Immune suppression and induction of gamma interferon by pertussis toxin

Vogel, Frederick R.; Klein, Thomas; Stewart, William E.; Igarashi, Takeshi; Friedman, Herman

doi:10.1128/iai.49.1.90-97.1985

Cited by 21 publications

(4 citation statements)

References 34 publications

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“…(19), precipitated in ammonium sulfate, and kept at 4°C . Before use, PT was resuspended in PBS and heat inactivated (at 100°C for 45 min) to eliminate its mitogenic effect (20) .…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Human T cell clones define S1 subunit as the most immunogenic moiety of pertussis toxin and determine its epitope map.

Magistris¹,

Romano²,

Bartoloni³

et al. 1989

The Journal of Experimental Medicine

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Human T lymphocyte clones specific for pertussis toxin (PT) were used to analyze the fine specificity of the response to PT, the basic component of new acellular vaccines against whooping cough. The majority (83%) of the clones specific for PT recognized S1, the subunit that in animal models has been shown to be highly immunogenic. To map T cell epitopes on S1, 18 S1-specific clones were tested for recognition of recombinant fragments representing NH2-terminal and COOH-terminal deletions of S1 and two recombinant S1 subunits containing amino acid substitutions. This approach led to the identification of three regions of the protein as the sequences containing T cell antigenic sites: 1-42, 181-211, and 212-235. Synthetic peptides were eventually used for a finer localization of the T cell epitopes. Two peptides, one of 13 residues (27-39) at the NH2 terminus and one of 24 residues (171-194) at the COOH terminus, stimulated proliferation of three and four clones, respectively. Both peptides are recognized in association with HLA DR1 molecules. These results stress the role of S1 in the immune response to PT and provide data useful for the development of a recombinant or synthetic antipertussis vaccine containing T cell epitopes from S1.

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“…(19), precipitated in ammonium sulfate, and kept at 4°C . Before use, PT was resuspended in PBS and heat inactivated (at 100°C for 45 min) to eliminate its mitogenic effect (20) .…”

Section: Methodsmentioning

confidence: 99%

“…(19), precipitated in ammonium sulfate, and kept at 4°C . Before use, PT was resuspended in PBS and heat inactivated (at 100°C for 45 min) to eliminate its mitogenic effect (20) . Subunits Sl, S2, S3, S4, S5 from B. pertussis, BPPSI, BBSI, and nine fragments of BPSI were expressed in Escherichia coli .…”

Section: Methodsmentioning

confidence: 99%

Human T cell clones define S1 subunit as the most immunogenic moiety of pertussis toxin and determine its epitope map.

Magistris¹,

Romano²,

Bartoloni³

et al. 1989

The Journal of Experimental Medicine

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“…The list of organisms includes: Vibrio cholera (Shenker et al 1980. Holmgren et al 1977 (Khansari et al 1981), Bordelella pertussis (Vogel et al 1985), Candida alhicans (Piccolella et al 1981), rubella, influenza, polio, influenza and parvovirus (Hurwitz & Hackett 1985, Engers et al 1981, Kauffmann et al 1974, Kantzler et al 1974, Soontiens & Van Der Veen 1973. Olson et al 1968).…”

Section: Immunosuppressive Properties Of Suspected Oral Pathogensmentioning

confidence: 99%

Immunologic dysfunction in the pathogenesis of periodontal diseases*

Shenker

1987

J Clinic Periodontology

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Despite significant progress in our understanding of the pathogenesis and etiology of periodontal diseases, the nature and contribution of the immune system to this disorder remains unclear. Several studies provide evidence for either a protective or destructive rôle. These conflicting findings are difficult to reconcile, since most interpretations tend to argue for a static contributory rôle (i.e., either protective or destructive) of the immune system. Current theories on the rôle of the immune response do not address these conflicting findings as well as the contradictory observation of a detectable immune response in the face of persistent infection in these patients. In this article, we present a model, based on available data, for the contribution of the immune system to the pathogenesis of periodontal disease. This model ascribes a dynamic rôle for the immune response. As documented in other infectious diseases, it is entirely possible, for example, that a state of immunologic dysfunction may occur in the earliest stages of periodontal disease progression; this may then be followed by a period of active immune reactivity (humoral and/or cellular) that would represent either a delayed or depressed response. This model is discussed in conjunction with recent findings that several suspected periodontal pathogens are capable of producing immunosuppressive agents. Many of the apparently contradictory clinical observations concerning the host immune response to oral pathogens and its correlation (or lack of) with both the progression and severity of periodontal disease may be accounted for in this model.

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“…Antibodies are necessary for control of infection in a mouse model [83] through their opsonization of bacteria for neutrophil killing and PT inhibits this process through its actions on neutrophil trafficking and recruitment [84]. PT suppression of antibody responses is supported by examples in the literature of the inhibitory effects of PT on B cell responses to lipopolysaccharide (LPS) [85], lymphocyte chemotaxis [86] and IgM production [87].…”

Section: Pt Effects On Inflammatory and Immune Responses To B Permentioning

confidence: 99%

Association of Pertussis Toxin with Severe Pertussis Disease

Scanlon

Skerry

Carbonetti

2019

Toxins

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Pertussis, caused by respiratory tract infection with the bacterial pathogen Bordetella pertussis, has long been considered to be a toxin-mediated disease. Bacteria adhere and multiply extracellularly in the airways and release several toxins, which have a variety of effects on the host, both local and systemic. Predominant among these toxins is pertussis toxin (PT), a multi-subunit protein toxin that inhibits signaling through a subset of G protein-coupled receptors in mammalian cells. PT activity has been linked with severe and lethal pertussis disease in young infants and a detoxified version of PT is a common component of all licensed acellular pertussis vaccines. The role of PT in typical pertussis disease in other individuals is less clear, but significant evidence supporting its contribution to pathogenesis has been accumulated from animal model studies. In this review we discuss the evidence indicating a role for PT in pertussis disease, focusing on its contribution to severe pertussis in infants, modulation of immune and inflammatory responses to infection, and the characteristic paroxysmal cough of pertussis.

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Immune suppression and induction of gamma interferon by pertussis toxin

Cited by 21 publications

References 34 publications

Human T cell clones define S1 subunit as the most immunogenic moiety of pertussis toxin and determine its epitope map.

Human T cell clones define S1 subunit as the most immunogenic moiety of pertussis toxin and determine its epitope map.

Immunologic dysfunction in the pathogenesis of periodontal diseases*

Association of Pertussis Toxin with Severe Pertussis Disease

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