1. Figure 1. Mechanism of migration of leucocytes from peripheral blood into inflamed tissues. Selectins ICAM-1 CD11a/CD18 CD11b/CD18 Chemokines: MCP-1 Chemotaxins: C5a chemokines Rolling Activation Adhesion Transmigration

2. Figure 2. Northern blot showing glomerular expression of MCP-1 mRNA correlated with monocyte infiltration

3. Figure 3. Schematic diagram showing regulation of the effects of IL ‑ 1 . Biological effects of IL ‑ 1 are tightly regulated, in part by its endogenous receptor antagonist (IL ‑ 1ra), as well as by expression of IL ‑ 1 type II receptor (IL ‑ 1RtII). IL ‑ 1RtII (68 kD) binds to IL ‑ 1  with high affinity (lower affinity for IL ‑ 1  and IL ‑ 1ra) without signal transduction. The extracellular domain of IL ‑ 1RtII can also be released as a soluble receptor selective for IL ‑ 1b. Hence, IL ‑ 1RtII is also know as a decoy receptor that may reduce the effect of IL ‑ 1 .

4. Figure 4. Northern blot showing synthesis of IL-1 decoy receptor in the glomeruli of IL-4 treated rats

5. Figure 5. Effect of IL-4 on glomerular macrophages (M  ) all M  activated M  0 2 4 6 8 Control IL-4 Cells/ glomerular section (gs) p=0.02 p=0.002

6. Figure 6. Blocking TNF-  prevented crescentic glomerulonephritis Control sTNFR 0 10 20 30 40 50 Crescents (%)

7. Figure 7. Delayed treatment with rolipram reduces urinary TNF-  vehiclerolipram 0 100 200 300 400 500 Urinary TNF-  (pg/17h) p = 0.05

8. Figure 8. Delayed treatment with rolipram reduces glomerular crescents vehiclerolipram 0 10 20 30 40 Crescents (quadrants/50 gs) p < 0.05

9. Figure 9. Short term treatment (day 0-7) with IL-4 reduction of renal injury at day 28 ControlIL-4 0 25 50 75 100 Crescents (%) p<0.01 Control IL-4 0 1 2 3 4 Tubular damage score p<0.01

10. Figure 10. IL-11 inactivated glomerular macrophages Activated M  ControlIL-11 0.0 0.5 1.0 1.5 2.0 *P<0.05 ED-3+ M  /gcs All M  ControlIL-11 0 10 20 30 40 50 NS ED-1+ M  /gs