Ask about this productRelated genes to: IL22 antibody
- Gene:
- IL22 NIH gene
- Name:
- interleukin 22
- Previous symbol:
- -
- Synonyms:
- ILTIF, IL-21, zcyto18, IL-TIF, IL-D110, TIFa, TIFIL-23, IL-22, MGC79382, MGC79384
- Chromosome:
- 12q15
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-12
- Date modifiied:
- 2019-04-23
- Gene:
- IL22RA1 NIH gene
- Name:
- interleukin 22 receptor subunit alpha 1
- Previous symbol:
- IL22R
- Synonyms:
- CRF2-9
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-10-16
- Date modifiied:
- 2015-12-11
Related products to: IL22 antibody
Related articles to: IL22 antibody
- Interleukin-22 (IL-22) is a cytokine that regulates tissue inflammation and repair, primarily through activation of STAT3 signaling. Although its protective effects in acute pancreatitis (AP) are well established, the specific contribution of its receptor, IL-22Ra1, and the underlying signaling mechanisms remain incompletely defined. Notably, the C-terminal region of IL-22Ra1, although devoid of tyrosine residues, has been reported to promote STAT3 activation through unconventional mechanisms. Here, we investigated the role of IL-22Ra1 and its C-terminal (STAT3-associated) domain in a mouse model of caerulein-induced AP. We show that deletion of the C-terminal region of IL-22Ra1 markedly reduces STAT3 activation in the pancreas, confirming its role in amplifying canonical signaling. Unexpectedly, this reduction does not worsen pancreatic injury. In contrast, both IL-22- and IL-22Ra1-deficient mice develop more severe pancreatitis, characterized by increased serum amylase levels, exacerbated inflammatory responses, and enhanced tissue damage. Notably, IL-22Ra1 deficiency results in a more severe phenotype than IL-22 deficiency alone, indicating that IL-22Ra1 mediates protective effects beyond IL-22 signaling. Consistently, acinar-to-ductal metaplasia during the regenerative phase is impaired in both IL-22- and IL-22Ra1-deficient mice but preserved upon C-terminal truncation. Together, these findings identify IL-22Ra1 as a central regulator of pancreatic protection through mechanisms that are independent of maximal STAT3 activation and extend beyond IL-22 itself, suggesting the involvement of additional IL-22Ra1 ligands. These results support the exploration of receptor-activating strategies, such as agonistic antibodies, to promote tissue protection and regeneration. - Source: PubMed
Publication date: 2026/07/28
Puigdevall LénaStewardson ClaraDhulst LysaHendrickx EmilieDumoutier Laure - Vulvovaginal candidiasis (VVC) affects >75% of women, with considerable morbidity and high medical cost burden. While Type 17 cytokines (IL-17, IL-22) are critical for oral and dermal immunity to C. albicans, their role in VVC has been less clear. Th17 gene signatures are potently upregulated in VVC, yet impairment of individual Th17 components (IL-17A, IL-17R subunits, IL-22) does not worsen disease. Rather, estrogen activity is tightly linked to VVC, leading to a paradigm that hormonal pathways, rather than immune defense, dominate susceptibility. Here, we reveal a previously unappreciated role for IL-1/Type 17 in VVC that operates independently of estrogenic hormones. In contrast to mice lacking IL-17A, IL-17RA, IL-22, or IL-22R individually, mice lacking IL-17RA and IL-22RA1 together (Il17raIl22ra1-/-) exhibited high fungal loads and exacerbated tissue damage and inflammation during estrogen-induced VVC. In human vulvar epithelial cells, IL-17 and IL-22 drive synergistic signaling. IL-1R signaling but surprisingly not IL-23 was upstream of this response. Il17raIl22ra1-/- mice expressed high IL-1β yet did not control disease, indicating that IL-1 is upstream but not downstream of Type 17 responses. Unexpectedly, Type 17-dependent control occurred in the absence of exogenous estrogen administration and persisted even when estrus was prevented by progesterone treatment. Collectively, these data indicate that susceptibility to VVC is driven not only by estrogen sensitization but through combinatorial loss of IL-17 and IL-22. - Source: PubMed
Publication date: 2026/05/07
Coleman Bianca MCook Melissa EKhan Md RobinVogel Amanda KWells Anthony JMiao JianVyas Shachi PTaylor Tiffany CAggor Felix E YPonde Nicole ODey IpsitaZou HenryJašarević EldinPeters Brian MGaffen Sarah L - This Mendelian randomization (MR) study investigates the causal relationships between circulating inflammatory proteins, blood metabolites, and Clostridium difficile colitis (CDC), with a focus on potential metabolic mediation. Bidirectional and mediation MR analyses were performed using genome-wide association study (GWAS) summary statistics from 3384 CDC cases and 406,048 controls. The primary MR methods included inverse variance weighting (IVW) and MR-Egger regression, with MR-PRESSO applied to detect and correct horizontal pleiotropy. Sensitivity analyses, including leave-one-out tests, were conducted to ensure the robustness of the findings. Mediation analysis was performed using a two-step MR framework to estimate the causal effects of inflammatory proteins on metabolites and, subsequently, the impact of these metabolites on CDC risk. Bidirectional MR identified 2 inflammatory proteins associated with CDC risk. Higher IL-2 receptor subunit beta (IL-2RB) levels were protective against CDC (OR = 0.827, 95% CI = 0.718-0.953, P < .01), whereas increased IL-22 receptor subunit alpha-1 (IL-22RA1) levels elevated CDC risk (OR = 1.300, 95% CI = 1.078-1.570, P < .01). Unidirectional MR identified 11 plasma metabolites associated with CDC, including a positive correlation with spermidine-to-choline ratio. Mediation MR analysis suggested that 17.4% (-6.21%, 41%) of IL-2RB's protective effect on CDC was mediated through this metabolite. Sensitivity analyses confirmed the robustness of these associations. Our findings suggest that higher IL-2RB levels were protective against CDC, while increased IL-22RA1 levels were associated with higher risk. The Spermidine-to-choline ratio partially mediated the protective effect of IL-2RB, suggesting a metabolic link between inflammation and CDC. - Source: PubMed
Dong GuofengWang LiYan PeilingLuo YongjianWu Jiao - Atopic dermatitis (AD) is a chronic inflammatory skin disease in which increased IL-22 expression contributes to epidermal hyperplasia and barrier defects. Temtokibart is a monoclonal antibody targeting IL-22RA1 (IL-22 receptor subunit alpha-1), blocking the signaling of IL-22 and potentially also of IL-20 and IL-24. - Source: PubMed
Publication date: 2025/11/11
Thaçi DiamantLaquer VivianLynde CharlesReich AdamSoong WeilyWorm MargittaArlert PetraBlemings AllanLitman ThomasMartel Britta COlesen MartinSørensen Ole EGooderham Melinda - Disease of a subgroup of patients with atopic dermatitis (AD) does not show sufficient improvement with current systemic therapies, highlighting the heterogeneity of the chronic inflammatory skin disease and the need for novel treatments. - Source: PubMed
Publication date: 2025/11/11
Wasserer SophiaLitman ThomasHebsgaard JosephineJargosch ManjaHillig ChristinaPilz Anna CarolineGarzorz-Stark NatalieBiedermann TiloBlanchetot ChristopheMenden MichaelMortensen Mette SidselSkak-Nielsen TineBertelsen MaleneUrsoe BirgitteLauffer FelixMartel Britta CEyerich KilianEyerich Stefanie