The Journal of Experimental Medicine
Torrey Pines Biolabs
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 176K)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ochsenbein, A. F.
Right arrow Articles by Zinkernagel, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ochsenbein, A. F.
Right arrow Articles by Zinkernagel, R. M.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?
© The Rockefeller University Press, 0022-1007/1999/10/1165/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 8, October 18, 1999 1165-1174

Protective T Cell–independent Antiviral Antibody Responses Are Dependent on Complement

Adrian F. Ochsenbeina, Daniel D. Pinschewera, Bernhard Odermatta, Michael C. Carrollb, Hans Hengartnera, and Rolf M. Zinkernagela
a Institute for Experimental Immunology, University Hospital, CH-8091 Zurich, Switzerland
b Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Correspondence to: Adrian F. Ochsenbein, Institute for Experimental Immunology, Schmelzbergstr. 12, CH-8091 Zurich, Switzerland. Tel:41-1-255-2989 Fax:41-1-255-4420 E-mail:aochsenb{at}pathol.unizh.ch.

Complement is part of the innate immune system and one of the first lines of host defense against infections. Its importance was evaluated in this study in virus infections in mice deficient either in soluble complement factors (C3-/-, C4-/-) or in the complement signaling complex (complement receptor [CR]2-/-, CD19-/-). The induction of the initial T cell–independent neutralizing immunoglobulin (Ig)M antibody response to vesicular stomatitis virus (VSV), poliomyelitis virus, and recombinant vaccinia virus depended on efficient antigen trapping by CR3 and -4–expressing macrophages of the splenic marginal zone. Neutralizing IgM and IgG antibody responses were largely independent of CR2-mediated stimulation of B cells when mice were infected with live virus. In contrast, immunizations with nonreplicating antigens revealed an important role of B cell stimulation via CR2 in the switch to IgG. The complement cascade was activated after infection with VSV via the classical pathway, and active complement cleavage products augmented the effector function of neutralizing IgM and IgG antibodies to VSV by a factor of 10–100. Absence of the early neutralizing antibody responses, together with the reduced efficiency of neutralizing IgM in C3-/- mice, led to a drastically enhanced susceptibility to disease after infection with VSV.

Key Words: complement, CD19, antiviral immunity, T cell independence, neutralizing antibodies


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS