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Clinical and Diagnostic Laboratory Immunology, March 1998, p. 211-218, Vol. 5, No. 2
Institute of Immunology and Rheumatology, The
National Hospital, Oslo, Norway,1 and
Section of Bacteriology, Department of Veterinary Microbiology,
University of Uppsala, Uppsala, Sweden2
Received 18 June 1997/Returned for modification 21 October
1997/Accepted 15 December 1997
We examined alternative and classical complement activation induced
by whole bacilli of Mycobacterium bovis BCG and
Mycobacterium tuberculosis products. After exposure to BCG,
there were higher levels of the terminal complement complex in sera
from Indian tuberculosis patients than in sera from healthy controls.
The addition of BCG with or without EGTA to these sera indicated that approximately 70 to 85% of the total levels of the terminal complement complex was formed by classical activation. Sera from Indian
tuberculosis patients contained more antibody to lipoarabinomannan
(LAM) than sera from healthy Indians. Levels of anti-LAM immunoglobulin
G2 (IgG2), but not anti-LAM IgM, correlated positively with classical activation induced by BCG in the sera. By flow cytometry, deposition of
C3 and terminal complement complex on bacilli incubated with normal
human serum was demonstrated. The anticomplement staining was
significantly reduced in the presence of EGTA and EDTA. Flow cytometry also revealed the binding of complement to BCG incubated with
rabbit anti-LAM and then with factor B-depleted serum. This indicates
that classical activation plays a major role in complement activation
induced by mycobacteria and that anti-LAM IgG on the bacilli can
mediate this response. Classical complement activation may be important
for the extent of phagocytosis of M. tuberculosis by
mononuclear phagocytes, which may influence the course after infection.
1071-412X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Involvement of Antilipoarabinomannan Antibodies in
Classical Complement Activation in Tuberculosis
*
Corresponding author. Mailing address: Institute of
Immunology and Rheumatology, The National Hospital, Fr. Qvamsgt. 1, N-0172 Oslo, Norway. Phone: 47 22 04 24 35. Fax: 47 22 35 36 05.
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