Since we observed that TREM-2 deficient AM produced more C1q (Fig. 4A, B, C and F) and that Trem-2−/− mice showed a modestly elevated neutrophil influx early during pneumococcal pneumonia (Fig. 1G), we speculated that classical complement activation could be increased in the pulmonary compartment of Trem-2−/− mice following S. pneumoniae infection and monitored levels of C3a and C5a, anaphylatoxins, which promote neutrophil influx [51]. The gene discussed is C3; the disease is pneumococcal pneumonia.