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pubmed:abstractText |
Guinea-pig spleen cells treated with complete Freund's adjuvant (CFA) produce eosinophil-directed chemotactic inhibitory factors (ECIF). The inhibition is selective for the response of eosinophils to delayed ECF-a, which had been isolated from 24-hr-old inflamed skin lesions induced by DNP-Ascaris extract in sensitized animals and had been confirmed as being a T lymphocyte-derived lymphokine. ECIF activity is absorbed by incubation with eosinophils, but not with macrophages or neutrophils. The cells spontaneously release ECIF; pretreatment with a protein synthesis inhibitor reduces ECIF production, indicating that protein synthesis is essential. The source of ECIF seems to be lymphocytes, probably T lymphocytes. ECIF activity is recovered in two separate fractions: one elutes near bovine serum albumin (MW 70,000) and the other near cytochrome c (MW 12,500). ECIF binds to peanut agglutinin- or Limulus polyphemus agglutinin-coupled agarose beads. Furthermore, ECIF activity is blocked when eosinophils are incubated with D-galactose or sialic acid. These results suggest that ECIF derived from T lymphocytes of CFA-treated animals modulate the delayed ECF-a-mediated tissue eosinophilia, and that terminal galactose and/or sialic acid residues are essential for ECIF activity.
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