PubMed · 1883263
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H Yoshida, K Maeda, Y Tanaka, S Anan. 1991. [Atopic dermatitis and eosinophils].. https://pubmed.ncbi.nlm.nih.gov/1883263/
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We have previously shown that irradiated BALL-1, a B lymphoma line, stimulates OKT4 T cells to produce a unique eosinophil chemotactic factor (ECF) which suppresses the respiratory burst of eosinophils. In the present experiments, we found that solubilized BALL-1 also stimulated peripheral blood mononuclear cells (PBMC) to produce ECF activity in a dose-dependent manner. PBMC treated with solubilized BALL-1 produced ECF within 24 h. ECF production-inducing factor (ECF-IF) had affinity with lentil lectin beads, suggesting that ECF-IF has glucose or mannose as carbohydrate moieties. Furthermore, we found that ECF-IF activity was comprised of at least four ECF-IF with different isoelectric points (pI): ECF-IF1 had a pI of 4-5, ECF-IF2 a pI of about 6, ECF-IF3 a pI of about 7, and ECF-IF4 a pI of about 8. ECF-IF1 stimulated PBMC to produce mainly an ECF with a pI of about 7-8, whereas the rest of ECF-IF induced an ECF with a different pI. The present results suggest that the membrane glycoproteins of some tumors, at least, partly contribute to tissue eosinophilia in the stroma of the malignant tumor by inducing ECF production from PBMC.
Human mononuclear leukocytes (MNL), probably OKT4-positive T cells, produced an eosinophil chemotactic factor (ECF) when they were cocultured with irradiated BALL-1, a B cell lymphoma line. Treatment of MNL, with anti-IL-2 antibody failed to suppress BALL-1-induced ECF production. Periodate-lysine-paraformaldehyde-fixed but not acetone- and ethanol-fixed BCLL induced evident ECF production. These results suggested that some cell surface molecules play a role in the induction of ECF production. Isoelectric point of BALL-1-induced ECF was around pH7, whereas that of IL-2-induced ECF was around pH 5. The molecular weight of BALL-1-induced ECF was between 10 and 30 kD. Although a combination of MoAb against IL-3, IL-5, and GM, CSF suppressed the activity of IL-2-induced ECF, it failed to suppress that of BALL-1-induced ECF. Furthermore, BALL-1-induced ECF suppressed fMLP-induced respiratory bursts of eosinophils, while IL-2-induced ECF failed. We propose that at least one reason for eosinophil infiltrate into the stroma of tumors is that the tumor cells stimulate T cells to produce BALL-1-induced ECF, and the eosinophils attracted by the ECF exhibit different functions from those by other ECF.
Although the eosinophilic granulocyte has been recognized as a blood cell type for more than 100 years, its functional significance has long remained an enigma. The introduction of successful isolation procedures resulted in rapidly progressive research efforts, but the concept of the functional role of this cell type made a full about turn between the 1970s and 1980s. In the 1970s, the role of the eosinophil was thought to be a homeostatic one, with its main task being to repair mast-cell-dependent tissue damage in parasitic and allergic disease. Further structural analysis and improved biological and clinical integration of such knowledge led to the completely revised concept of the 1980s: the eosinophil is now seen as the main culprit in the damage that accompanies allergic disease, as a result of mistaken identity between the parasite (where cytotoxic power against the aggressor is desirable) and the allergen (where the eosinophil's cytotoxic power results in self-damage). The latest research news about cytokine-dependent regulatory mechanisms governing the eosinophilic reaction supports our hope that by specific blocking of tissue hormones, such as the lymphocyte-derived IL-5, elegant ways of manipulating hypereosinophilic reactions will be found in the near future.