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Host protection upon vaccination usually results from the complex interplay of humoral and cellular components of the immune system. Exploring hepatitis B surface antigen (HBsAg)-specific T cell responses and their correlation with humoral responses under immunosuppression, we analyzed 51 renal transplant recipients, differing in HBV vaccine–specific antibody titers (non [NRs]-, low [LRs]-, and high responders [HRs]) and in 22 healthy controls (HCs) in a cross-sectional study. HBsAg-specific T cells were analyzed by flow cytometry according to expression of activation markers CD40L and/or CD69, and the cytokines IFNγ, IL-2, TNFα, and IL-17. No significant differences in responder rate and magnitude of HBsAg-specific T cell responses were found between HCs and HRs. Interestingly, HBsAg-specific Th-cells were also observed in 50% of humoral NRs. Frequencies of HBsAg-specific CD40L+ Th-cells were significantly higher in HRs compared to LRs (p = 0.009) and in LRs in comparison to NRs (p = 0.043). All but NRs showed a predominance of multi-potent HBsAg-specific TNFα+IL-2+ Th-cells. As expected, HBsAg-specific CD8+T cells were rarely found. In conclusion, mounting of hepatitis B vaccine-specific T cell responses is possible in kidney transplant recipients despite immunosuppression. Detection of HBV-specific Th-cells in a significant proportion of humoral NRs contributes to the current discussion on conferring immune protection by cellular memory in such patients.

Host protection upon vaccination usually results from the complex interplay of humoral and cellular components of the immune system. Exploring hepatitis B surface antigen (HBsAg)‐specific T cell responses and their correlation with humoral responses under immunosuppression, we analyzed 51 renal transplant recipients, differing in HBV vaccine–specific antibody titers (non [NRs]‐, low [LRs]‐, and high responders [HRs]) and in 22 healthy controls (HCs) in a cross‐sectional study. HBsAg‐specific T cells were analyzed by flow cytometry according to expression of activation markers CD40L and/or CD69, and the cytokines IFNγ, IL‐2, TNFα, and IL‐17. No significant differences in responder rate and magnitude of HBsAg‐specific T cell responses were found between HCs and HRs. Interestingly, HBsAg‐specific Th‐cells were also observed in 50% of humoral NRs. Frequencies of HBsAg‐specific CD40L+ Th‐cells were significantly higher in HRs compared to LRs (p = 0.009) and in LRs in comparison to NRs (p = 0.043). All but NRs showed a predominance of multi‐potent HBsAg‐specific TNFα+IL‐2+ Th‐cells. As expected, HBsAg‐specific CD8+T cells were rarely found. In conclusion, mounting of hepatitis B vaccine‐specific T cell responses is possible in kidney transplant recipients despite immunosuppression. Detection of HBV‐specific Th‐cells in a significant proportion of humoral NRs contributes to the current discussion on conferring immune protection by cellular memory in such patients. Flow cytometric analysis of hepatitis B surface antigen‐specific T cells and their correlation with humoral responses under immunosuppression reveal that 50% of humoral nonresponders show mounting of sufficient vaccination‐specific T cell immunity.