Granulocyte-macrophage colony-stimulating activty (GM-CSA) can be produced by a variety of normal cell types including mononuclear phagocytes, activated T lymphocytes, endothelial cells, and fibroblasts. Recent evidence shows that a major role of the monocyte-macrophage is the recruitment of environmental cells, i.e., fibroblasts, to produce GM-CSA. In this study we have identified interleukin 1 (IL-i) as a monokine that stimulates fibroblasts to produce and release GM-CSA and prostaglandin E2 (PGE2). Both purified human monocyte-derived IL-I and human recombinant ILiA (10-10 M) can be substituted for monocyteconditioned medium in stimulating fibroblast GM-CSA and PGE2 production. Both forms of IL-1 stimulate fibroblasts to produ6e GM-CSA and PGE2 in a dose-dependent fashion. The fibroblkst-stimulating activity found in monocyte-conditioned medium was completely blocked by anti-I-iA. We conclude that monocytes produce IL-1, and that monocyte-derived IL-i induces fibroblasts to produce GM-CSA and PGE2.

Conditioned medium prepared from human autopsy lung tissue contains high level activity of colony stimulating factor which stimulates granulocytes and macrophage colony formation in both mouse and human bone marrow. The lung colony stimulating factor has been purified about 2250-fold by methods including hydroxylapatite chromatography, preparative gel electrophoresis, preparative isoelectric focusing, and gel filtration chromatography. The final specific activity was 2.7 X 10(6) units/mg. The purified factor has a molecular weight of 41 000 as determined by gel filtration. It is stable at the pH range of 6.5--10 and 56 degrees C for 30 min but sensitive to protease digestion and periodate oxidation. On polyacrylamide gel electrophoresis, it migrates in the alpha-globulin post-albumin region. Upon isoelectrofocusing lung colony stimulating factor appears heterogeneous with isoelectric points of 3.7--4.3. Treatment with neuraminidase did not affect its activity, but caused a change in electrophoretic mobility and isoelectric point. Antibody produced by immunizing rabbits with partially purified lung colony stimulating factor exerted strong inhibitory activity on the factor from lung as well as on colony stimulating factor from other human sources including serum, urine, and placenta.

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Angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) can best be described as a disorder of T-cells resulting in amplification of the B-cell response and clinical symptoms of lymphadenopathy, fever, hepatosplenomegaly, and a variety of blood abnormalities. Pure red cell aplasia (PRCA), an autoimmune disorder resulting in selective aplasia of the erythroid series, has only rarely been associated with AILD. Herein we report three cases of AILD and PRCA. Serum from one patient was available for study and contained a dose-dependent inhibitor of the CFU-E but not CFU-GM cultures from normal bone marrow. This activity was found in the globulin fraction after ammonium sulfate precipitation. Patients with AILD are known to make antibodies to many autologous epitopes, and the most well-characterized mechanism of PRCA involves antibodies to red cell precursors. Our serum data are consistent with the hypothesis that such an antibody existed in our patient. Aggressive treatment of these patients resulted in transient improvement in two; however, all three died without achieving a durable complete remission with two dying of infectious complications.