Therefore, the resting MT was only determined for the right thenar musculature since the majority of subjects were right-handed and thus the correlations were calculated only for the left hemisphere. Another limiting factor might be that we included in the study not only right handed subjects but also a few lefthanded and ambidextrous individuals since we did not wish to reduce the group size by including only right-handed subjects. In a previous large-scale normative study there was no significant difference in MT between the dominant and non-dominant hand thus the inclusion of non right-handed subjects and the stimulation of their non-dominant hand should not distort the results of the study. An alternative solution to the handedness issue could have been to perform the measurements for the dominant hand in all subjects, but then we would have faced the problem of combining the thickness results of both hemispheres. Another limitation in the study is the elapsed time between the MRI scanning and the TMS experiment which for some subjects was several months. We acknowledge that especially in the case of progressive neurodegenerative diseases the timing in the data collection is essential and differences in timing may have an impact on the results. Due to both funding and technical issues we were forced to use older MRI scans when available for the subjects. Fortunately, the majority of the subjects were scanned within a few weeks before the TMS, the average time difference being 2.4 months. Furthermore, the time difference between the measurements was taken into account in the statistical modelling as a covariate of no interest. The obligate intracellular bacterium Chlamydia pneumoniae infects the respiratory tract and replicates in bronchial epithelial cells. The cells are infected by elementary bodies of C. pneumoniae which develop within hours post infectionem into reticulate bodies. The latter form divides several times and within 48 to 72 h a microscopically visible intracellular inclusion is generated. In vitro, the replication of C. pneumoniae is impaired by IFNc. This cytokine exerts its effect indirectly via the induction of two enzymes: the inducible isoform of the nitric oxide synthase and indolamine 2,3 dioxygenase. The former enzyme generates nitric oxide, which is toxic for bacteria and impairs replication of C. pneumoniae, while the latter degrades the aminoacid tryptophan, which is required by C. pneumoniae. In vivo, the replication of the bacterium is also controlled by IFNc, as chlamydial burden in IFNc receptor-deficient mice is significantly higher than in wild type mice. Based on these findings it is obvious that IFNc is crucial to control and confine pneumonia caused by C. pneumoniae. The cellular source of IFNc in vivo during pulmonary infection with C. pneumoniae was analyzed by Rothfuchs et al. Accordingly, NK cells neither contributed to IFNc-secretion by bronchoalveolar lavage mononuclear cells nor protected mice. In contrast, IFNc-secreting CD4+ or CD8+ T-cells were protective since they impaired replication of C. pneumoniae. Thus, IFNcsecreting cells of the adaptive immune Life Science Reagents system contribute to host defense against the bacterium.