Ir gene control of the murine secretory IgA response to cholera toxin

Elson, Charles O.; Ealding, W

doi:10.1002/eji.1830170320

Cited by 59 publications

(39 citation statements)

References 26 publications

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“…Therefore, these results suggest that the serum antibody response to the cell fraction of the orally administered lactic acid bacteria was closely related to the proliferative response ofPP to the cell fraction. This is consistent with the results of Elson and Ealding, 22) who have found that the serum antibody response produced by cholera toxin feeding was due to the immune response of PP to the cholera toxin, rather than of other lymphoid tissues such as the spleen.…”

Section: Discussionsupporting

confidence: 92%

Immune Response of Mice to Orally Administered Lactic Acid Bacteria

Takahashi

Oka

Iwana

et al. 1993

Bioscience, Biotechnology, and Biochemistry

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Section: Discussionsupporting

confidence: 92%

Immune Response of Mice to Orally Administered Lactic Acid Bacteria

Takahashi

Oka

Iwana

et al. 1993

Bioscience, Biotechnology, and Biochemistry

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“…In addition, recent evidence suggests that an innate component of the immune system may also play a role in the host response to cholera (9,22,26). Studies with experimental animals have shown that the mucosal immune response to cholera toxin is T cell dependent and that CD4 T helper cells have an important role (7,12,13). However, not much is known about the role of the adaptive cellular immune responses in patients with cholera.…”

mentioning

confidence: 99%

Cholera Caused by Vibrio cholerae O1 Induces T-Cell Responses in the Circulation

et al. 2009

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Considerable effort is being made to understand the acute and memory antibody responses in natural cholera infection, while rather less is known about the roles of cellular immune responses involving T and B lymphocytes. We studied responses in adult patients hospitalized with cholera caused by Vibrio cholerae O1. Peripheral blood mononuclear cells from patients (n ‫؍‬ 15) were analyzed by flow cytometry after stimulation with V. cholerae O1 membrane protein (MP) or toxin-coregulated pilus antigen (TcpA). The gamma interferon (IFN-␥) and interleukin-13 (IL-13) responses in stimulated-lymphocyte supernatants were studied. The responses were compared with those of healthy controls (n ‫؍‬ 10). Vibrio cholerae O1 is a common causative agent of acute watery diarrhea in children and adults in the developing world (1,3,10, 19). After colonizing the proximal small intestine, this bacterium produces cholera toxin, which induces a profuse secretory diarrhea. Cholera remains a key public health problem that results in epidemics in resource-poor settings.It is believed that the immune response to cholera is initiated by antigen presentation in the Peyer's patches of the gastrointestinal mucosa, followed by migration of the stimulated antigen-specific B cells to regional lymph nodes and differentiation of these cells into specific antibody-secreting cells (28). Stimulation of the common mucosal immune system leads to production of both local and systemic antibodies (2, 15, 27) to virulence antigens of V. cholerae (25,28).Natural cholera infection is believed to give rise to long-term protection against subsequent disease. Robust systemic and mucosal antibodies are produced to the V. cholerae lipopolysaccharide, to cholera toxin, and to colonization factors, including the major subunit of the toxin-coregulated pilus, TcpA (2, 24, 25, 28). We have recently shown that there is induction of memory B-cell responses following infection, which may play a role in longer-lasting protection (14). In addition, recent evidence suggests that an innate component of the immune system may also play a role in the host response to cholera (9,22,26). Studies with experimental animals have shown that the mucosal immune response to cholera toxin is T cell dependent and that CD4 T helper cells have an important role (7, 12, 13). However, not much is known about the role of the adaptive cellular immune responses in patients with cholera. The aim of the present study was to decipher the role of T-and B-cellmediated immune responses in natural cholera infection in adults hospitalized with dehydrating illness, who were followed from the acute stage to convalescence. MATERIALS AND METHODSStudy group and recruitment. V. cholerae O1-infected adult male patients (n ϭ 15) who were between 18 and 49 years old were recruited into this study from the hospital of the International Centre for Diarrhoeal Disease Research, Dhaka, Bangladesh (ICDDR, B), and the degree of dehydration and clinical severity of the disease in the patients were assessed by a physicia...

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“…Various studies in mice have shown that oral tolerance is influenced by strain, 20,21 age at first feeding, [22][23][24] and the dose and nature of antigen. 25,26 Cholera toxin, a potent mucosal adjuvant for secretory IgA production in some mouse strains, 27,28 has been shown to activate T H2 cells and promote production of IL-4 and IgE antibodies. 29,30 We recently used a combination of experimental conditions to generate the first murine model of IgE-mediated cow's milk hypersensitivity (CMH), which closely resembles the clinical features of immediate cow's milk allergy in human subjects.…”

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confidence: 99%

A murine model of peanut anaphylaxis: T- and B-cell responses to a major peanut allergen mimic human responses

Li¹,

Serebrisky²,

Lee³

et al. 2000

Journal of Allergy and Clinical Immunology

397

377

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Background: Peanut allergy affects 0.6% of the US population. At the present time, allergen avoidance is the only therapeutic option. Animal models of food-induced anaphylaxis would facilitate attempts to design novel immunotherapeutic strategies for the treatment of peanut allergy. Objective: The purpose of this study was to develop a murine model of IgE-mediated peanut hypersensitivity that closely mimics human peanut allergy. Methods: C3H/HeJ mice sensitized orally with freshly ground whole peanut and cholera toxin as adjuvant were challenged orally 3 and 5 weeks later with crude peanut extract. Anaphylactic reactions were determined. T-and B-cell responses to Ara h 1 and Ara h 2, the major peanut allergens, were characterized by evaluating splenocyte proliferative responses and IgE antibody concentrations. Furthermore, IgE antibodies in the sera of patients with peanut allergy and mice were compared for antibody binding to Ara h 2 isoforms and allergenic epitopes. Results: Peanut-specific IgE was induced by oral peanut sensitization, and hypersensitivity reactions were provoked by feeding peanut to sensitized mice. The symptoms were similar to those seen in human subjects. Ara h 1-and Ara h 2-specific antibodies were present in the sera of mice with peanut allergy. Furthermore, these Ara h 2-specific IgE antibodies bound the same Ara h 2 isoforms and major allergenic epitopes as antibodies in the sera of human subjects with peanut allergy.

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Ir gene control of the murine secretory IgA response to cholera toxin

Cited by 59 publications

References 26 publications

Immune Response of Mice to Orally Administered Lactic Acid Bacteria

Immune Response of Mice to Orally Administered Lactic Acid Bacteria

Cholera Caused by Vibrio cholerae O1 Induces T-Cell Responses in the Circulation

A murine model of peanut anaphylaxis: T- and B-cell responses to a major peanut allergen mimic human responses

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