In situ hybridization (ISH) of human glioblastoma tissue sections revealed expression of interleukin‐1 (IL‐1)α and/or β and IL‐1 receptor types I and II (IL‐1R I and II) in the majority of cases evaluable. To understand the function of IL‐1‐family members in human glioblastomas, we have studied 6 glioblastoma cell lines. RT‐PCR, ISH, ELISA and ¹²⁵I‐IL‐1‐binding assays revealed expression of IL‐1 and high‐affinity receptors for human (h)IL‐1 in all but 1 cell line. Using a colony growth assay in semi‐solid media for testing serial plating efficacy (PE, number of colonies per number of cells seeded in %), only the IL‐1R‐negative cell line was not influenced by recombinant human (rh)IL‐1α or ‐β, whereas IL‐1 down‐regulated the self‐renewal of clonogenic cells of the other glioblastomas. Tritiated thymidine uptake was down‐regulated by rhIL‐1 in all cell lines studied. Cell viability remained unchanged by rhIL‐1. Wherever growth modulation by rhIL‐1 was detected, it could be reversed by either soluble IL‐1R I or II or by rhIL‐1 receptor antagonist (ra). IL‐1ra not only was able to reverse rhIL‐1‐induced growth modulation but alone could modulate glioblastoma growth in comparison with control in cell lines producing IL‐1. Our results show the presence of public autocrine loops for IL‐1 leading to growth inhibition in some glioblastomas. To understand these loops, we have studied expression and function of IL‐1ra in glioblastomas. ISH of human glioblastoma tissue sections revealed expression of hIL‐1ra in all 8 cases evaluable. In 4 of 6 cell lines, IL‐1ra was found in the supernatant under constitutive conditions, the IL‐1R‐negative line being among the 2 non‐producers. The other non‐producing cell line, HTB 17, showed expression of hIL‐1R II. Most interestingly, a neutralizing antibody against IL‐1ra down‐regulated growth of IL‐1‐ and IL‐1ra‐producing glioblastoma cells to approx. 30% of the controls. Thus, public autocrine loops for IL‐1 in human glioblastomas exist and result in growth inhibition. An autocrine production of IL‐1‐antagonizing molecules such as IL‐1ra by these tumors can counteract this IL‐1 function and represent a basic escape mechanism supporting malignant growth in some glioblastomas. Int. J. Cancer 71: 1066‐1076, 1997. © 1997 Wiley‐Liss Inc.