Interleukin-22 (IL-22) is a secreted cytokine of the IL-10 family that plays critical roles in innate immunity, tissue repair, and inflammation at barrier surfaces. Unlike most cytokines, IL-22 acts primarily on non-immune cells (epithelial cells, hepatocytes) through the IL-22R1/IL-10RB receptor complex, activating JAK-STAT signaling to promote antimicrobial defense, epithelial proliferation, and tissue regeneration. IL-22 is produced mainly by activated T cells (Th17/Th22) and innate lymphoid cells (ILC3) in response to infection and inflammation. Its activity is tightly regulated by the soluble antagonist IL-22BP (IL-22RA2), creating a balanced system essential for maintaining barrier integrity while preventing excessive tissue responses.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005125 cytokine activity | IBA GO_REF:0000033 | ACCEPT | Summary: Cytokine activity is a well-established core molecular function of IL-22. Multiple lines of evidence confirm IL-22 functions as a secreted signaling molecule that binds to cell surface receptors (IL-22R1/IL-10RB) to mediate intercellular communication. The IBA annotation is based on phylogenetic inference from well-characterized orthologs across vertebrates. Reason: IL-22 is definitively a cytokine - it is a secreted protein that signals through specific receptors to mediate immune and tissue responses. This is supported by extensive structural, biochemical, and functional studies since its discovery in 2000. The protein binds IL-22R1 with high affinity and signals through JAK-STAT pathways, fulfilling all criteria for cytokine activity. Supporting Evidence: PMID:10875937 We report the identification of a novel human cytokine, distantly related to interleukin (IL)-10, which we term IL-22. IL-22 is produced by activated T cells. IL-22 is a ligand for CRF2-4, a member of the class II cytokine receptor family. PMID:10954742 IL-10-related T cell-derived inducible factor (IL-TIF or IL-21) is a new cytokine structurally related to IL-10 and originally identified in the mouse as a gene induced by IL-9 in T cells and mast cells. |
| GO:0005615 extracellular space | IBA GO_REF:0000033 | ACCEPT | Summary: IL-22 is definitively localized to the extracellular space as a secreted cytokine. The protein contains a signal peptide (aa 1-33) that directs it through the secretory pathway, and mature IL-22 functions in the extracellular environment where it binds to receptors on target cells. The IBA annotation is well-supported by phylogenetic conservation. Reason: IL-22 is a secreted protein that functions in the extracellular space. Multiple structural and functional studies confirm its extracellular localization, including crystal structures of IL-22 bound to its receptor and functional assays showing it acts on cell surface receptors. This is a core aspect of IL-22 biology. Supporting Evidence: file:human/IL22/IL22-uniprot.txt Subcellular location: Secreted. [Signal peptide prediction based on analysis of experimentally verified cleavage sites - PROTEIN SEQUENCE OF 34-48] file:human/IL22/IL22-deep-research.md IL-22 is a secreted protein. It contains an N-terminal signal peptide (amino acids 1β33) that directs it into the endoplasmic reticulum/Golgi secretory pathway, after which the mature cytokine is released into the extracellular space. |
| GO:0050728 negative regulation of inflammatory response | IBA GO_REF:0000033 | MODIFY | Summary: IL-22 has complex, context-dependent effects on inflammation. While it can have anti-inflammatory effects through tissue protection and barrier maintenance, it also has well-documented pro-inflammatory activities in many contexts, particularly in autoimmune diseases like psoriasis and rheumatoid arthritis. The negative regulation annotation captures only one aspect of IL-22 function. Reason: IL-22 has dual pro- and anti-inflammatory effects depending on context. In acute injury, it promotes tissue repair and can limit inflammation through barrier protection. However, in chronic inflammation (psoriasis, IBD), IL-22 often drives pathogenic inflammation. A more accurate annotation would be "regulation of inflammatory response" (GO:0050727) or maintaining both positive and negative regulation terms to capture this duality. Proposed replacements: regulation of inflammatory response positive regulation of response to external stimulus Supporting Evidence: PMID:10875937 In contrast to IL-10, IL-22 does not inhibit the production of proinflammatory cytokines by monocytes in response to LPS nor does it impact IL-10 function on monocytes file:human/IL22/IL22-deep-research.md IL-22 can also have pro-inflammatory properties β for example, by sustaining chronic inflammation in autoimmune diseases... IL-22 effects are context-dependent: in an environment with ongoing infection or tissue stress, IL-22 is generally beneficial (enhancing antimicrobial immunity and repair), but in an already inflamed tissue without active infection, continual IL-22 signaling may contribute to pathogenic inflammation. |
