Acute Shock Induced by Antigen Vaccination in NOD Mice

Overbergh, Lutgart; Decallonne, Brigitte; Brănișteanu, Dumitru; Valckx, Dirk; Kasran, Ahmad; Bouillon, Roger; Mathieu, Chantal

doi:10.2337/diabetes.52.2.335

Cited by 27 publications

(14 citation statements)

References 45 publications

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“…However, the predominant immune response in BALB/c mice was a Th2 response as suggested by the predominance of IgG1 after immunization. This result was as expected, as BALB/c mice have a bias toward this type of immune response (36,52).…”

Section: Figsupporting

confidence: 77%

Comparison of Antibody- and Cell-Mediated Immune Responses After Intramuscular Hepatitis C Immunizations of BALB/c Mice

et al. 2005

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Current treatments for hepatitis C infection have limited efficacy, and there is no vaccine available. The goal of this study was to compare the immune response to several immunization combinations against hepatitis C virus (HCV). Six groups of mice were immunized at weeks 0, 4, and 8 with different combinations of a candidate HCV vaccine consisting of 100 microg recombinant HCV core/E1/E2 (rHCV) DNA plasmid and/or 25 microg rHCV polyprotein and 50 microL Montanide ISA- 51. Four weeks after the last injection, all groups of mice were sacrificed and blood samples and spleens were collected for measuring the levels of specific HCV antibodies (total IgG, IgG1, and IgG2a). Cell proliferation and intracellular interferon-gamma were also measured. Among the groups of immunized mice, only the mice immunized with rHCV DNA plasmid, rHCV polyprotein, and montanide (group D) and mice immunized with rHCV polyprotein and montanide (group F) demonstrated a significant increase in the total IgG titer after immunization. IgG1 was the predominant antibody detected in both groups D and F. No IgG2a was detected in any of the groups. Proliferation assays demonstrated that splenocytes from group D and group C (rHCV DNA primed/rHCV polyprotein boost) developed significant anti-HCV proliferative responses. The combination of an rHCV DNA plasmid, rHCV polyprotein, and montanide induced a high antibody titer with a predominance of IgG1 antibodies and recognized the major neutralization epitopes in HVR1. In contrast, group C did not show an increase in anti-HCV antibodies, but did show a proliferative response.

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Section: Figsupporting

confidence: 77%

Comparison of Antibody- and Cell-Mediated Immune Responses After Intramuscular Hepatitis C Immunizations of BALB/c Mice

et al. 2005

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“…Deleterious immune responses varied depending on the antigens and the route of administration. Interestingly, Liu et al noted that anaphylaxis could be prevented by lowering the dose or altering the isoelectric point of the peptide to neutral pH [12,19,20].…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Human alpha 1-antitrypsin therapy induces fatal anaphylaxis in non-obese diabetic mice

Lu¹,

Parker²,

Pileggi

et al. 2008

Clinical and Experimental Immunology

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SummaryPrevious studies have shown that human alpha-1 antitrypsin (hAAT) gene delivery prevents type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. Furthermore, hAAT protein administration prolongs acceptance of islet allografts. Therefore, we evaluated the use of purified hAAT protein therapy to prevent T1D in NOD mice. Female NOD, non-obese resistant (NOR), Balb/c and C57BL/6 mice were injected intraperitoneally with vehicle alone or vehicle containing hAAT, human albumin or mouse albumin (or mg/injection/mouse; 2¥/week). Preparations of clinical-grade hAAT included API®, Aralast®, Prolastin® and Zemaira®. Surprisingly, hAAT administration was associated with a high rate of fatal anaphylaxis. In studies seeking T1D prevention at 4 weeks of age, 100% mice died after six injections of hAAT. When administrated at 8-10 weeks of age, most (80-100%) NOD mice died following the fourth injection of hAAT, while 0% of Balb/c and C57BL/6 mice and 10% of NOR mice died. Interestingly, repeated injections of human albumin, but not mouse albumin, also induced sudden death in NOD mice. Antibodies to hAAT were induced 2-3 weeks after hAAT administration and death was prevented by treatment with anti-platelet-activating factor along with anti-histamine. In studies of disease reversal in NOD mice, using the four pharmaceutical grade formulations of hAAT, anaphylactic deaths were observed with all hAAT preparations. The propensity for fatal anaphylaxis following antigenic administration appears to be NOD-but not hAATspecific. The susceptibility of NOD mice to hypersensitivity provides a significant limitation for testing of hAAT. Development of strategies to avoid this unwanted response is required to use this promising therapeutic agent for T1D.

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“…Symptoms were evaluated according to the following scoring system [8]: 0, no symptoms; 1, scratching and rubbing around the nose and head; 2, puffiness around the eyes and mouth, diarrhoea, pilar erecti, reduced activity, and/or decreased activity with increased respiratory rate; 3, wheezing, laboured respiration, and cyanosis around the mouth and tail; 4, no activity after prodding or tremor and convulsion; and 5, death. Dexamethasone (Dexa, 50 µg/100 µl in saline) was injected intraperitoneally in D-gal-treated mice 2, 24, and 48 hours before BSA challenge [9]. …”

Section: Methodsmentioning

confidence: 99%

Splenocyte proliferation and anaphylaxis induced by BSA challenge in a D-galactose-induced aging mouse model

Park

Choi

2016

cejoi

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We previously found a cross-reactive autoantibody that bound to bovine serum albumin generated in a D-galactose-induced aging mouse model. Also, we confirmed that other reducing sugars (glucose and fructose) could induce the formation of autoantibody, and only following subcutaneous injection, not oral or intraperitoneal administration. Mice that had never been exposed to bovine serum albumin produced an anti-bovine serum albumin autoantibody following repeated subcutaneous injection of D-galactose (D-gal). In this study, we investigated the involvement of the adaptive immune system in the production of this autoantibody. In particular, we examined bovine serum albumin-induced splenocyte proliferation and bovine serum albumin-induced active cutaneous and systemic anaphylaxis in D-gal-treated mice. We find our results particularly interesting: bovine serum albumin stimulates splenocyte proliferation and induces both active cutaneous and systemic anaphylaxis in D-gal-treated mice. In summary, our results suggest that adaptive immune response participates in the autoantibody formation against bovine serum albumin in D-gal-treated mice.

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Acute Shock Induced by Antigen Vaccination in NOD Mice

Cited by 27 publications

References 45 publications

Comparison of Antibody- and Cell-Mediated Immune Responses After Intramuscular Hepatitis C Immunizations of BALB/c Mice

Comparison of Antibody- and Cell-Mediated Immune Responses After Intramuscular Hepatitis C Immunizations of BALB/c Mice

Human alpha 1-antitrypsin therapy induces fatal anaphylaxis in non-obese diabetic mice

Splenocyte proliferation and anaphylaxis induced by BSA challenge in a D-galactose-induced aging mouse model

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