AIM: To evaluate, whether humoral hepatitis-B-vaccine non-responders also fail to mount a T cell response and to compare these results to normal vaccinees. METHODS: Fourty-seven health care employees were enrolled in ...AIM: To evaluate, whether humoral hepatitis-B-vaccine non-responders also fail to mount a T cell response and to compare these results to normal vaccinees. METHODS: Fourty-seven health care employees were enrolled in this study including all available non- responders (n = 13) with an anti-HBsAg titer < 10 kU/L and all available low-responders (n = 12) with an anti- HBsAg titer < 100 kU/L. Also, 12 consecutive anti-HBsAg negative pre-vaccination subjects were enrolled as well as 10 subjects (+7 from the vaccinated group) with titers > 1000 kU/L as controls. PBMC from all subjects were analyzed by IFN-γ and IL-4 ELISPOT assays for the presence of hepatitis B surface antigen (HBsAg) reactive T cells. RESULTS: Non-responders and low-responders had no or only very limited T cell responses, respectively. Indi- viduals responding to vaccination with the induction of a high anti-HBsAg titer showed a strong T cell response after the third vaccination. Surprisingly, these individuals showed response even before the first vaccination. T cell response to control antigens and mitogens was similar in all groups. CONCLUSION: Our data suggest that there is no gen- eral immune deficiency in non-/low-responders. Thus, we hypothesize that the induction of anti-HBsAg re- sponses by vaccination is significantly dependent on the pre-existing T cell repertoire against the specific antigen rather than the presence of a general T cell defect.展开更多
We have previously demonstrated the ability of malaria parasites to interfere with specific immune responses. CD4 T cells specific to parasite antigens, but not CD4 T cells specific to an irrelevant antigen, ovalbumin...We have previously demonstrated the ability of malaria parasites to interfere with specific immune responses. CD4 T cells specific to parasite antigens, but not CD4 T cells specific to an irrelevant antigen, ovalbumin (OVA), are de- leted via apoptosis during malaria infection. It is of interest, therefore, to investigate the immune responses that developed following vaccination with the 19 kDa carboxylterminus of the merozoite surface protein 1 (MSP119) in mice that had previ- ously experienced malaria infection. In this study, pre-exposure of mice to Plasmodium yoelii elicited native anti-MSP119 an- tibody responses, which could be boosted by vaccination with recombinant MSP119 . likewise, infection of MSP119-primed mice with Plasmodium yoelii ( P . yoelii) led to an increase of anti-MSP119 antibodies. MSP119 vaccination of malaria pre- exposed mice or immunization by infection/cure of MSP119-primed mice enabled the mice to survive challenge infection, with the former group having slightly lower parasitaemia. The data suggest that exposure to malaria infection primes a natural im- mune response which can be boosted by vaccination. This information is relevant to the development of a vaccine for use in individuals living in malaria-endemic areas.展开更多
基金Supported by Sofia-Kovalevskaja Award of the Alexander von Humboldt Foundation (JL Schultze), No. 37888309, Koeln Fortune (MR Weihrauch)
文摘AIM: To evaluate, whether humoral hepatitis-B-vaccine non-responders also fail to mount a T cell response and to compare these results to normal vaccinees. METHODS: Fourty-seven health care employees were enrolled in this study including all available non- responders (n = 13) with an anti-HBsAg titer < 10 kU/L and all available low-responders (n = 12) with an anti- HBsAg titer < 100 kU/L. Also, 12 consecutive anti-HBsAg negative pre-vaccination subjects were enrolled as well as 10 subjects (+7 from the vaccinated group) with titers > 1000 kU/L as controls. PBMC from all subjects were analyzed by IFN-γ and IL-4 ELISPOT assays for the presence of hepatitis B surface antigen (HBsAg) reactive T cells. RESULTS: Non-responders and low-responders had no or only very limited T cell responses, respectively. Indi- viduals responding to vaccination with the induction of a high anti-HBsAg titer showed a strong T cell response after the third vaccination. Surprisingly, these individuals showed response even before the first vaccination. T cell response to control antigens and mitogens was similar in all groups. CONCLUSION: Our data suggest that there is no gen- eral immune deficiency in non-/low-responders. Thus, we hypothesize that the induction of anti-HBsAg re- sponses by vaccination is significantly dependent on the pre-existing T cell repertoire against the specific antigen rather than the presence of a general T cell defect.
文摘We have previously demonstrated the ability of malaria parasites to interfere with specific immune responses. CD4 T cells specific to parasite antigens, but not CD4 T cells specific to an irrelevant antigen, ovalbumin (OVA), are de- leted via apoptosis during malaria infection. It is of interest, therefore, to investigate the immune responses that developed following vaccination with the 19 kDa carboxylterminus of the merozoite surface protein 1 (MSP119) in mice that had previ- ously experienced malaria infection. In this study, pre-exposure of mice to Plasmodium yoelii elicited native anti-MSP119 an- tibody responses, which could be boosted by vaccination with recombinant MSP119 . likewise, infection of MSP119-primed mice with Plasmodium yoelii ( P . yoelii) led to an increase of anti-MSP119 antibodies. MSP119 vaccination of malaria pre- exposed mice or immunization by infection/cure of MSP119-primed mice enabled the mice to survive challenge infection, with the former group having slightly lower parasitaemia. The data suggest that exposure to malaria infection primes a natural im- mune response which can be boosted by vaccination. This information is relevant to the development of a vaccine for use in individuals living in malaria-endemic areas.
