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
- 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 - is the most important infectious cause of tubal infertility and is frequently detected in the human gastrointestinal tract. , a murine pathogen, closely resembles the human pathogen . Our previous studies showed that the pGP3-deficient mutant was restricted to the large intestine following intracolonic inoculation, suggesting that the pGP3-deficient mutant was killed by the tissue beyond the large intestine. Here, we report that the intra-ilenum, but not the intra-jejunum, to bypass the gastric barrier rescued the colonization of pGP3-deficient , suggesting that pGP3 is required to overcome host factors of the jejunum to help reach the colon. Moreover, mice genetically deficient in IL-22 not only rescued the colonization of pGP3-deficient following intrajejunal inoculation but also rescued the colonization of pGP3-deficient in the whole gastrointestinal tract tissues following intracolonic inoculation on day 14, suggesting a critical role of IL-22 in regulating chlamydial spread. Importantly, IL-22RA1 flox/flox and Villin-cre mice rescued the colonization of pGP3-deficient following intrajejunal inoculation, suggesting that intestinal epithelial-specific IL-22RA1 signaling is important for the spread of pGP3-deficient from the small intestine to the large intestine. These observations provide a platform for further research on intestinal IL-22RA1 signaling in regulating bacterial spread in the intestine. Therefore, host factors identified in the gastrointestinal tract may also contribute to the female lower genital tract barrier during sexually transmitted diseases. - Source: PubMed
Publication date: 2025/09/17
Tian QiFang GuangchiMa JingyueWang LuyingZuo ZonghuiZhang Tianyuan