As adenosine receptors have various affinities to their ligand, work in my lab is exploring the hypothesis that these receptors have a time-dependent role in infection where at the onset of S. pneumoniae infection and resulting tissue damage, a moderate rise in extracellular adenosine results in selective engagement of the high-affinity receptors A1 and/or A3 mediating host protection, while continued damage and adenosine buildup later on stimulate the lower-affinity A2A and/or A2B receptors. Here, IGKV2D-29 is linked to infection.