| GO:0007165 signal transduction | IEA GO_REF:0000108 | MODIFY | Summary: Signal transduction is too general a term for IL-22. While IL-22 does activate signal transduction pathways (JAK-STAT, MAPK, PI3K/AKT) in target cells, this annotation lacks specificity. More precise terms describing IL-22 receptor binding or cytokine-mediated signaling would be more informative. Reason: This overly broad term provides little functional information. IL-22 specifically activates JAK-STAT signaling through its receptor complex. More specific annotations like "cytokine-mediated signaling pathway" (GO:0019221) or "JAK-STAT cascade" (GO:0007259) would be more appropriate. Proposed replacements: cytokine-mediated signaling pathway cell surface receptor signaling pathway via JAK-STAT Supporting Evidence: PMID:10875937 Cell lines were identified that respond to IL-22 by activation of STATs 1, 3, and 5 PMID:10954742 Recombinant human IL-TIF was found to activate signal transducer and activator of transcription factors-1 and -3 in several hepatoma cell lines. |
| GO:0005125 cytokine activity | IEA GO_REF:0000043 | ACCEPT | Summary: Duplicate annotation of cytokine activity via automated keyword mapping. While correct, this duplicates the IBA annotation above which is based on stronger phylogenetic evidence. Reason: This is a correct annotation - IL-22 is definitively a cytokine. The IEA evidence is based on UniProt keyword mapping which correctly identifies IL-22 as a cytokine. Having multiple evidence codes for the same core function is acceptable and provides complementary support. Supporting Evidence: file:human/IL22/IL22-uniprot.txt RecName: Full=Interleukin-22; Short=IL-22; AltName: Full=Cytokine Zcyto18 |
| GO:0005576 extracellular region | IEA GO_REF:0000120 | ACCEPT | Summary: Correct localization annotation. IL-22 functions in the extracellular region as a secreted cytokine. This broader term (extracellular region) is appropriate alongside the more specific extracellular space annotation. Reason: IL-22 is correctly annotated to the extracellular region. As a secreted cytokine, it functions outside cells in the extracellular environment. This annotation is consistent with experimental evidence and complements the more specific extracellular space annotation. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consequently, the functional location of IL-22 is the extracellular region, where it diffuses to interact with receptors on target cell surfaces. |
| GO:0005615 extracellular space | IEA GO_REF:0000120 | ACCEPT | Summary: Duplicate annotation of extracellular space localization via automated methods. While correct, this duplicates the IBA annotation which has stronger phylogenetic support. Reason: Correct annotation supported by multiple lines of evidence. IL-22 is a secreted protein that functions in the extracellular space. Multiple evidence codes for the same correct annotation provide complementary support. Supporting Evidence: file:human/IL22/IL22-uniprot.txt Subcellular location: Secreted. |
| GO:0005515 protein binding | IPI PMID:12513909 Comparison of interleukin-22 and interleukin-10 soluble rece... | MODIFY | Summary: Generic protein binding annotation that provides minimal functional information. IL-22 specifically binds IL-22R1 and IL-10RB receptors. This should be replaced with the more specific "interleukin-22 receptor binding" term. Reason: While IL-22 does bind proteins (its receptors), the generic "protein binding" term is uninformative. The specific annotation "interleukin-22 receptor binding" (GO:0045518) or "cytokine receptor binding" (GO:0005126) would be more appropriate and informative. Proposed replacements: interleukin-22 receptor binding cytokine receptor binding Supporting Evidence: PMID:12513909 Comparison of interleukin-22 and interleukin-10 soluble receptor complexes |
