TY - JOUR
T1 - In situ suppression of dealyed-type hypersensitivity
T2 - Another mechanism for sustaining the immune privilege of the anterior chamber
AU - Benson, J. L.
AU - Niederkorn, J. Y.
N1 - Copyright:
Copyright 2004 Elsevier B.V., All rights reserved.
PY - 1991
Y1 - 1991
N2 - 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.
AB - 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.
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M3 - Article
C2 - 1937568
AN - SCOPUS:0025923830
SN - 0019-2805
VL - 74
SP - 153
EP - 159
JO - Immunology
JF - Immunology
IS - 1
ER -