Live varicella vaccine polarizes the mucosal adjuvant action of cholera toxin or its B subunit on specific Th1-type helper T cells with a single nasal coadministration in mice
✍ Scribed by Keiko Sasaki; Michio Kato; Tsuyoshi Takahashi; Sadayuki Ochi; Yoshio Ichinose; Kimiyasu Shiraki; Yoshizo Asano; Masaaki Iwanaga; Takao Tsuji
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 109 KB
- Volume
- 70
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
This study was undertaken to determine whether the specific Th1‐ or Th2‐cell response to varicella‐zoster virus was induced predominantly by a mucosal adjuvant, cholera toxin, in mice. A commercially available live varicella vaccine (Oka strain) and cholera toxin or its B subunit were administered simultaneously via the nasal route. Delayed‐type hypersensitivity to the Oka vaccine was induced, but the systemic neutralizing antibody response was low. The delayed‐type hypersensitivity evoked after a single administration was relatively higher than that on administration three times. When spleen cells from mice immunized once with the vaccine and cholera toxin or its B subunit were restimulated with the live vaccine in vitro, there was greater thymidine uptake and production of interleukin‐ 2 (IL‐2) than controls, but only a low level of IL‐4 production. The production of IL‐2 induced by the B subunit of cholera toxin was less than that by cholera toxin and a mutant of Escherichia coli enterotoxin on co‐immunization with the vaccine in mice. Cholera toxin and its B subunit have been reported to induce predominantly a specific Th2‐type T‐cell response to various antigens. However, the Oka vaccine is an antigen that polarizes the activation of specific Th1/Th2‐type T cells by cholera toxin or its B subunit to the Th1‐type side. Cholera toxin and its B subunit are thus useful mucosal adjuvants for inducing cellular immunity to the Oka vaccine similar to Escherichia coli enterotoxin. J. Med. Virol. 70: 329–335, 2003. © 2003 Wiley‐Liss, Inc.