| GO:0005515 protein binding | IPI PMID:18599299 Structure of IL-22 bound to its high-affinity IL-22R1 chain. | MODIFY | Summary: Generic protein binding annotation from structural study of IL-22/IL-22R1 complex. Should be replaced with specific receptor binding annotation. Reason: This paper specifically describes the crystal structure of IL-22 bound to IL-22R1, demonstrating specific receptor binding rather than generic protein binding. The annotation should use "interleukin-22 receptor binding" (GO:0045518). Proposed replacements: interleukin-22 receptor binding Supporting Evidence: PMID:18599299 Structure of IL-22 bound to its high-affinity IL-22R1 chain |
| GO:0005515 protein binding | IPI PMID:18675809 Crystal structure of the IL-22/IL-22R1 complex and its impli... | MODIFY | Summary: Another generic protein binding annotation from IL-22/IL-22R1 structural study. Should specify receptor binding. Reason: This paper describes the crystal structure of the IL-22/IL-22R1 complex and signaling mechanism, demonstrating specific receptor binding. Should use "interleukin-22 receptor binding" (GO:0045518) instead of generic protein binding. Proposed replacements: interleukin-22 receptor binding Supporting Evidence: PMID:18675809 Crystal structure of the IL-22/IL-22R1 complex and its implications for the IL-22 signaling mechanism |
| GO:0005515 protein binding | IPI PMID:20462497 Structure and mechanism of receptor sharing by the IL-10R2 c... | MODIFY | Summary: Generic protein binding annotation describing IL-10RB interaction. Should specify receptor binding activity. Reason: This paper describes receptor sharing by IL-10R2 (IL-10RB), which is part of the IL-22 receptor complex. The annotation should specify "interleukin-22 receptor binding" or "cytokine receptor binding" rather than generic protein binding. Proposed replacements: interleukin-22 receptor binding cytokine receptor binding Supporting Evidence: PMID:20462497 Structure and mechanism of receptor sharing by the IL-10R2 common chain |
| GO:0051384 response to glucocorticoid | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: Automated annotation suggesting IL-22 expression responds to glucocorticoids. While IL-22 production can be modulated by glucocorticoids in immune cells, this is not a core function of the IL-22 protein itself. Reason: IL-22 expression can be regulated by glucocorticoids as part of anti-inflammatory responses, but this represents regulation of IL-22 production rather than a core function of the IL-22 protein. This is a secondary/regulatory aspect rather than a defining characteristic of IL-22. Supporting Evidence: file:human/IL22/IL22-deep-research.md anti-inflammatory cytokines like IL-10 or regulatory T cells can suppress IL-22 production [glucocorticoids act similarly as anti-inflammatory agents] |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-448480 | ACCEPT | Summary: Correct annotation from Reactome pathway showing IL-22 binding to IL-22RA1:JAK1 receptor complex in the extracellular space. Multiple Reactome annotations provide pathway-specific evidence. Reason: IL-22 functions in the extracellular region where it binds to its receptor complex. This Reactome annotation is based on curated pathway knowledge and is correct. Supporting Evidence: Reactome:R-HSA-448480 IL22 binds IL22RA1:JAK1 receptor complex [occurs in extracellular region] |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-448741 | ACCEPT | Summary: Correct annotation showing IL-22 binding to its soluble antagonist IL-22RA2 (IL-22BP) in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region where it can be bound and neutralized by IL-22BP. This regulatory interaction occurs in the extracellular space. Supporting Evidence: PMID:11481447 We demonstrate that IL-22RA2 binds specifically to IL-22 and neutralizes IL-22-induced proliferation |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8854645 | ACCEPT | Summary: Another correct Reactome annotation showing IL-22 receptor complex formation in the extracellular region. Reason: Correctly shows IL-22 in the extracellular region as part of receptor complex assembly with IL-10RB:TYK2. Multiple Reactome pathways provide consistent evidence for extracellular localization. Supporting Evidence: Reactome:R-HSA-8854645 IL22:IL22RA1:JAK1 binds IL10RB:TYK2 |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8986995 | ACCEPT | Summary: Correct Reactome annotation documenting IL-22 signaling pathway events in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region in this Reactome pathway. Multiple independent Reactome pathways consistently place IL-22 in the extracellular space where it interacts with its receptors. