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Regression models assessed associations with failure to achieve seroprotective antibodies to H1, H3, and B influenza strains. RESULTS: A total of 96 women were enrolled in the study at a median gestation of 22 weeks with a BMI range of 18-49 kg/m(2). Paired sera samples were available for 90/96 (94%). Most pregnant women (72/90, 80%) demonstrated seroprotective antibody titres to all three influenza vaccine antigens (A(H1N1)pdm09, A(H3N2), B/Yamagata) following vaccination. Compared with women with BMI < 30 kg/m(2), those with high BMI were less likely to fail to achieve seroprotective antibodies, however this was not statistically significant (RR 0.42, 95% CI 0.

11-1.68; p = 0.22). A greater proportion of women vaccinated during their second (47/53, 93%) or third trimester (18/25, 72%) demonstrated seroprotection to all three vaccine antigens following vaccination compared with women vaccinated during their first trimester (7/12, 58%). CONCLUSION: High BMI did not impair seroprotection levels following influenza vaccination in pregnant women. Gestation at vaccination may be an important consideration for optimising vaccine protection for pregnant women and their newborns. Further assessment of first trimester influenza vaccine responses Adelaide, Adelaide, SA, Australia.

Polysaccharides : Hospital, at the Peter Doherty Institute for Infection and Immunity, Melbourne, the Peter Doherty Institute for Infection and Immunity, Melbourne, VIC, Hospital, at the Peter Doherty Institute for Infection and Immunity, Melbourne, Melbourne, at the Peter Doherty Institute for Infection and Immunity, Melbourne, Investigators on clinical vaccine trials sponsored by Industry. Their institution (Women’s and Children’s Hospital) receives funding for Investigator led research and/or sponsored vaccine trials from Industry, including GSK, Pfizer, Sanofi, Novavax and Merck.  None of the authors receive any personal payments from Industry. S Lambert, LC Giles, SG Sullivan and LM Goodchild have no conflicts to declare. IG Barr has shares in an influenza vaccine producing company.  The WHO Collaborating Centre for Reference and Research on Influenza receives funds from Seqirus Limited and from the IFPMA for its influenza surveillance activities.  The WHO Collaborating Centre for Reference and Research on Influenza is funded by the Australian Government Department of Health.

  The funding bodies were not involved in the collection, analysis or interpretation of data, the writing of the article, or the decision to submit the article for publication.treatment of several T cell-mediated experimental autoimmune diseases, including experimental allergic encephalomyelitis, thyroiditis, and adjuvant arthritis. The aim of this study was to determine whether T-cell vaccination could be used to down-regulate specifically the antibody response to AChR in experimental autoimmune myasthenia gravis (EAMG), an antibody-mediated disorder. We produced T cells specific for the acetylcholine receptor (AChR) by immunizing Lewis rats with torpedo AChR, harvesting the regional lymph node cells, and restimulating them in vitro with AChR. Polysucrose 400 Sweetener was expanded with IL2. The cells were then activated with concanavalin A (Con-A) and exposed to high hydrostatic pressure to augment their immunogenicity. We found that rats vaccinated with these cells did not manifest decreased antibody titers to AChR, when challenged.

In fact, the antibody response to AChR was consistently potentiated by the vaccine treatment. This result could not be attributed to antigen carryover by the vaccinating cells or to induction of anti-idiotypic antibodies. Despite these results showing overall enhancement of the AChR antibody response, we found evidence of AChR-specific suppressor cells in the spleens of the vaccinated animals. Our observations indicate that T-cell vaccination can elicit both a positive immune response and a suppressive response in the same animal. If the T-cell vaccination strategy is to be useful for the treatment of MG, methods for amplifying the suppressive effect will need to be developed.basophils, and a platelet-activating factor.from rabbit platelets, a complement-independent mechanism which has been implicated in the deposition of immune complexes in acute serum sickness of rabbits.