IL6是一種白細(xì)胞介素，具有調(diào)節(jié)免疫反應(yīng)和炎癥反應(yīng)的作用。最新研究表明，IL6在心血管疾病、惡性腫瘤和神經(jīng)系統(tǒng)疾病等多種疾病的發(fā)生和發(fā)展中發(fā)揮重要作用。研究還發(fā)現(xiàn)，針對(duì)IL6的治療方法在臨床實(shí)踐中取得了很好的療效，可以有效減輕疾病的癥狀和改善患者的生活質(zhì)量。

Cytokine with a wide variety of biological functions in immunity, tissue regeneration, and metabolism. Binds to IL6R, then the complex associates to the signaling subunit IL6ST/gp130 to trigger the intracellular IL6-signaling pathway. The interaction with the membrane-bound IL6R and IL6ST stimulates 'classic signaling', whereas the binding of IL6 and soluble IL6R to IL6ST stimulates 'trans-signaling'. Alternatively, 'cluster signaling' occurs when membrane-bound IL6:IL6R complexes on transmitter cells activate IL6ST receptors on neighboring receiver cells.; IL6 is a potent inducer of the acute phase response. Rapid production of IL6 contributes to host defense during infection and tissue injury, but excessive IL6 synthesis is involved in disease pathology. In the innate immune response, is synthesized by myeloid cells, such as macrophages and dendritic cells, upon recognition of pathogens through toll-like receptors (TLRs) at the site of infection or tissue injury. In the adaptive immune response, is required for the differentiation of B cells into immunoglobulin-secreting cells. Plays a major role in the differentiation of CD4(+) T cell subsets. Essential factor for the development of T follicular helper (Tfh) cells that are required for the induction of germinal-center formation. Required to drive naive CD4(+) T cells to the Th17 lineage. Also required for proliferation of myeloma cells and the survival of plasmablast cells.; Acts as an essential factor in bone homeostasis and on vessels directly or indirectly by induction of VEGF, resulting in increased angiogenesis activity and vascular permeability. Induces, through 'trans-signaling' and synergistically with IL1B and TNF, the production of VEGF. Involved in metabolic controls, is discharged into the bloodstream after muscle contraction increasing lipolysis and improving insulin resistance. 'Trans-signaling' in central nervous system also regulates energy and glucose homeostasis. Mediates, through GLP-1, crosstalk between insulin-sensitive tissues, intestinal L cells and pancreatic islets to adapt to changes in insulin demand. Also acts as a myokine. Plays a protective role during liver injury, being required for maintenance of tissue regeneration. Also has a pivotal role in iron metabolism by regulating HAMP/hepcidin expression upon inflammation or bacterial infection. Through activation of IL6ST-YAP-NOTCH pathway, induces inflammation-induced epithelial regeneration.

1. STA3 facilitates TLR4-dependent IL-6 and IL-8 production via IL-6 receptor-positive feedback in endometrial cells. PMID: 26813342
2. when a confluent endometrial epithelial cell barrier is faced with infection and damage, chemokines attract immune cells to the uterine lumen, but IL6 is solely secreted apically to ensure immune cells are only exposed to IL6 once they reach the lumen. PMID: 25740541
3. The results revealed that the peak expression of IL6 and 21 was on DPV 28 which correlated well with the FMDV antibody titer and plummeted to the prevaccination titer level by 60 DPV. PMID: 24555796
4. Exposure to follicular fluid transiently increased the transcript levels of IL8 and PTGS2, and decreased the expression of SOD2, GPX3, DAB2, and NR3C1. TNF and IL6 levels were also decreased while those of NAMPT were unaffected. PMID: 24186266
5. Testicular IL-1 alpha and IL-1 beta concentrations were highest in the early post-natal period; however, IL-1 bioactivity and IL-6 concentrations were greatest in the immediate pre-pubertal period. PMID: 19144032
6. The results showed that the expression of TNF-alpha, iNOS, and IL-6 in alveolar macrophages was up-regulated by stimulation with the recombinant Mce4A protein of M. bovis; in contrast, expression of IL-12 was unaffected.[IL-6, IL-12] PMID: 17530193
7. results show for the first time that interleukin-6 (IL6), in the presence of its soluble receptor (sIL-6R), induces activation of JAK1, JAK2, and STAT1/STAT3 proteins in bovine articular chondrocytes. PMID: 12419823
8. Mechanical injury potentiates the catabolic effects of TNFalpha and IL-6/sIL-6R in causing proteoglycan degradation in human and bovine cartilage. PMID: 19790045

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Secreted.

IL-6 superfamily

KEGG: bta:280826

STRING: 9913.ENSBTAP00000019865

UniGene: Bt.3686