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PubMed1995

Characterization of mycobacterial antigens and antibodies in circulating immune complexes from pulmonary tuberculosis.

Circulating immune complexes (CICs) in serum samples from patients with pulmonary tuberculosis (bacteriologically positive [S+C+] and bacteriologically negative [S-C-]) and controls (NHC) have been measured by using C1q binding assay (C1qBA) and 3.5% polyethylene glycol precipitation and measurement of absorbance at 280 nm (PEG-OD 280). Although C1qBA did not show any difference between tuberculous and normal serum samples, PEG-OD 280 was significantly elevated in tuberculous samples. The effect of chemotherapy on CIC levels was studied. During the treatment, initially (for up to 2 months) there was a rise in CIC levels and later a fall, coinciding with bacterial clearance. Anti-purified protein derivative antibodies of class immunoglobulin G (IgG) and immunoglobulin M were measured in the serum samples and PEG precipitates. Anti-mycobacterial antibody measurement in CICs was more discriminatory between the groups than serum antibody. For characterization of the complexed antibody, the PEG precipitates were used in the Western blot and the patterns were compared. S+C+ CICs contained antibodies for a wide range of antigens ranging from 100 Kd to 10 Kd. However, none of the NHC-CICs contained antibodies for antigens < 70 Kd. Thus, when using the criterion of positivity for antibodies to antigens < 70 Kd as a marker for pulmonary tuberculosis, 24 of 24 (100%) of the S+C+ CICs were positive. Similarly, 11 of 16 (70%) of the S-C- CICs contained antibodies for antigens < 70 Kd.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Bacterial↗
PubMed2005

Ipr1 gene mediates innate immunity to tuberculosis.

An estimated eight million people are infected each year with the pathogen Mycobacterium tuberculosis, and more than two million die annually. Yet only about 10% of those infected develop tuberculosis. Genetic variation within host populations is known to be significant in humans and animals, but the nature of genetic control of host resistance to tuberculosis remains poorly understood. Previously we mapped a new genetic locus on mouse chromosome 1, designated sst1 (for supersusceptibility to tuberculosis 1). Here we show that this locus mediates innate immunity in sst1 congenic mouse strains and identify a candidate gene, Intracellular pathogen resistance 1 (Ipr1), within the sst1 locus. The Ipr1 gene is upregulated in the sst1 resistant macrophages after activation and infection, but it is not expressed in the sst1 susceptible macrophages. Expression of the Ipr1 transgene in the sst1 susceptible macrophages limits the multiplication not only of M. tuberculosis but also of Listeria monocytogenes and switches a cell death pathway of the infected macrophages from necrosis to apoptosis. Our data indicate that the Ipr1 gene product might have a previously undocumented function in integrating signals generated by intracellular pathogens with mechanisms controlling innate immunity, cell death and pathogenesis.

Animals↗
PubMed1996

Suppression of adjuvant arthritis in rats by oral administration of type II collagen in combination with type I interferon.

The oral administration of 3 micrograms but not 300 micrograms of type II collagen (CII) significantly suppressed adjuvant arthritis in rats that was induced by immunization with Mycobacterium tuberculosis. Feeding 5000 units of type I interferon was also effective in downregulating the disease. More suppression of adjuvant arthritis was observed when both CII and interferon were orally given. Delayed-type hypersensitivity responses to M. tuberculosis were inhibited in interferon- but not in CII-fed animals. There were no delayed responses to CII in M. tuberculosis-immunized rats fed either CII or interferon. However, the delayed response to M. tuberculosis plus CII was significantly reduced by CII as well as interferon given orally. Feeding both CII and interferon was more effective in suppressing the delayed responses to M. tuberculosis plus CII. A similar suppression was observed in proliferative responses of lymph-node cells to M. tuberculosis, CII, or M. tuberculosis plus CII in-vitro. These results suggest that the suppression of adjuvant arthritis by oral administration of CII is due to tolerance to CII in which a bystander suppression mechanism appears to be involved. Orally administered interferon seems to suppress nonspecifically cellular immune responses. The oral administration of CII in combination with interferon may be a novel way to treat T cell-mediated diseases.

