SOCS1 and parasitic infectious disease: [29], [30] Furthermore, as shown by Whyte et al. in context with parasite infection, SOCS-1 may confine classically activated M1 macrophage formation and foster alternatively activated - potentially anti-atherogenic - M2 macrophage generation. [3] Thus, these observations support the pro-atherogenic impact of SOCS-1 deficiency in this mouse model. The fact that we hardly detected any M2 macrophages regardless of the genotype examined may reflect the mainly pro-inflammatory sub-intimal environment at this particular time of plaque development. [31].