IL-12- and IL-2-induced tumor regression in a new murine model of oral squamous-cell carcinoma is promoted by expression of the CD80 co-stimulatory molecule and interferon-gamma

Int J Cancer. 2000 May 1;86(3):368-74. doi: 10.1002/(sici)1097-0215(20000501)86:3<368::aid-ijc11>3.0.co;2-1.

Abstract

Therapy with IL-12 or IL-2 induces tumor regression in only a few patients with head-and-neck squamous cell carcinoma (SCC), and the factors promoting responsiveness have not been well defined. In this study, we examined whether combined IL-12 and IL-2 therapy can induce tumor regression in a new murine model of oral SCC and determined if the anti-tumor response is promoted by expression of the immune co-stimulatory molecule CD80 and cytokine IFN-gamma. In CD80-positive or -negative subclones of a BALB/c oral SCC line in syngeneic mice, we showed that systemic rIL-12 alone was comparable in effectiveness to combined therapy with IL-12 and peri-tumoral rIL-2, inducing complete regression of the CD80(+) line B7E11-4scid. However, therapy with these cytokines had no effect on growth of the CD80(-) subclone B7E3-4scid and did not induce complete regression of the CD80(+) subclone B7E11-4scid in congenic BALB/c IFN-gamma knockout mice, indicating that expression of the CD80 co-stimulatory molecule and IFN-gamma contributes to tumor regression. In cytokine-treated mice that rejected the CD80(+) SCC line, an increase in infiltrating CD4(+) lymphocytes and apoptotic bodies within the tumor specimens was observed, and resistance to rechallenge with the same tumor was detected in 50% of recipients, consistent with an immune response. Our results provide evidence that regression of oral head-and-neck SCC may be induced by therapy with systemic IL-12 and that expression of the CD80 co-stimulatory molecule by SCC and IFN-gamma by the host promote IL-12 induced regression of SCC.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Angiogenesis Inhibitors / pharmacology
  • Angiogenesis Inhibitors / therapeutic use*
  • Animals
  • B7-1 Antigen / biosynthesis
  • B7-1 Antigen / genetics*
  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / genetics*
  • Carcinoma, Squamous Cell / metabolism
  • Carcinoma, Squamous Cell / pathology
  • Disease Models, Animal
  • Gene Expression Regulation, Neoplastic* / drug effects
  • Interferon-gamma / biosynthesis
  • Interferon-gamma / genetics*
  • Interleukin-12 / pharmacology
  • Interleukin-12 / therapeutic use*
  • Interleukin-2 / pharmacology
  • Interleukin-2 / therapeutic use*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mouth Neoplasms / drug therapy*
  • Mouth Neoplasms / genetics*
  • Mouth Neoplasms / metabolism
  • Mouth Neoplasms / pathology
  • Recombinant Proteins / pharmacology
  • Recombinant Proteins / therapeutic use

Substances

  • Angiogenesis Inhibitors
  • B7-1 Antigen
  • Interleukin-2
  • Recombinant Proteins
  • Interleukin-12
  • Interferon-gamma