The Adjuvant Effect of Silicone-Gel on Antibody Formation in Rats

1993 ◽  
Vol 22 (2) ◽  
pp. 151-161 ◽  
Author(s):  
John O. Naim ◽  
Raymond J. Lanzafame ◽  
Carel J. van Oss
1981 ◽  
Vol 76 (1) ◽  
pp. 93-98
Author(s):  
Nelson M. Vaz ◽  
Robert E. Kane ◽  
James M. Lynch

Linear relationships were found between the dose of A1(OH)3 adjuvant and the titer of anti-OVA antibodies formed by BDF1 mice. Mice immunized with OVA, DNP-KLH and then boosted with DNP-OVA formed anti-DNP antibodies only when A1(OH)3 was added to the injection of DNP-KLH; addition of A1(OH)3 to the priming injection of OVA decreased, rather than increased antibody formation.


1962 ◽  
Vol 60 (4) ◽  
pp. 411-426 ◽  
Author(s):  
J. R. Farthing ◽  
L. B. Holt

The characteristics of Gram-negative organisms and some of the underlying reasons for their adjuvant action with diphtheria toxoid are described.The adjuvant effect was shown by an earlier production of antitoxin, with a maintained differential advantage over controls, but with the usual decline in titre with passage of time. The adjuvant effect only occurred with a primary stimulus. There was no adsorption between toxoid and vaccine and mixture of the two was not necessary, but the vaccine had to be given simultaneously with or within 24 hr. following injection of the toxoid. There was evidence for believing that these adjuvants decreased the minimal stimulating dose of antigen and caused hyperplasia of antibody-producing cells. No direct link could be found between the characteristic stress symptoms caused by lipopolysaccharides and their ability to enhance antibody formation.


2004 ◽  
Vol 95 (2) ◽  
pp. 94-96 ◽  
Author(s):  
Soren Thor Larsen ◽  
Rikke Hansen ◽  
Otto Melchior Poulsen ◽  
Gunnar Damgard Nielsen

1952 ◽  
Vol 95 (5) ◽  
pp. 429-447 ◽  
Author(s):  
Jonas E. Salk ◽  
Angela M. Laurent

Untoward reactions at the site of inoculation were not observed in monkeys vaccinated with influenza virus incorporated in a water-in-oil emulsion without acid-fast bacilli. Studies were then made to measure some of the dimensions of antigenicity of these emulsions to evaluate the extent of the immunologic adjuvant effect. This included measurements of height and persistence of the antibody response to inoculation and measurements of the extent to which the vaccine could be diluted and still induce antibody formation; i.e., antigenic extinction. In addition, comparisons were made of the rates of development of hemagglutination-inhibiting, virus-neutralizing, and complement-fixing antibody activities to determine the relationship among these three properties of the serum of immunized animals. It was found that levels of antibody many fold higher were induced by the virus-adjuvant mixtures as compared with virus in an aqueous menstruum, and that the level of antibody induced was related to the quantity of antigen incorporated in the emulsion. The stock vaccine when emulsified could be diluted 100,000-fold and was still active in antibody formation whereas a 100-fold dilution of the antigen without emulsification was essentially ineffective. Equivalent quantities of virus in 0.1 ml. or 1.0 ml. of emulsion induced antibody responses that were indistinguishable with respect to level or persistence. In comparing the course of antibody development it was found that hemagglutination-inhibiting, virus-neutralizing, and complement-fixing antibodies develop at different rates; careful analysis of the data derived from the present study together with other observations warrant the conclusion that these antibody activities are not present in constant proportion and are independent of one another. The implications of this observation and of the others mentioned above are discussed.


Pathobiology ◽  
1971 ◽  
Vol 37 (4) ◽  
pp. 302-312
Author(s):  
E. Elekes ◽  
K. Merétey ◽  
V. Várterész

1990 ◽  
Vol 64 (04) ◽  
pp. 564-568 ◽  
Author(s):  
Lloyd E Lippert ◽  
Lyman Mc A Fisher ◽  
Lawrence B Schook

SummaryApproximately 14% of transfused hemophiliacs develop an anti-factor VIII inhibitory antibody which specifically neutralizes factor VIII procoagulant activity. In this study an association of the major histocompatibility complex (MHC) with inhibitor antibody formation was evaluated by restriction fragment length polymorphism (RFLP) analysis using BamHI, EcoRI, HindII, PstI, PvuII and TaqI digested genomic DNA probed with DP beta, DQ alpha, DQ beta and DR beta class II MHC gene probes. The RFLP patterns for 16 non-inhibitor and 11 inhibitor hemophiliac patients were analyzed. These 24 enzyme:probe combinations generated 231 fragments. Fifteen (15) fragments associated with the inhibitor phenotype; odds ratios ranged from 5.1 to 45 and lower bounds of 95% confidence intervals were > 1.000 for all 15 fragments. Five (5) fragments associated with non-inhibitors, with odds ratios ranging from 6.4 to 51.7. This report establishes a MHC related genetic basis for the inhibitor phenotype. No statistically significant differences in the distribution of serologically defined HLA-DR phenotypes were observed between the inhibitor and non-inhibitor groups.


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