| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Host/Isotype | Mouse IgG1 |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human |
| Immunogen | Purified recombinant fragment of human IL36G |
| Formulation | Purified antibody in PBS with 0.05% sodium azide |
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以下是3-4条关于IL-36G抗体的参考文献及其摘要内容：
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1. **标题**: *"Efficacy and Safety of Spesolimab for the Treatment of Generalized Pustular Psoriasis: A Phase II Trial"*
**作者**: Bachelez H, et al.
**摘要**: 该研究报道了抗IL-36受体单抗Spesolimab在泛发性脓疱型银屑病(GPP)患者中的II期临床试验结果，显示其能快速缓解炎症症状并改善皮肤病变，验证了IL-36通路作为治疗靶点的有效性。
2. **标题**: *"Targeting IL-36 in Hidradenitis Suppurativa: A Phase I Study of ANB019 (Imsidolimab)"*
**作者**: Marovt M, et al.
**摘要**: 本研究评估了抗IL-36G单抗Imsidolimab在化脓性汗腺炎患者中的安全性和初步疗效，结果显示其显著降低局部炎症标志物，支持进一步临床开发。
3. **标题**: *"IL-36 Signaling in Psoriatic Inflammation: Mechanisms and Therapeutic Potential"*
**作者**: Tortola L, et al.
**摘要**: 文章通过小鼠模型和患者样本分析，阐明IL-36G在银屑病中的促炎作用，并证明阻断IL-36通路(如使用中和抗体)可减轻皮肤炎症和病理损伤。
4. **标题**: *"Emerging Role of IL-36 Cytokines in Inflammatory Skin Diseases: From Pathogenesis to Targeted Therapy"*
**作者**: Gabay C, et al.
**摘要**: 综述总结了IL-36家族(包括IL-36G)在银屑病、特应性皮炎等疾病中的病理机制，并讨论靶向IL-36的单克隆抗体在临床试验中的进展与挑战。
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**备注**：部分研究针对IL-36受体(如Spesolimab)而非直接靶向IL-36G，但因其与IL-36G信号通路密切相关，常被纳入相关文献讨论。如需更精确的IL-36G抗体研究，建议进一步检索最新靶向分子开发的论文。
Interleukin-36 gamma (IL-36γ), a pro-inflammatory cytokine belonging to the IL-1 family, plays a critical role in modulating innate and adaptive immune responses. Primarily expressed in epithelial tissues, IL-36γ binds to the IL-36 receptor (IL-36R) and activates downstream signaling pathways, including NF-κB and MAPK, to promote the release of inflammatory mediators. Dysregulated IL-36γ signaling is implicated in chronic inflammatory and autoimmune diseases, particularly psoriasis, where it drives keratinocyte hyperproliferation and immune cell infiltration.
IL-36γ-targeting antibodies have emerged as promising therapeutic agents to block pathological IL-36/IL-36R interactions. These antibodies are designed to neutralize IL-36γ activity, thereby suppressing excessive inflammation and tissue damage. Preclinical studies demonstrate their efficacy in reducing disease severity in psoriasis-like models and other IL-36-mediated conditions, such as generalized pustular psoriasis (GPP) and inflammatory bowel disease (IBD). Several anti-IL-36γ antibodies are currently in clinical trials, highlighting their potential as precision therapies for patients unresponsive to conventional treatments. By selectively inhibiting IL-36γ, these antibodies aim to achieve a favorable safety profile compared to broad immunosuppressants, addressing a significant unmet need in chronic inflammatory disease management.
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