Debard N, Buzoni-Gatel D, Bout D
Laboratoire d'Immunologie des Maladies Infectieuses, Faculté des Sciences Pharmaceutiques, Tours, France.
Infect Immun. 1996 Jun;64(6):2158-66. doi: 10.1128/iai.64.6.2158-2166.1996.
SAG1 protein of Toxoplasma gondii was evaluated as a protective antigen in mucosal immunization with cholera toxin as an adjuvant. CBA/J mice intranasally immunized with a combination of SAG1 and cholera toxin exhibited significantly fewer cysts in the brain after oral infection with the 76K strain of T. gondii than control mice. This acquired protection lasted at least 5 months. Protected mice developed high levels of serum anti-SAG1 immunoglobulin G antibodies as well as an enhanced systemic cellular response, as assessed by the proliferation of splenocytes in response to SAG1 restimulation in vitro. This cellular proliferation was associated with an increase of interleukin-2 and interleukin-5 synthesis and with barely detectable gamma interferon production. Splenic immune T cells were shown to convey modest protection to recipients against development of brain cysts following oral infection with T. gondii. Significant production of anti-SAG1 immunoglobulin A was induced in intestinal secretions of protected mice. These results indicate that intranasal immunization with SAG1 and cholera toxin can induce mucosal and systemic immune responses and affords partial and long-lasting resistance against the establishment of chronic toxoplasmosis.
将弓形虫SAG1蛋白作为保护性抗原,以霍乱毒素作为佐剂进行黏膜免疫。用SAG1和霍乱毒素联合经鼻免疫的CBA/J小鼠,在经口感染76K株弓形虫后,其脑中的包囊明显少于对照小鼠。这种获得性保护至少持续5个月。受保护的小鼠产生了高水平的血清抗SAG1免疫球蛋白G抗体以及增强的全身细胞反应,这通过体外重新刺激SAG1后脾细胞的增殖来评估。这种细胞增殖与白细胞介素-2和白细胞介素-5合成的增加以及几乎检测不到的γ干扰素产生有关。脾脏免疫T细胞显示出能为受体提供适度保护,使其在经口感染弓形虫后免受脑包囊的形成。在受保护小鼠的肠道分泌物中诱导产生了大量抗SAG1免疫球蛋白A。这些结果表明,用SAG1和霍乱毒素经鼻免疫可诱导黏膜和全身免疫反应,并对慢性弓形虫病的建立提供部分和持久的抵抗力。