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consistent with this, Reactome and other pathway databases localize IL-22 to the extracellular region in human pathways. |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8987014 | ACCEPT | Summary: Correct Reactome annotation documenting IL-22 signaling pathway events in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region in this Reactome pathway. Multiple independent Reactome pathways consistently place IL-22 in the extracellular space where it interacts with its receptors. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consistent with this, Reactome and other pathway databases localize IL-22 to the extracellular region in human pathways. |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8987042 | ACCEPT | Summary: Correct Reactome annotation documenting IL-22 signaling pathway events in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region in this Reactome pathway. Multiple independent Reactome pathways consistently place IL-22 in the extracellular space where it interacts with its receptors. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consistent with this, Reactome and other pathway databases localize IL-22 to the extracellular region in human pathways. |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8987070 | ACCEPT | Summary: Correct Reactome annotation documenting IL-22 signaling pathway events in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region in this Reactome pathway. Multiple independent Reactome pathways consistently place IL-22 in the extracellular space where it interacts with its receptors. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consistent with this, Reactome and other pathway databases localize IL-22 to the extracellular region in human pathways. |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8987132 | ACCEPT | Summary: Correct Reactome annotation documenting IL-22 signaling pathway events in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region in this Reactome pathway. Multiple independent Reactome pathways consistently place IL-22 in the extracellular space where it interacts with its receptors. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consistent with this, Reactome and other pathway databases localize IL-22 to the extracellular region in human pathways. |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8987236 | ACCEPT | Summary: Correct Reactome annotation documenting IL-22 signaling pathway events in the extracellular region. Reason: IL-22 is correctly localized to the extracellular region in this Reactome pathway. Multiple independent Reactome pathways consistently place IL-22 in the extracellular space where it interacts with its receptors. Supporting Evidence: file:human/IL22/IL22-deep-research.md Consistent with this, Reactome and other pathway databases localize IL-22 to the extracellular region in human pathways. |
| GO:0006953 acute-phase response | NAS PMID:11481447 A soluble class II cytokine receptor, IL-22RA2, is a natural... | ACCEPT | Summary: IL-22 induces acute-phase response in hepatocytes, a well-documented function. IL-22 stimulates production of acute phase proteins like serum amyloid A, haptoglobin, and alpha-1-antichymotrypsin in liver cells. Reason: Induction of acute-phase response is a core biological function of IL-22. Multiple studies demonstrate IL-22 activates STAT3 in hepatocytes to induce acute phase reactants. This is one of the originally discovered functions of IL-22 and remains a key aspect of its role in inflammation and innate immunity. Supporting Evidence: PMID:10954742 IL-TIF stimulation of HepG2 human hepatoma cells up-regulated the production of acute phase reactants such as serum amyloid A, alpha1-antichymotrypsin, and haptoglobin. PMID:11481447 Because IL-22 induces the expression of acute phase reactants, IL-22RA2 may play an important role as an IL-22 antagonist in the regulation of inflammatory responses. |
| GO:0006954 inflammatory response | NAS PMID:10954742 Human interleukin-10-related T cell-derived inducible factor... | ACCEPT | Summary: IL-22 participates in inflammatory responses, though its effects are complex and context-dependent. IL-22 can promote inflammation in autoimmune diseases but also has tissue-protective anti-inflammatory effects. Reason: IL-22 is involved in inflammatory response, though its role is nuanced. It contributes to inflammation through acute phase protein induction and tissue responses, but also promotes tissue repair. This broad annotation captures IL-22s involvement in inflammatory processes. Supporting Evidence: PMID:10954742 IL-TIF expression was found to be rapidly increased after lipopolysaccharide (LPS) injection, suggesting that this cytokine contributes to the inflammatory response in vivo. file:human/IL22/IL22-deep-research.md IL-22 serves as a key mediator of the innate immune response (GO:0045087) and the inflammatory response (GO:0006954) during infection and injury. |
