Formation of IgE-binding factors by rat T lmphocytes. III. Mechanisms of selective formation of IgE-suppressive factors by treatment with complete Freund's adjuvant

M. Hirashima, J. Yodoi, T. F. Huff, K. Ishizaka

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Splenic lymphocytes of rats treated by repeated injections of complete Freund's adjuvants (CFA) spontaneously released soluble factors that had affinity for IgE and selectively suppressed the IgE response (IgE-suppressive factors). The factors lacked affinity for lentil lectin. The serum of CFA-treated rats and culture filtrates of their spleen cells induced normal mesenteric lymph node (MLN) cells to form IgE-suppressive factors. Analysis of the cellular mechanisms for the induction of IgE-suppressive factors in CFA-treated animals revealed that their macrophages formed 'inducers' of IgE-binding factors; their splenic lymphocytes released another soluble factor(s) that could modulate the nature of the IgE-binding factors. Culture filtrates of splenic, adherent cells from the CFA-treated animals induced normal MLN cells to form IgE-binding factors, but the factors failed to suppress the IgE response. However, normal MLN cells formed IgE-suppressive factors when they were incubated with a mixture of culture filtrates of adherent and nonadherent cells from CFA-treated rats or with culture filtrates of nonadherent cells and IgE. Approximately one-half of IgE-binding factors induced by IgE or 'inducer' alone had affinity for lentil lectin. If the IgE-binding factors were induced in the presence of culture filtrates of splenic lymphocytes from CFA-treated animals, however, the majority of the factors lacked affinity for the lectin. The same culture filtrate prevented the IgE-induced increase in Fc(ε)R(+) cells in both B cell and T cell populations. The results indicate that splenic lymphocytes release lymphokines that prevent the glycosylation of the precursor molecules of both Fc(ε)R and IgE-binding factors, thereby preventing the expression of Fc(ε)R and increasing the ratio of the IgE-suppressive factors to the total IgE-binding factors. The source of the glycosylation-inhibiting factors appears to be a subset of T cells lacking W 3/25 markers, whereas the source of the IgE-suppressive factors is W 3/25(+) T cells. Macrophage-derived 'inducers' of IgE-binding factors had affinity for Poly U Sepharose and could be recovered from the beads by elution with 1 M NaCl. The results indicate that collaboration between 'inducers' derived from adherent cells and 'glycosylation-inhibiting factors' from W 3/25(-)T cells results in the formation of IgE-suppressive factors by W 3/25(+) T cells.

Original languageEnglish (US)
Pages (from-to)1810-1816
Number of pages7
JournalJournal of Immunology
Issue number5
StatePublished - 1981

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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