Cobalamin (Cbl) is an essential co-factor for the generation of energy from proteins and fat within the citrate cycle and purine and pyrimidine synthesis in the folic acid cycle. Thus, proliferating cells require Cbl for cell division. In response to activation, one of the main functions of lymphocytes (T- and B-cells) is the initiation of the cell cycle followed by proliferation. Interestingly, the influence of Cbl on T-cell activation has not been investigated so far. In peripheral blood, Cbl is bound to the transport protein Transcobalamin II (TCII) and this complex binds to proliferating cells via the TCII receptor (CD320). In this thesis, we analyzed the expression levels of CD320 on human T-cells and their respective subsets in time course analyses following activation with agonistic anti-CD3/anti-CD28 antibodies. CD320 expression under these conditions was measured using qPCR, Western Blot and flow cytometry. We could show that there is a significant correlation between the up-regulation of CD320 expression and the time after T-cell stimulation in vitro. In contrast to other activation markers such as CD25, CD320 was not expressed within the first two days following activation but strongly expressed at later time points. Furthermore, the functional effects of TCII blockade were studied using an anti-TCII monoclonal antibody. Under these conditions, T-cell proliferation was reduced by approximately 50% indicating that Cbl is an important cofactor also for T-cell proliferation. In conclusion, we here described the up-regulation of CD320 on activated T-cells for the first time. Furthermore, we gave first implications about the influence of Cbl on T-cell activation. Thus, we here provide a novel principle of how metabolic mechanisms modulate T-cell functions.