| GO:0045518 interleukin-22 receptor binding | NAS PMID:10875937 Interleukin (IL)-22, a novel human cytokine that signals thr... | ACCEPT | Summary: IL-22 specifically binds to the IL-22 receptor complex composed of IL-22R1 (IL-22RA1) and IL-10RB (IL-10R2). This is a core molecular function that has been extensively characterized through structural and biochemical studies. Reason: Interleukin-22 receptor binding is a defining molecular function of IL-22. The protein binds with high affinity to IL-22R1 and forms a signaling complex with IL-10RB. This specific receptor binding activity distinguishes IL-22 from other IL-10 family members and is essential for all IL-22 biological functions. Supporting Evidence: PMID:10875937 IL-22 is a ligand for CRF2-4, a member of the class II cytokine receptor family... A new member of the interferon receptor family, which we term IL-22R, functions as a second component together with CRF2-4 to enable IL-22 signaling. file:human/IL22/IL22-deep-research.md IL-22 binds to a heterodimeric receptor complex composed of IL-22RA1 (a cell-type specific Ξ±-chain on epithelial and stromal cells) and the shared IL-10RB (IL-10R2) Ξ²-chain. |
| GO:0050832 defense response to fungus | IC file:human/IL22/IL22-deep-research.md | NEW | Summary: IL-22 mediates defense responses against fungal pathogens at barrier surfaces by inducing antimicrobial peptides. This function is directly stated in the deep research but not currently annotated. Reason: IL-22 plays a documented role in antifungal defense through antimicrobial peptide induction. The deep research explicitly states IL-22 strengthens barriers against both bacteria AND fungi, but only bacterial defense is currently annotated. Supporting Evidence: file:human/IL22/IL22-deep-research.md IL-22 stimulates epithelial cells (in the skin, gut, lung, etc.) to produce antimicrobial peptides (such as Ξ²-defensins, S100 proteins, Reg3 lectins in mice) and mucus, thereby strengthening the barrier against pathogenic bacteria and fungi |
| GO:0010631 epithelial cell migration | IC file:human/IL22/IL22-deep-research.md | NEW | Summary: IL-22 promotes epithelial cell migration and spreading, which is important for wound healing and tissue repair. This is a direct effect of IL-22 signaling. Reason: IL-22 directly promotes epithelial cell migration through its signaling pathways. This is distinct from proliferation and is an important component of wound healing. Supporting Evidence: file:human/IL22/IL22-deep-research.md epithelial cell migration (IL-22 was shown to promote epithelial cell spreading and mobility) |
| GO:0043066 negative regulation of apoptotic process | IC file:human/IL22/IL22-deep-research.md | NEW | Summary: IL-22 promotes cell survival and protects cells from apoptosis, particularly in hepatocytes and epithelial cells. This anti-apoptotic effect is mediated through STAT3 activation and upregulation of survival proteins. Reason: Cell survival/anti-apoptosis is a core function of IL-22, particularly important for its tissue-protective effects. Multiple studies demonstrate IL-22 prevents apoptosis in target cells. Supporting Evidence: file:human/IL22/IL22-deep-research.md These signaling cascades promote target cell survival, proliferation, and repair, enabling tissues to withstand and recover from inflammatory damage file:human/IL22/IL22-deep-research.md IL-22 acts as a survival factor for hepatocytes via STAT3 activation, reducing liver damage... In vitro, IL-22 could prevent hepatocyte apoptosis file:human/IL22/IL22-deep-research.md linking this cytokine to numerous gene expression programs involved in inflammation, cell survival (e.g. upregulating Bcl-2/Bcl-x_L) |
| GO:0070257 positive regulation of mucus secretion | IC file:human/IL22/IL22-deep-research.md | NEW | Summary: IL-22 stimulates mucus production by epithelial cells at barrier surfaces, which is an important component of antimicrobial defense and barrier function. Reason: Mucus production is specifically mentioned as an IL-22-induced protective mechanism at mucosal barriers. This is distinct from antimicrobial peptide production and represents an important barrier defense function. Supporting Evidence: file:human/IL22/IL22-deep-research.md IL-22 stimulates epithelial cells (in the skin, gut, lung, etc.) to produce antimicrobial peptides (such as Ξ²-defensins, S100 proteins, Reg3 lectins in mice) and mucus, thereby strengthening the barrier against pathogenic bacteria and fungi file:human/IL22/IL22-deep-research.md IL-22 plays a paradoxical role: it is generally protective for the intestinal mucosa (promoting wound healing and mucus production) |
