Natural antibody and complement mediate neutralization of influenza virus in the absence of prior immunity

被引:212
作者
Jayasekera, Jerome P.
Moseman, E. Ashley
Carroll, Michael C.
机构
[1] CBR, Biomed Res Inst, Boston, MA 02115 USA
[2] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA
关键词
D O I
10.1128/JVI.02128-06
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Early control of virus replication by the innate immune response is essential to allow time for the generation of a more effective adaptive immune response. As an important component of innate immunity, complement has been shown to be necessary for protection against numerous microbial infections. This study was undertaken to investigate the role of complement in neutralizing influenza virus. Results demonstrated that the classical pathway of complement mediated serum neutralization of influenza virus. Although nonimmune serum neutralized influenza virus, the mechanism of virus neutralization (VN) required antibody, as sera from RAG1-deficient mice lacked VN activity; moreover, purified natural immunoglobulin M (IgM) restored VN activity to antibody-deficient sera. The mechanism of VN by natural IgM and complement was associated with virion aggregation and coating of the viral hemagglutinin receptor; however, viral lysis did not significantly contribute to VN. Additionally, reconstitution of RAG1-deficient mice with natural IgM resulted in delayed morbidity during influenza virus infection. Collectively, these results provide evidence that natural IgM and the early components of the classical pathway of complement work in concert to neutralize influenza virus and that this interaction may have a significant impact on the course of influenza viral pneumonia.
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页码:3487 / 3494
页数:8
相关论文
共 37 条
[1]   COMPLEMENT-DEPENDENT NEUTRALIZATION OF INFLUENZA-VIRUS BY A SERUM MANNOSE-BINDING LECTIN [J].
ANDERS, EM ;
HARTLEY, CA ;
READING, PC ;
EZEKOWITZ, RAB .
JOURNAL OF GENERAL VIROLOGY, 1994, 75 :615-622
[2]   Human serum IgM glycosylation - Identification of glycoforms that can bind to mannan-binding lectin [J].
Arnold, JN ;
Wormald, MR ;
Suter, DM ;
Radcliffe, CM ;
Harvey, DJ ;
Dwek, RA ;
Rudd, PM ;
Sim, RB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (32) :29080-29087
[3]   2-MURINE NATURAL POLYREACTIVE AUTOANTIBODIES ARE ENCODED BY NONMUTATED GERM-LINE GENES [J].
BACCALA, R ;
QUANG, TV ;
GILBERT, M ;
TERNYNCK, T ;
AVRAMEAS, S .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (12) :4624-4628
[4]   B-1 and B-2 cell-derived immunoglobulin M antibodies are nonredundant components of the protective response to influenza virus infection [J].
Baumgarth, N ;
Herman, OC ;
Jager, GC ;
Brown, LE ;
Herzenberg, LA ;
Chen, JZ .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 192 (02) :271-280
[5]  
BEEBE DP, 1983, J IMMUNOL, V130, P1317
[6]   Accelerated development of IgG autoantibodies and autoimmune disease in the absence of secreted IgM [J].
Boes, M ;
Schmidt, T ;
Linkemann, K ;
Beaudette, BC ;
Marshak-Rothstein, A ;
Chen, JZ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (03) :1184-1189
[7]  
Boes M, 1998, J IMMUNOL, V160, P4776
[8]   ANTI-PHOSPHOCHOLINE ANTIBODIES FOUND IN NORMAL MOUSE SERUM ARE PROTECTIVE AGAINST INTRAVENOUS INFECTION WITH TYPE-3 STREPTOCOCCUS-PNEUMONIAE [J].
BRILES, DE ;
NAHM, M ;
SCHROER, K ;
DAVIE, J ;
BAKER, P ;
KEARNEY, J ;
BARLETTA, R .
JOURNAL OF EXPERIMENTAL MEDICINE, 1981, 153 (03) :694-705
[9]   The classical pathway is the dominant complement pathway required for innate immunity to Streptococcus pneumoniae infection in mice [J].
Brown, JS ;
Hussell, T ;
Gilliland, SM ;
Holden, DW ;
Paton, JC ;
Ehrenstein, MR ;
Walport, MJ ;
Botto, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (26) :16969-16974
[10]   LYSIS OF RNA TUMOR-VIRUSES BY HUMAN-SERUM - DIRECT ANTIBODY-INDEPENDENT TRIGGERING OF CLASSICAL COMPLEMENT PATHWAY [J].
COOPER, NR ;
JENSEN, FC ;
WELSH, RM ;
OLDSTONE, MBA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1976, 144 (04) :970-984