Our choice of partners, so they say, is subconsciously directed by an immune system aiming to making itself more diverse and robust. This strategy seems to work quite well if one looks at the highly complex structures that underlie human immunology, which still surprises with unexpected enigmas even after decades of intense research. Another recent proof of this phenomena is the study by Eller et al. 1 in this issue of JASN that describes a surprisingly aggravated course of glomerulonephritis in mice lacking the chemokine receptor CCR7. The family of chemokines and their receptors are important mediators of directional leukocyte trafficking under inflammatory and homeostatic conditions. Given the complexity of the immune system and the multitude of different leukocytes, guidance by the chemokine family is much needed to facilitate the interaction of the right leukocyte subsets at the right time and in the right location. CCR7 is particularly crucial in the initiation of antigen-specific immune responses.2 Upon encountering a danger signal, antigen-bearing dendritic cells upregulate CCR7 and become responsive to the corresponding ligands CCL19 and CCL21, which are expressed in secondary lymphoid organs. Likewise, naive T helper cells bear CCR7 on their surface and are similarly directed to lymph nodes and spleen. Here, these two cell types interact in a favorable environment to initiate …