2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

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

      Clinical and Experimental Immunology
      Antigen Presentation, immunology, Antigen-Presenting Cells, Antigens, CD, Antigens, CD14, Antigens, CD80, Antigens, CD86, Cell Line, Coculture Techniques, methods, HLA-DP Antigens, HLA-DP beta-Chains, HLA-DR Antigens, HLA-DR3 Antigen, Hepatitis B Surface Antigens, Hepatitis B Vaccines, Humans, Immunity, Cellular, Leukocyte Count, Leukocytes, Mononuclear, Membrane Glycoproteins, T-Lymphocytes

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The mechanisms causing non-responsiveness to hepatitis B surface antigen (HBsAg) vaccines in man remain elusive. The increased incidence of non-responsiveness in subjects with HLA-DR3(+) or -DR7(+) haplotypes suggests that immune response mechanisms governed by genes of the MHC are involved. Homozygotes for these two haplotypes are found almost exclusively in the non-responder (NR) population. It is conceivable that antigen-presenting cells (APC) of NR are defective in the uptake of HBsAg and that they are unable to present this Ag adequately. Previously, we demonstrated that DR2(+), DR7(+) and DP4(+) 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 HBsAg-presentation. 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 non-responsiveness of these subjects.

          Related collections

          Author and article information

          Comments

          Comment on this article