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IL11

Official Full Name
interleukin 11
Organism
Homo sapiens
GeneID
3589
Background
The protein encoded by this gene is a member of the gp130 family of cytokines. These cytokines drive the assembly of multisubunit receptor complexes, all of which contain at least one molecule of the transmembrane signaling receptor IL6ST (gp130). This cytokine is shown to stimulate the T-cell-dependent development of immunoglobulin-producing B cells. It is also found to support the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells. Alternatively spliced transcript variants encoding distinct isoforms have been found for this gene. [provided by RefSeq, Jun 2012]
Synonyms
AGIF; IL-11;
Bio Chemical Class
Cytokine: interleukin
Protein Sequence
MNCVCRLVLVVLSLWPDTAVAPGPPPGPPRVSPDPRAELDSTVLLTRSLLADTRQLAAQLRDKFPADGDHNLDSLPTLAMSAGALGALQLPGVLTRLRADLLSYLRHVQWLRRAGGSSLKTLEPELGTLQARLDRLLRRLQLLMSRLALPQPPPDPPAPPLAPPSSAWGGIRAAHAILGGLHLTLDWAVRGLLLLKTRL
Open
Disease
Thrombocytopenia
Approved Drug
0
Clinical Trial Drug
1 +
Discontinued Drug
0

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Detailed Information

Interleukin-11 (IL-11), a member of the IL-6 cytokine family, has long been recognized for its involvement in hematopoietic regulation, tissue repair, and tumorigenesis. However, recent studies have revealed that IL-11 plays a significantly more critical role in various physiological and pathological processes than previously understood. This review summarizes the molecular mechanisms by which IL-11 promotes tissue fibrosis, tumorigenesis, inflammation regulation, metabolic abnormalities, and aging, along with its potential clinical applications.

Molecular Structure and Signaling Mechanisms of IL-11

IL-11 is a multifunctional cytokine with a molecular weight of approximately 19 kDa. Its signaling depends on the formation of a hexameric signaling complex composed of IL-11, its specific receptor IL-11Rα, and the common signaling receptor glycoprotein 130 (GP130). Upon activation of the classical signaling pathway, this complex recruits Janus kinases (JAKs), leading to phosphorylation of tyrosine residues in the cytoplasmic region of GP130, which subsequently activates signal transducer and activator of transcription 1/3 (STAT1/3), regulating downstream target gene expression.

Beyond the classical signaling pathway, IL-11 also exerts its biological functions through two non-classical mechanisms: trans-signaling (where soluble IL-11Rα, generated by ADAM10 protease cleavage, binds to soluble IL-11) and cis-presentation (where soluble IL-11 is presented to adjacent cells expressing GP130 after binding to IL-11Rα on the cell surface), thereby broadening its regulatory scope.

Figure 1: TGFβ stimulates fibroblasts to upregulate IL11 via SMAD signaling, leading to ERK-mediated translation of profibrotic genes through IL-11/gp130 signaling, while STAT3 activation by IL-11 is minimal and likely irrelevant to fibrogenesis. Figure 1. Autocrine IL-11 signaling underlies fibroblast activation. (Ng B, et al., 2020)

 IL-11's Mechanistic Network in Aging Promotion

The molecular mechanisms by which IL-11 promotes aging involve three interrelated pathophysiological processes, forming a vicious cycle:

Abnormal Metabolic Regulation: IL-11 suppresses AMPK activity while activating the mTORC1 signaling pathway, blocking thermogenesis in adipose tissue (decreasing UCP1 expression), leading to a loss of metabolic flexibility and metabolic "stasis," which accelerates aging.

Chronic Inflammation Activation: IL-11 activates pro-inflammatory transcription factors such as NF-κB and STAT3, recruits macrophages to infiltrate adipose tissue and the liver, triggering a low-grade chronic inflammation state, a core driving factor in aging.

Activation of Cellular Senescence Pathways: IL-11 induces DNA damage response (DDR) pathways, promoting telomere attrition and mitochondrial dysfunction, accelerating cellular senescence, and forming a senescence-associated secretory phenotype (SASP), which amplifies inflammation and tissue damage.

Anti-IL-11 therapy breaks this vicious cycle by intervening in all three interconnected pathophysiological processes, achieving a dual effect of extending healthspan and lifespan.

IL-11's Immune Regulatory Function

IL-11 exhibits complex and diverse regulatory effects in both innate and adaptive immune responses. In innate immunity, IL-11 directly regulates macrophage function, inhibiting the production of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-12. In a mouse endotoxemia model, IL-11 significantly reduced serum levels of TNF-α and IL-1β, exerting anti-inflammatory protective effects.

In adaptive immunity, IL-11 participates in the differentiation regulation of B cells and T cells. Research shows that IL-11 promotes the production of immunoglobulin G (IgG) and immunoglobulin M (IgM) by B cells, although it has no direct effect on purified B cells, suggesting that it may regulate B cell function through indirect mechanisms. Additionally, IL-11 induces differentiation of purified naïve CD4^+ T cells into T helper 2 (Th2) and Th17 phenotypes, participating in the regulation of adaptive immune responses.

IL-11 Receptor Mutations and Associated Genetic Diseases

Gene mutations in components of the IL-11 signaling pathway can lead to several genetic diseases. Complete loss of GP130 function (encoded by the IL6ST gene) causes lethal Stüve-Wiedemann syndrome, with affected infants typically dying within days of birth. Partial loss of GP130 signaling can lead to skeletal developmental abnormalities, immune defects, and high immunoglobulin E syndrome (HIES), characterized by distinctive facial malformations, recurrent infections, and elevated serum IgE levels.

Specific loss of IL-11 signaling (caused by IL11RA gene mutations) mainly results in cranial suture synostosis and dental developmental abnormalities but does not lead to HIES, suggesting that isolated loss of IL-11 signaling is insufficient to cause the full HIES phenotype. These genetic findings further support the important role of IL-11 in multi-system development and homeostasis maintenance.

References:

  1. Widjaja AA, Lim WW, Viswanathan S, et al. Inhibition of IL-11 signalling extends mammalian healthspan and lifespan. Nature. 2024;632(8023):157-165.
  2. Ng B, Cook SA, Schafer S. Interleukin-11 signaling underlies fibrosis, parenchymal dysfunction, and chronic inflammation of the airway. Exp Mol Med. 2020;52(12):1871-1878.
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