Antigen-Specific Activation of Effector Macrophages by IFN-γ Producing (T(H)1) T Cell Clones. Failure of IL-4-Producing (T(H)2) T Cell Clones to Activate Effector Function in Macrophages

Document Type

Article

Publication Date

1-1-1989

Description

IFN-γ-producing (T(H)1) and IL-4-producing (T(H)2) clones were assayed for their ability to directly induce cytostatic activity in macrophages generated from splenic myeloid precursors (M∅-c). In the presence, but not in the absence, of antigen, T(H)1 clones activated the M∅-c to inhibit the growth of P815 tumor cells in vitro. T(H)2 clones were not able to activate such effector activity in the M∅-c. The M∅-c did effectively present Ag to the T(H)2 clones as evidenced by the proliferation of T(H)2 cells cultured with Ag in the presence, but not in the absence, of M∅-c. Therefore, although both T(H)1 and T(H)2 were activated by cognate interaction with antigen presenting M∅-c, only T(H)1:M∅-c interactions displayed reciprocity resulting in activation of the M∅-c. T(H)1-derived lymphokines or rIFN-γ, in the presence of LPS, could activate proteose-peptone elicited M∅, resident peritoneal M∅, and M∅-c whereas neither T(H)2-derived lymphokines nor rIL4 could induce detectable activity in any of the 3 M∅ populations. IFN-γ, in the absence of LPS, could activate the elicited M∅ and to a lesser and more variable degree, the resident M∅. Only the Mα-c consistently required both IFN-γ and LPS for induction of cytostatic activity. Since M∅-c consistently required at least two signals for activation, the ability of T(H)1-derived lymphokines to synergize with T(H)2 cells in M∅ activation was examined. T(H)2 could activate the Ag-presenting M∅-c in the presence of IFN-γ. The ability of added IFN-γ to synergize with T(H)2 indicates that the cognate interaction between T(H)2 and antigen presenting M∅-c does result in delivery of at least one of the signals required for M∅ activation.

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