Staining for iC3b and C3/C3 fragments in inflamed and normal human lung. Left column. Lung from control “normal” human (HT840-1, -2). 10×. Staining for iC3b and C3/C3 fragments in normal human lung tissue was characterized by weak to strong staining of frequent intravascular, interstitial, and perivascular extracellular proteinaceous material, as well as peribronchiolar interstitium and/or alveolar septae. This is consistent with the spontaneous tickover of CAP activity and with normal methods of inactivating C3b to iC3b. Staining for C3/C3 fragments was more intense than staining for iC3b. Staining with TT30 is less intense (likely because of differences in concentration and signal amplification, as well as binding avidity) but follows the same pattern as for iC3b and C3/C3 fragments. TT30 staining is blocked by inclusion of an anti-CR2 mAb. Right column. Inflamed lung from asthmatic human (113285a3-1). 10×. Staining for iC3b and C3/C3 fragments in peribronchiolar interstitium and/or alveolar septa is of greater intensity and extends further into smaller airways than in the normal lung. Staining with TT30 is more intense and more broadly distributed, after the iC3b and C3/C3 fragment staining patterns. This is consistent with the targeting of TT30 to sites of C3 fragment deposition by binding of the CR2 portion. This binding is blocked by addition of an anti-CR2 mAb.