No abstract available.
Interleukin-1*

No abstract available.
Humans ; Interleukin-1* ; Periodontitis*

No abstract available.
Humans* ; Interleukin-1* ; Keratinocytes*

BACKGROUND: The severity of several chronic inflammatory diseases was reported to be associated with polymorphism of the IL-1 receptor antagonist gene(IL-lrn). OBJECTIVE: This study was performed to study the polymorphism of the IL-1rn in vitiligo and in the normal Korean population. METHODS: Thirty one cases of vitiligo and seventy nine normal Koreans as control were studied for the polymorphism of IL-1 rn. RESULTS: The frequency of allele 2 of the IL- I rn in 31 patients with vitiligo was compared with that of the 79 healthy controls. The frequency of allele 2 was 1.6% in vitiligo patients and 3.8% in the normal controls. CONCLUSION: There was no significant difference in the frequency of allele 2 between the vitiligo patients and normal controls.
Alleles ; Humans ; Interleukin-1* ; Vitiligo*

No abstract available.
Interleukin 1 Receptor Antagonist Protein*

Cytokines play a pivotal role in maintaining bone homeostasis. Osteoclasts (OCs), the sole bone resorbing cells, are regulated by numerous cytokines. Macrophage colony-stimulating factor and receptor activator of NF-κB ligand play a central role in OC differentiation, which is also termed osteoclastogenesis. Osteoclastogenic cytokines, including tumor necrosis factor-α, IL-1, IL-6, IL-7, IL-8, IL-11, IL-15, IL-17, IL-23, and IL-34, promote OC differentiation, whereas anti-osteoclastogenic cytokines, including interferon (IFN)-α, IFN-β, IFN-γ, IL-3, IL-4, IL-10, IL-12, IL-27, and IL-33, downregulate OC differentiation. Therefore, dynamic regulation of osteoclastogenic and anti-osteoclastogenic cytokines is important in maintaining the balance between bone-resorbing OCs and bone-forming osteoblasts (OBs), which eventually affects bone integrity. This review outlines the osteoclastogenic and anti-osteoclastogenic properties of cytokines with regard to osteoimmunology, and summarizes our current understanding of the roles these cytokines play in osteoclastogenesis.
Cytokines ; Homeostasis ; Interferons ; Interleukin-1 ; Interleukin-10 ; Interleukin-11 ; Interleukin-12 ; Interleukin-15 ; Interleukin-17 ; Interleukin-23 ; Interleukin-27 ; Interleukin-3 ; Interleukin-33 ; Interleukin-4 ; Interleukin-6 ; Interleukin-7 ; Interleukin-8 ; Macrophage Colony-Stimulating Factor ; Necrosis ; Osteoblasts ; Osteoclasts ; RANK Ligand

No abstract available.
Humans ; Interleukin-1* ; Interleukin-6* ; Plasma* ; Tumor Necrosis Factor-alpha*

We investigated the question of whether cholesterol catabolite can influence expression of inflammatory cytokines via Toll-like receptors (TLR) in monocytic cells. Treatment of THP-1 monocytic cells with 27-hydroxycholesterol (27OHChol) resulted in induction of gene transcription of TLR6 and elevated level of cell surface TLR6. Addition of FSL-1, a TLR6 agonist, to 27OHChol-treated cells resulted in transcription of the IL-1alpha gene and enhanced secretion of the corresponding gene product. However, cholesterol did not affect TLR6 expression, and addition of FSL-1 to cholesterol-treated cells did not induce expression of IL-1alpha . Using pharmacological inhibitors, we investigated molecular mechanisms underlying the expression of TLR6 and IL-1alpha. Treatment with Akt inhibitor IV or U0126 resulted in significantly attenuated expression of TLR6 and IL-1alpha induced by 27OHChol and 27OHChol plus FSL-1, respectively. In addition, treatment with LY294002, SB202190, or SP600125 resulted in significantly attenuated secretion of IL-1alpha . These results indicate that 27OHChol can induce inflammation by augmentation of TLR6-mediated production of IL-1alpha in monocytic cells via multiple signaling pathways.
Cholesterol ; Cytokines ; Inflammation ; Interleukin-1 ; Interleukin-1alpha* ; Toll-Like Receptors*

No abstract available.
Animals ; Interleukin-1 ; Interleukin-1beta ; Islets of Langerhans ; Rats

Humans ; Interleukin Inhibitors ; Interleukin-1 ; Neoplasms ; Pericarditis/drug therapy* ; Recurrence