In situ suppression of dealyed-type hypersensitivity: Another mechanism for sustaining the immune privilege of the anterior chamber

J. L. Benson, J. Y. Niederkorn

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20 Scopus citations


Immunological rejection of a highly immunogenic, syngeneic tumour (UV5C25) in the anterior chamber (AC) of BALB/c mice was analysed. Hosts developed systemic, tumour-specific cytotoxic T lymphocyte (CTL) activity (P < 0.001) as well as systemic, tumour-specific delayed-type hypersensitivity (DTH) (P < 0.001). Histopathological featurs of tumour rejection were consistent with that of a CTL-mediated process [i.e., piecemeal necrosis of individual tumour cells by tumour-infiltrating lymphocytes (TIL)]. There was no evidence of ischaemic necrosis, perivascular cuffing, infarction, or vascular damage, as expected of a DTH-mediated process. In an effort to selectively eliminate CTL or DTH effector cells and hence alter the pattern of tumour rejection, mice were treated with anti-CD8 or anti-CD4 antibodies, respectively. Elimination of either cell population not only eliminated both systemic CTL and DTH activity to this tumour, but also resulted in progressive tumour growth . Analysis of TIL from untreated tumour-bearing hosts demonstrated tumour-specific cytolysis (P < 0.01) as well as the presence of DTH effector cells (P < 0.01). These results indicate that while both DTH and CTL effector cells are present in the AC, only the latter are active in tumour resolution in the AC; DTH effectors are active systemically, but suppressed locally. Further, these data also suggest the requirement of a CD8+ cell population for the development of a systemic DTH response to this tumour.

Original languageEnglish (US)
Pages (from-to)153-159
Number of pages7
Issue number1
StatePublished - Jan 1 1991


ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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