Defects of hepatitis B surface antigen (HBsAg) presentation and recognition in patients with end stage of renal disease (ESRD) was studied. The patients showed an impaired response to hepatitis B vaccination (NR: non-responders). One hundred and thirty seven ESRD-adult patients and 54 children were included in the study. Low response to HBV vaccination in ESRD-patients resulted from failure of monocytes in processing of HBsAg and impaired function of antigen specific, responder CD4+ T cells. Defects of monocytes involved diminished internalization of HBsAg and low expression of adhesion as well as accessory molecules (ICAM-1, HLA-DR,respectively), decrease in synthesis of IL-1β. Failure in function of CD4+ T cells involved: a) low proliferative response of CD4 T cells stimulated by autologous monocytes, presenting HBsAg, b) impaired expression of TCR/CD3 receptor complex on CD4+ T cells, c) low synthesis of IL-6, IL-2 and IFN-γ and increase in IL-10 expression. The intensification of defects of antigen presentation and recognition was determined by individual immunogenetic configuration, degree of uremia and advanced age. Immunogenetic features were defined as extended HLA haplotype of class I, II (transplantation antigens) and III (complement allotypes). It concerned more frequent expression of HLA-A1, B8, DR3 haplotypes as well as C4A, 6Q0 and Bf S0.7S of complement allotypes. Uremia by itself had only limited effect on response to HBV vaccination: when the plasma creatinine level was not higher then 6 mg%, the relatively good response to HBV vaccination was observed. Children, especially before introduction of dialysis (plasma creatinine < 6 mg%), revealed a good response to HBsAg.
|Number of pages||9|
|Journal||Central-European Journal of Immunology|
|Publication status||Published - Jan 1 1996|
ASJC Scopus subject areas
- Immunology and Allergy