During the bridging phase, up-regulation of MHC class I and II genes were measured, enabling antigen presentation to both CD4 + Th-cells and cytotoxic CD8 + T-cells. Several studies focused on the role of Th-cells because of their important contribution to protect against B. pertussis. Nevertheless, the CTLs seem also important for protection against B. pertussis, indicated by CTL infiltration in lungs and formation of MDL-29951 FHA-specific IFNa?-producing CTLs upon B. pertussis infection as was previously found in mice and humans. In addition, the bridging phase was characterized by simultaneous gene expression of several receptors on innate immune cells in the lungs and spleen. Interestingly, this included MAIRs, TREMs, semaphorins and DAP12, which is the first evidence that these receptors might play a role in B. pertussis infection. Especially DAP12, which is abundantly expressed in lungs, interacts with other membrane receptors and influences cytokine expression. Coupled to MAIR-II, DAP12 is an inhibitor of Bcell responses. Together with TREM2, DAP12 downregulates TLR and FcR expression. Overall, these former receptors function as an important bridge between innate and adaptive immune responses, determining the strength and direction of the adaptive immune response by the successive activation of lymphocytes, such as CTLs, Th-cells, and B-cells. Since the exact role of these receptors in the protection against B. pertussis remains unresolved, additional research is needed to find whether targeting of these receptors might be a viable strategy to elicit desired immune responses. In summary, the bridging phase suggests the presence of APCs and myeloid cells, such as DCs and neutrophils based on gene expression of membrane markers. However, this was not validated by histological data. Finally, the adaptive phase was recognized by the formation of T-cell and Tioxolone B-cell responses and a broad humoral response. In this same period, the naive mice were able to clear B. pertussis from their lungs. Gene expression, cytokine secretion and cellular analysis revealed presence of activated CD4 + Th-cells. The highest number of CD4 + Th-cells was detected at 14 days p.i., which is in agreement with a study showing the largest influx of Th17 cells in the lungs after B. pertussis infection at 14 days p.i.. Phenotyping of CD4 + Th-cells, based on cytokine profiles in serum and lung and expression of specific transcription factors or membrane markers, suggests a broad Th-response in the present study. The Th1 response in the lungs was characterized by Ifng and Stat1 expression. Gene expression of the mucosal homing receptor Ccr6, Card11, Ccl19, Ccl21a, Ccl21c, and signature cytokines Il17a and Il17f might indicate Th17 cells in the lungs. Upon restimulation of splenocytes with purified B. pertussis antigens, Prn- and FHA-specific Th1 and Th17 type CD4 + T-cells could be detected in the memory phase. In addition, enhanced IL-9 levels in serum suggest activation of Th9 cells and Th17 cells as these cells produce large amounts of IL-9. However, Tregs, NKT-cells and mast cells are also sources of IL-9. In summary, the different phases of T-cell development were mapped; the expansion phase of naive T-cells in the spleen, the effector phase in the lungs, contraction phase in the spleen and finally the specific memory T-cells. Data from this study suggests generation of local specific Th1/ Th17 cells in the lungs.