Administration, Oral↗
PubMed1955

EXPERIMENTAL studies of vaccination, allergy, and immunity in tuberculosis. I. Design for a research programme.

With the growing popularity of BCG vaccination in tuberculosis control programmes, the tuberculin test has become a widely accepted means of determining the success of vaccination, despite persistent disagreement in scientific circles about the relation between skin sensitivity to tuberculin and acquired resistance to tuberculosis. With little hope today of solving the allergy-immunity problem by studies on human beings, and because of the urgent practical need for guide-lines for international mass BCG campaigns, a research programme in laboratory animals has been patterned on extensive studies of BCG vaccination and post-vaccination allergy in school-children.The programme, composed of a series of separate but interrelated projects, is not primarily concerned with the academic intricacies of the allergy-immunity problem. Rather, it has more directly practical objectives. First, to reproduce as nearly as possible in animals what is now being done in vaccination programmes in human beings, in order to compare, in the two species, the responses that are readily observable in man. Secondly, by challenging the vaccinated animals with virulent organisms, to study the association between those responses and resistance to virulent infection. Finally, from the results so obtained, to determine whether and to what extent some observable response to vaccination can be used (by analogy) as a practical guide to the successful vaccination of man.The experimental design takes into account variation in the animals, the vaccines, the challenge infection, and other pertinent factors. Large numbers of animals and randomization procedures have been necessary to ensure that all kinds of variation-biological, sampling, observer errors, etc.-are reduced to a minimum and distributed by chance among the various experimental groups. Observations and techniques common to the projects so far undertaken in the programme are described in the last section of the paper.

Animals↗
PubMed2000

Negligible genetic diversity of mycobacterium tuberculosis host immune system protein targets: evidence of limited selective pressure.

A common theme in medical microbiology is that the amount of amino acid sequence variation in proteins that are targets of the host immune system greatly exceeds that found in metabolic enzymes or other housekeeping proteins. Twenty-four Mycobacterium tuberculosis genes coding for targets of the host immune system were sequenced in 16 strains representing the breadth of genomic diversity in the species. Of the 24 genes, 19 were invariant and only six polymorphic nucleotide sites were identified in the 5 genes that did have variation. The results document the highly unusual circumstance that prominent M. tuberculosis antigenic proteins have negligible structural variation worldwide. The data are best explained by a combination of three factors: (i) evolutionarily recent global dissemination in humans, (ii) lengthy intracellular quiescence, and (iii) active replication in relatively few fully immunocompetent hosts. The very low level of amino acid diversity in antigenic proteins may be cause for optimism in the difficult fight to control global tuberculosis.

Acyltransferases↗
PubMed2006

Protective immunity to tuberculosis with Ag85B-ESAT-6 in a synthetic cationic adjuvant system IC31.

In this study, we evaluated the potential of a novel synthetic adjuvant designated IC31 for the ability to augment the immune response and protective efficacy of the well-known mycobacterial vaccine antigen, Ag85B-ESAT-6. The IC31 adjuvant, consisting of a vehicle based on the cationic peptide KLKL(5)KLK and the immunostimulatory oligodeoxynucleotide ODN1a signalling through the TLR9 receptor, was found to promote highly efficient Th1 responses. The combination of Ag85B-ESAT-6 and IC31 exhibited significant levels of protection in the mouse aerosol challenge model of tuberculosis and a detailed analysis of the immune response generated revealed the induction of CD4 T cells giving rise to high levels of IFN-gamma secretion. Furthermore, the combination of Ag85B-ESAT-6/IC31 was found to confer efficient protection in the guinea pig aerosol model of tuberculosis infection and is at present moving towards clinical testing.

Adjuvants, Immunologic↗