Saunders Michael N, Rival Claudia M, Mandal Mahua, Cramton Kayla, Rad Laila M, Janczak Katarzyna W, Williams Laura A, Angadi Amogh R, O'Konek Jessica J, Shea Lonnie D, Erickson Loren D
Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, United States.
Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, United States.
Front Allergy. 2024 Aug 9;5:1437523. doi: 10.3389/falgy.2024.1437523. eCollection 2024.
IgE antibodies against the mammalian oligosaccharide allergen galactose-α-1,3-galactose (αGal) can result in a severe allergic disease known as alpha-gal syndrome (AGS). This syndrome, acquired by tick bites that cause αGal sensitization, leads to allergic reactions after ingestion of non-primate mammalian meat and mammalian-derived products that contain αGal. Allergen-specific immunotherapies for this tickborne allergic syndrome are understudied, as are the immune mechanisms of allergic desensitization that induce clinical tolerance to αGal. Here, we reveal that prophylactic administration of αGal glycoprotein-containing nanoparticles to mice prior to tick protein-induced αGal IgE sensitization blunts the production of Th2 cytokines IL-4, IL-5, and IL-13 in an αGal-dependent manner. Furthermore, these effects correlated with suppressed production of αGal-specific IgE and hypersensitivity reactions, as measured by reduced basophil activation and histamine release and the systemic release of mast cell protease-1 (MCPT-1). Therapeutic administration of two doses of αGal-containing nanoparticles to mice sensitized to αGal had partial efficacy by reducing the Th2 cytokine production, αGal-specific IgE production, and MCPT-1 release without reducing basophil activation or histamine release. These data identify nanoparticles carrying encapsulated αGal glycoprotein as a potential strategy for augmenting αGal-specific immune tolerance and reveal diverse mechanisms by which αGal nanoparticles modify immune responses for established αGal-specific IgE-mediated allergic reactions.
针对哺乳动物寡糖过敏原半乳糖-α-1,3-半乳糖(αGal)的IgE抗体可导致一种严重的过敏性疾病,称为α-半乳糖综合征(AGS)。这种综合征是通过蜱叮咬导致αGal致敏而获得的,在摄入含有αGal的非灵长类哺乳动物肉和哺乳动物衍生产品后会引发过敏反应。针对这种蜱传播的过敏综合征的过敏原特异性免疫疗法以及诱导对αGal临床耐受性的过敏脱敏免疫机制的研究都很少。在这里,我们发现,在蜱蛋白诱导的αGal IgE致敏之前,给小鼠预防性施用含αGal糖蛋白的纳米颗粒,会以αGal依赖的方式抑制Th2细胞因子IL-4、IL-5和IL-13的产生。此外,这些效应与αGal特异性IgE的产生抑制和过敏反应相关,通过减少嗜碱性粒细胞活化和组胺释放以及肥大细胞蛋白酶-1(MCPT-1)的全身释放来衡量。对已对αGal致敏的小鼠进行两剂含αGal纳米颗粒的治疗性给药具有部分疗效,可减少Th2细胞因子产生、αGal特异性IgE产生和MCPT-1释放,但不会降低嗜碱性粒细胞活化或组胺释放。这些数据确定携带封装的αGal糖蛋白的纳米颗粒是增强αGal特异性免疫耐受性的潜在策略,并揭示了αGal纳米颗粒改变已建立的αGal特异性IgE介导的过敏反应免疫反应的多种机制。