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Involvement of the complement system in the protection of mice from challenge with respiratory syncytial virus Long strain following passive immunization with monoclonal antibody 18A2B2.

Abstract：

:Passive immunization of mice with 131 micrograms of the non-neutralizing monoclonal antibody (mAb) 18A2B2, directed against the A subgroup epitope of the G glycoprotein of respiratory syncytial virus Long strain (RSV), confers protection against viral i.n. challenge. The role of the Fc fragment of this antibody as well as the involvement of antibody-dependent cellular cytotoxicity (ADCC) and complement-mediated cytolysis towards protection was evaluated in vivo. Passive immunization with the Fab fragment alone (618-907 micrograms mouse-1) was unable to confer protection in mice. Furthermore, we passively immunized with the mAb 18A2B2 SCID beige mice, which are deficient in natural killer (NK) cell activity, to ascertain the role of NK cells in the protective mechanism. These mice were free of virus 5 days following viral challenge, indicating that NK cells do not contribute significantly towards the protective action of this antibody. Moreover, passively immunized BALB/c mice decomplemented with 8-10 U of cobra venom factor (CoVF) and DBA/2J mice (C5 deficient) were only partially protected. These findings suggest that in mice the alternative and classical pathways of the complement system are involved in the passive protection mechanism conferred by the non-neutralizing mAb 18A2B2. To our knowledge, it is the first description of a protective mechanism in mice that involves a non-neutralizing antibody and the complement system.

journal_name

Vaccine

journal_title

Vaccine

authors

Corbeil S,Seguin C,Trudel M

doi

10.1016/0264-410x(95)00222-m

subject

Has Abstract

pub_date

1996-04-01 00:00:00

pages

521-5

issue

6

eissn

0264-410X

issn

1873-2518

pii

0264410X9500222M

journal_volume

14

pub_type

杂志文章

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