Immunoglobulin G subclass responses to mycobacterial lipoarabinomannan in HIV‐infected and non‐infected patients with tuberculosis

SUMMARY Immunoglohulin G subclass responses to lipoarabinomannan (LAM) of Mycobacterium tuberculosis were determined by ELISA in both HIV‐1 antibody positive (n=31) and negative (n=43) patients with tuberculosis (TB), Responses were also studied in a group of healthy controls (n= 16) and HIV‐1 antib...

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Published in:Clinical and experimental immunology 1993-01, Vol.91 (1), p.25-29
Main Authors: COSTA, C. T. K. A., KHANOLKAR‐YOUNG, S., ELLIOTT, A. M., WASUNNA, K. M. A., McADAM, K. P. W. J.
Format: Article
Language:English
Subjects:
Adolescent
Adult
AIDS/HIV
Antigens, Bacterial - immunology
Biological and medical sciences
ELISA
Female
HIV
HIV Infections - complications
HIV Infections - immunology
human immunodeficiency virus
Humans
Immunodeficiencies
Immunodeficiencies. Immunoglobulinopathies
Immunoglobulin G - analysis
Immunoglobulin G - classification
immunoglobulin G subclasses
Immunopathology
lipoarabinomannan
Lipopolysaccharides - immunology
Male
Medical sciences
Mycobacterium - immunology
Mycobacterium tuberculosis
Sex Factors
tuberculosis
Tuberculosis, Pulmonary - complications
Tuberculosis, Pulmonary - immunology
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Summary:SUMMARY Immunoglohulin G subclass responses to lipoarabinomannan (LAM) of Mycobacterium tuberculosis were determined by ELISA in both HIV‐1 antibody positive (n=31) and negative (n=43) patients with tuberculosis (TB), Responses were also studied in a group of healthy controls (n= 16) and HIV‐1 antibody positive (n=60) individuals without TB. IgG2 antibodies were the predominant subclass, being present in 25 of 43 non‐HIV‐infected TB patients (58%) and in 11 of 31 HIV‐infected TB patients (35%). However. HIV+ TB patients also showed IgG4 (n= 16; 52%). and IgG1 (n=4, 13%) responses to LAM. whereas these subclasses were absent in sera from HIV TB patients. Individuals in both non‐tuberculous control groups showed no antibody responses to LAM. The influence of HIV infection on B cell responses to LAM, and possible mechanisms for antibody‐mediated regulation of immunity to TB, are explored.
ISSN:0009-9104
1365-2249
DOI:10.1111/j.1365-2249.1993.tb03348.x