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Nucleoprotein‐specific nonneutralizing antibodies speed up LCMV elimination independently of complement and F cγ R
Author(s) -
Straub Tobias,
Schweier Oliver,
Bruns Michael,
Nimmerjahn Falk,
Waisman Ari,
Pircher Hanspeter
Publication year - 2013
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.201343565
Subject(s) - lymphocytic choriomeningitis , biology , virology , virus , nucleoprotein , antibody , immunity , immune system , humoral immunity , neutralizing antibody , cd8 , microbiology and biotechnology , immunology
CD 8 + T cells have an essential role in controlling lymphocytic choriomeningitis virus ( LCMV ) infection in mice. Here, we examined the contribution of humoral immunity, including nonneutralizing antibodies ( A bs), in this infection induced by low virus inoculation doses. Mice with impaired humoral immunity readily terminated infection with the slowly replicating LCMV strain A rmstrong but showed delayed virus elimination after inoculation with the faster replicating LCMV strain WE and failed to clear the rapidly replicating LCMV strain D ocile, which is in contrast to the results obtained with wild‐type mice. Thus, the requirement for adaptive humoral immunity to control the infection was dependent on the replication speed of the LCMV strains used. Ab transfers further showed that LCMV ‐specific I g G A bs isolated from LCMV immune serum accelerated virus elimination. These A bs were mainly directed against the viral nucleoprotein ( NP ) and completely lacked virus neutralizing activity. Moreover, m A bs specific for the LCMV NP were also able to decrease viral titers after transfer into infected hosts. Intriguingly, neither C 3 nor F cγ receptors were required for the antiviral activity of the transferred A bs. In conclusion, our study suggests that rapidly generated nonneutralizing A bs specific for the viral NP speed up virus elimination and thereby may counteract T ‐cell exhaustion.