| GO:0072089 stem cell proliferation | IC file:human/IL22/IL22-deep-research.md | NEW | Summary: IL-22 promotes intestinal stem cell proliferation, which is crucial for epithelial regeneration after injury. This is a specific and important function distinct from general epithelial proliferation. Reason: IL-22 specifically drives stem cell proliferation in the intestine, which is mechanistically distinct from differentiated epithelial cell proliferation. This function is key to IL-22s regenerative capacity. Supporting Evidence: file:human/IL22/IL22-deep-research.md IL-22 has been shown to drive intestinal stem cell proliferation and epithelial regeneration after acute injury in the gut, largely via STAT3 activation in those cells |
| GO:0002225 positive regulation of antimicrobial peptide production | IEA | NEW | Summary: IL-22 stimulates epithelial cells to produce antimicrobial peptides such as Ξ²-defensins, S100 proteins, and Reg3 lectins at mucosal surfaces as part of barrier defense Reason: This is a hallmark function of IL-22 at mucosal surfaces, where it strengthens epithelial barriers by inducing antimicrobial peptide production in skin, gut, and lung epithelial cells Supporting Evidence: file:human/IL22/IL22-deep-research.md IL-22 stimulates epithelial cells (in the skin, gut, lung, etc.) to produce antimicrobial peptides (such as Ξ²-defensins, S100 proteins, Reg3 lectins in mice) and mucus, thereby strengthening the barrier against pathogenic bacteria and fungi |
| GO:0042060 wound healing | IEA | NEW | Summary: IL-22 promotes epithelial regeneration for wound healing Reason: IL-22 plays an essential role in regenerating epithelial cells after injury to maintain barrier function and prevent further tissue damage. It induces proliferation and antimicrobial peptide production in keratinocytes and intestinal epithelial cells. Supporting Evidence: PMID:17204547 IL-22-mediated liver cell regeneration |
| GO:0042742 defense response to bacterium | IEA | NEW | Summary: IL-22 induces antimicrobial peptides for bacterial defense Reason: IL-22 induces production of antimicrobial peptides (Ξ²-defensins, S100 proteins, RegIIIΞ³) in epithelial cells at mucosal surfaces. This provides critical defense against bacterial pathogens at barrier sites like intestine and lung. Supporting Evidence: file:human/IL22/IL22-deep-research.md IL-22 induces antimicrobial peptide production |
| GO:0045087 innate immune response | IEA | NEW | Summary: IL-22 mediates innate immunity at epithelial barriers Reason: IL-22 is a key mediator of innate immunity at epithelial surfaces, inducing antimicrobial peptide production and maintaining barrier integrity. Unlike other cytokines, IL-22 acts on tissue cells rather than immune cells to coordinate innate defense. Supporting Evidence: file:human/IL22/IL22-deep-research.md IL-22 targets epithelial cells rather than immune cells |
| GO:0050673 epithelial cell proliferation | IEA | NEW | Summary: IL-22 induces epithelial cell proliferation for tissue repair Reason: IL-22 directly stimulates proliferation of epithelial cells including keratinocytes, intestinal epithelial cells, and hepatocytes. This proliferative response is essential for tissue regeneration and barrier restoration after injury. Supporting Evidence: PMID:17204547 IL-22-mediated liver cell regeneration |
| GO:0007259 cell surface receptor signaling pathway via JAK-STAT | IEA | NEW | Summary: IL-22 binding to its heterodimeric receptor (IL-22RA1/IL-10RB) activates JAK1 and TYK2 tyrosine kinases, leading to STAT3 phosphorylation and downstream signaling Reason: The JAK-STAT pathway (particularly STAT3) is the central and primary signaling mechanism triggered by IL-22 upon receptor binding, essential for all IL-22 functions Supporting Evidence: file:human/IL22/IL22-deep-research.md Upon ligand binding, this receptor activates the JAK1 and TYK2 tyrosine kinases, leading to phosphorylation of STAT3 and downstream signaling via the ERK, PI3K/AKT, and STAT3 pathways. The JAK-STAT pathway (particularly STAT3) is the central pathway triggered by IL-22 |
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