to induce anti-inflammatory response via p38 MAPK activation. Conclusion: Mtbhsp60 induces anti-inflammatory response upon endocytosis. Blockage of endocytosis predominantly leads to pro-inflammatory cytokine production. Significance: This information is important to tailor the Mtbhsp60-triggered IL-10 signaling to specifically block the excess nonprotective Th2-type response.

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“…In this study, we found that the plasma level of IFN-γ of HS group increased significantly with the increasing TLR2 expression. In addition, TLR2 activator, pam3cys, activates TLR2 via ERK-MAPK signalling pathway and enhances the Th2 immune response (Netea et al 2005). Therefore, the expression of TLR2 can regulate the Th1/Th2 balance and make it shift towards Th2.…”

Section: Discussionmentioning

confidence: 99%

Effects of γ-aminobutyric acid on the thymus tissue structure, antioxidant activity, cell apoptosis, and cytokine levels in chicks under heat stress

Chen¹,

Xie²,

Zhou³

et al. 2016

CZECH J ANIM SCI

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ABSTRACT:This study aims to investigate the effect of dietary γ-aminobutyric acid (GABA) on the development of thymus tissue structure and function in chicks under heat stress. One-day-old male Wenchang chicks were randomly divided into control group (CK), heat stress group (HS), and GABA+HS group. The chicks from GABA+HS group were administered 0.2 ml of GABA solution daily by oral gavage (50 mg/kg of body weight). Chicks from HS and GABA+HS groups were subjected to heat stress treatment at 40 ± 0.5°C for 2 h every day. Blood and thymus tissue were collected from the chicks at the end of weeks 1-6. Results showed that the thymus weight and index, thickness of cortex, cortex/medulla ratio, number of lymphocytes, activity of superoxide dismutase, total antioxidant capacity, and glutathione peroxidase, and plasma level of tumor necrosis factor-α in HS group were significantly lower than in CK group (P < 0.05). The Toll-like receptor 2 (TLR2) expression in the late stage of heat stress, malondialdehyde (MDA) content, thymocyte apoptosis rate, number of lymphocytes in the S and G2/M phases, and plasma levels of interleukin-4 and interferon-γ in HS group were significantly higher than in CK group (P < 0.05). In contrast, the integrity of thymus tissue structure of GABA+HS group was improved compared with HS group. The TLR2 expression in the early stage of heat stress and the activity of antioxidant enzymes in GABA+HS group were significantly higher than in HS group (P < 0.05), and the MDA content, thymocyte apoptosis rate, number of lymphocytes in the S and G2/M phases, and plasma level of IL-4 and IFN-γ in GABA+HS group were significantly lower than in HS group (P < 0.05). We concluded that heat stress caused structure damage to thymus tissue of chicks, changed the plasma levels of cytokines, reduced the antioxidant activity, and increased cell apoptosis in chick thymus. GABA alleviated the negative effects on the development of chick thymus, improved the immune function of thymus, and played a protective role by regulating the plasma levels of cytokines and antioxidant activity of thymus tissue.

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From the Th1/Th2 Paradigm towards a Toll-Like Receptor/T-Helper Bias

Cited by 160 publications

References 60 publications

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

Type I Interferons Mediate the Innate Cytokine Response to Recombinant Fowlpox Virus but Not the Induction of Plasmacytoid Dendritic Cell-Dependent Adaptive Immunity

Endocytosis of Mycobacterium tuberculosis Heat Shock Protein 60 Is Required to Induce Interleukin-10 Production in Macrophages*

Effects of γ-aminobutyric acid on the thymus tissue structure, antioxidant activity, cell apoptosis, and cytokine levels in chicks under heat stress

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