Interaction of IL-1β, IL-6 and tumour necrosis factor-alpha (TNF-α) in human T cells activated by murine antigens

Panzer, Simon; Madden, Michael C.; Matsuki, Kazumasa

doi:10.1111/j.1365-2249.1993.tb08203.x

Cited by 31 publications

(17 citation statements)

References 40 publications

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“…We therefore suggest that positive feedback by IL-6 on IL-1␤ secretion occurs with stress and that the role is to partially negate the downregulatory effect of corticosterone on IL-1␤. This suggestion is supported by an earlier in vitro finding of IL-6-stimulated upregulation of IL-1␤ mRNA in human T cells (51). However, because this suggestion is based in part on the assumption of transiently elevated IL-6, which was no longer evident under the basal conditions at death, it can only be proven definitively in vivo, by assessment of multiple time points after an acute stressor when IL-6 will also be sufficiently elevated to be easily detectable.…”

Section: Circulating Parameterssupporting

confidence: 70%

Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6

Smith¹,

Wilson²,

Louw³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Intermittent psychological stress was induced in adult rats by 2 h/day of immobilization stress for 4 days, with or without blocking the function of IL-6 by using an anti-IL-6 antibody. Basal concentrations of serum corticosterone, IL-1β, IL-6, and TNF-α were assessed 24 h after the last intervention, as were levels of glucocorticoid receptors (GR) and activities of glucocorticoid-inducible enzymes (tyrosine aminotransferase and glutamine synthetase) in muscle and liver. Whole blood cultures were used to assess both spontaneous and LPS-induced reactivity of peripheral blood mononuclear cells. Stress increased corticosterone concentration in a manner partially modulated by IL-6. Serum IL-1β concentration was downregulated during stress when IL-6 was blocked ( P < 0.01). LPS-induced IL-6 secretion by peripheral blood mononuclear cells in vitro correlated positively with serum IL-1β concentration in antibody-treated groups, independently of stress ( R = 0.70 in nonstressed and R = 0.78 in stressed rats; both P < 0.05), whereas serum corticosterone concentration correlated positively with LPS-induced secretion of IL-6 only in control rats ( R = 0.66; P < 0.05). Reductions in liver GR levels indicated independent effects of stress (34.5%) and anti-IL-6 antibody (16.7%) and additive effects for both (62.5%). Similar results are reported for vastus muscle. Conversely, stress increased tyrosine aminotransferase and glutamine synthetase activities in muscle and liver with a significant ( P < 0.05) effect of anti-IL-6 antibody only seen in stressed livers. In conclusion, IL-6 plays a role in maintaining circulating IL-1β concentration after multiple exposures to stress, thus promoting a continued elevation of corticosterone release; in peripheral tissues, IL-6 antagonizes the effects of glucocorticoids, especially at the level of GR concentration.

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Section: Circulating Parameterssupporting

confidence: 70%

Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6

Smith¹,

Wilson²,

Louw³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Furthermore, IL-1␤ increases the expression of I-A, B7-2, CD40, and ICAM-1 in LC, all of which are crucial in stimulating T cells (40). At the T cell level, IL-1␤ promotes T cell proliferation by up-regulating T cell production of IL-2 and IL-2R (41). It is unclear whether LC production of IL-1␤ acts in an autocrine fashion on the LC, on the T cells, or both.…”

Section: Discussionmentioning

confidence: 99%

Vasoactive Intestinal Peptide Modulates Langerhans Cell Immune Function

Kodali¹,

Ding²,

Huang³

et al. 2004

The Journal of Immunology

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Epidermal nerves lie in close proximity to Langerhans cells (LC) and are capable of releasing peptides that modulate LC function, including calcitonin gene-related peptide and pituitary adenylate cyclase-activating polypeptide. The neuropeptide vasoactive intestinal peptide (VIP) has also been found in cutaneous nerves and mRNA, for the VIP receptor vasoactive intestinal peptide receptor type 1, and vasoactive intestinal peptide receptor type 2 have been found in murine LC and the LC-like cell line XS106. We examined the effects of VIP on LC function and cutaneous immunity. VIP inhibited elicitation of a delayed-type hypersensitivity response in previously immunized mice by epidermal cells enriched for LC content pulsed with Ag in vitro. VIP also inhibited the ability of unseparated epidermal cells to present Ag to a T cell clone and hybridoma and the ability of highly enriched LCs to present to the T cell clone. Inhibition of presentation to the hybridoma was observed with an antigenic peptide that does not require processing, suggesting that VIP is active at a step independent of Ag processing. To elucidate the mechanism(s) by which VIP may mediate these effects, we determined the effects of VIP on LC cytokine production using the XS106 cell line as a surrogate for LC. VIP augmented the production of the IL-10 in LPS-stimulated XS106 cells while down-regulating IL-12 and IL-1β production. Thus, VIP, like pituitary adenylate cyclase-activating polypeptide and calcitonin gene-related peptide, down-regulates LC function and the associated immune response.

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“…LC are the only source of cutaneous IL-1 g [26], and IL-1 g induces LC migration and increases expression of I-A, B7-2, CD40, and ICAM-1 in LC [27,28]. IL-1 g also promotes T cell proliferation, up-regulating production of IL-2 and IL-2 receptor [29]. In contrast, IL-10 attenuates Th1-mediated immune responses.…”

Section: Discussionmentioning

confidence: 99%

Pituitary adenylate cyclase‐activating polypeptide inhibits cutaneous immune function

et al. 2003

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Epidermal nerves are closely associated with Langerhans cells (LC) and may be able to release factors, such as calcitonin gene-related peptide and epinephrine, that affect LC function. LC and the LC-like cell line XS106 express mRNA for the pituitary adenylate cyclase-activating polypeptide (PACAP) receptors VPAC1 and VPAC2. We examined whether PACAP regulates cutaneous immunity. Intradermal administration of PACAP prior to application of a contact sensitizer at the injected site inhibited the induction of contact hypersensitivity. Pretreatment of murine epidermal cells enriched for LC content (˚12% LC) with PACAP inhibited their ability to elicit delayed-type hypersensitivity in previously immunized mice. In vitro, PACAP suppressed the ability of both murine epidermal cells and highly purified LC (˚95%) to present antigen to a T cell clone and hybridoma. Furthermore, in LC and the XS106 cell line, PACAP inhibited the LPS/GM-CSF-induced stimulation of IL-1 g secretion and augmented IL-10 production. PACAP also down-regulated CD86 expression in LPS/GM-CSF-stimulated XS106 cells. The immunosuppressive effects of PACAP may be due to modulation of cytokine production and CD86 expression.

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Interaction of IL-1β, IL-6 and tumour necrosis factor-alpha (TNF-α) in human T cells activated by murine antigens

Cited by 31 publications

References 40 publications

Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6

Illuminating the interrelated immune and endocrine adaptations after multiple exposures to short immobilization stress by in vivo blocking of IL-6

Vasoactive Intestinal Peptide Modulates Langerhans Cell Immune Function

Pituitary adenylate cyclase‐activating polypeptide inhibits cutaneous immune function

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