Humoral Immune Response After Hepatitis-B-Vaccination: Kinetics of Anti-HBS Antibodies and Demonstration of HLA Antigens

Usonis, Vytautas; Kühnl, P.; Brede, H. D.; Doerr, H. W.

doi:10.1016/s0176-6724(86)80011-6

Cited by 8 publications

(14 citation statements)

References 15 publications

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“…Under these controlled conditions, 38 out of 40 patients (95%) had protective anti-HBs antibody levels after only three injections. Comparable data were found in several studies (Deinhardt 1984, Mckan et al 1983, Usonis et al 1986).…”

Section: Discussionsupporting

confidence: 81%

“…In previous studies, the absence or the presence of detectable anti-HBs antibodies appeared to be in association with certain HLA phenotypes (Cayzer et al 1987, Usonis et al 1986). However (1) the determinism of the latent period of the anti-HBs response and (2) the serum levels of anti-HBs antibodies has been poorly documented.…”

Section: Discussionmentioning

confidence: 82%

“…Early reports on this subject (Usonis et al 1986) did not allow a clear conclusion on the existence of HLA associated IR gene. Recently, the vaccination against hepatitis B virus (HBV) offered a tempting way of research in this field.…”

mentioning

confidence: 95%

“…conflicting results (Krawitt et al 1981, Opeltz & Terasaki 1W8). Several reports of immune responses to HBsAG in human vaccination led to apparent evidence of an HLA linked determinism of the anti-HBsAG antibody production (Cayzer et al 1987, Usonis et al 1986). However, these studies are limited to the response to several antigenic systems of the hepatitis B virus or vaccine.…”

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confidence: 99%

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HLA linked immune response to S and pre‐S2 gene products in hepatitis B vaccination

et al. 1989

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In order to detect a possible HLA linked genetic control of human immune responses to hepatitis B virus, forty healthy adult persons of the same age typed for HLA-A, -B and -DR antigens, were vaccinated against virus hepatitis B and sequentially tested for anti-HBs and anti-pre-S2 antibodies. They received three injections of Hevac-B Pasteur vaccine, the second 1 month and the third 3 months after the first. Following the third immunization, 38 individuals (95%) had a protective level of anti-HBs antibodies and 17 (42.3%) had a positive level of anti-pre-S2 antibodies. HLA-A11 antigen was significantly more frequent (pc = 0.007) among anti-HBs high responders than low responders. In addition, anti-HBs high responders were more frequently HLA-DR1, and less frequently HLA-DR4 and DR7 positive; corrected values, however, were not significant. Anti-pre-S2 high responders showed an apparent increase of HLA-B7, B14 or DR3 antigens, when compared to low responders (pc not significant).

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 82%

mentioning

confidence: 95%

mentioning

confidence: 99%

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HLA linked immune response to S and pre‐S2 gene products in hepatitis B vaccination

et al. 1989

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“…[4], who observed a significant excess of HLA-DR7 and a total absence of HLA-DR1 in hepatitis B non-responders (NR). Subsequent studies demonstrated that HLA class II alleles that are associated strongly with high response (or protect from non/poor response) are: DRB1*01 ( DR1 ), DRB1*11 ( DR5 ), DRB1*15 ( DR2 ), DQB1*0501, DPB1*0401, whereas alleles strongly associated with non/poor response are: DRB1*03, DRB1*07, DQB1*02, DPB1*1101 [1,[5][6][7][8][9][10][11][12]. In addition to the associations between single HLA class II alleles and anti-HBs response mentioned above, several associations with extended haplotypes have been reported.…”

Section: Introductionmentioning

confidence: 99%

Non-responsiveness to hepatitis B surface antigen vaccines is not caused by defective antigen presentation or a lack of B7 co-stimulation

Desombere

Cao

Gijbels

et al. 2005

Clinical and Experimental Immunology

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SummaryThe mechanisms causing non-responsiveness to hepatitis B surface antigen (HBsAg) vaccines in man remain elusive. The increased incidence of nonresponsiveness in subjects with HLA-DR3 + + + + NR were able to present HBsAg. In the present paper we demonstrate that six DR0301 + + + + NR, five of which are homozygous for this marker, were able to take up, process and present HBsAg to HBsAg-specific, DR0301-restricted T cell lines. Non-fractionated peripheral blood mononuclear cells (PBMC) from the DR0301 + + + + NR did not proliferate to HBsAg in vitro , whereas they proliferated vigorously upon stimulation with tetanus toxoid, thus ruling out the presence of a generalized immunodeficiency. We therefore conclude that HLA-DR0301 + + + + NR vaccinees are not deficient in their HBsAgpresentation. Because it was demonstrated that recently activated T cells can apparently bypass the requirement for B7, we may have overlooked the role of the B7-co-stimulation in our set-up that used HBsAg-specific T cell lines. Therefore we examined the expression of B7 co-stimulatory molecules on NR-APC. CD86 was normally present on these cells and was not down-regulated after culturing the PBMC in the presence of HBsAg. We conclude that CD86 expression on CD14 + + + + monocytes of DR0301-and DR07-homozygous poor responders is not deficient and cannot be the mechanism underlying the nonresponsiveness of these subjects.Keywords: antigen presentation, DRB1*0301, HBsAg, hepatitis B vaccines, non-response I ntroductionFor nearly two decades, vaccines against hepatitis B virus (HBV) have been administered routinely and the antibodies to the hepatitis B surface antigen (HBsAg) they elicit are clearly effective in preventing infections with HBV. About 5% of healthy vaccine recipients fail to produce protective levels of antibodies (defined as an antibody level £ 10 IU/l) to the hepatitis B vaccine after standard immunization. This phenomenon has been observed in all surveys of vaccine effectiveness, irrespective of the HBsAg vaccine employed [1][2][3], and its cause remains largely unknown.Variations in immune response are often associated with polymorphism of the major histocompatibility complex (MHC). The suggestion that MHC-linked immune response genes may control the human response to HBsAg was first made in 1981 by Walker et al . [4], who observed a significant excess of HLA-DR7 and a total absence of HLA-DR1 in hepatitis B non-responders (NR). Subsequent studies demonstrated that HLA class II alleles that are associated strongly with high response (or protect from non/poor response) are: DRB1*01 ( DR1 ), DRB1*11 ( DR5 ), DRB1*15 ( DR2 ), DQB1*0501, DPB1*0401, whereas alleles strongly associated with non/poor response are: DRB1*03, DRB1*07, DQB1*02, ,9,13-18] and, in particular, homozygotes for these extended haplotypes were seen more frequently [1,19,20]. In our studies, for example, six of seven DRB1*07 homozygous individuals and five of six DRB1*0301 homozygous individuals were found to be NR.We and other groups have reported t...

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Correlation between in vivo humoral and in vitro cellular immune responses following immunization with hepatitis B surface antigen (HBsAg) vaccines

Leroux‐Roels

Vanhecke

Michielsen

et al. 1994

Vaccine

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Humoral Immune Response After Hepatitis-B-Vaccination: Kinetics of Anti-HBS Antibodies and Demonstration of HLA Antigens

Cited by 8 publications

References 15 publications

HLA linked immune response to S and pre‐S2 gene products in hepatitis B vaccination

HLA linked immune response to S and pre‐S2 gene products in hepatitis B vaccination

Non-responsiveness to hepatitis B surface antigen vaccines is not caused by defective antigen presentation or a lack of B7 co-stimulation

Correlation between in vivo humoral and in vitro cellular immune responses following immunization with hepatitis B surface antigen (HBsAg) vaccines

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