TY - JOUR
T1 - Immunological analysis of a destructive pattern of intraocular tumor resolution
AU - Niederkorn, Jerry Y.
AU - Knisely, Terrence L.
N1 - Funding Information:
unrestricted grant from Research to Prevent Blindness, New York. Dr. Niederkorn is a Research to Prevent Blindness - Olga Keith Wiess Scholar. Dr. Knisely is supported in part by a grant from the Texas Department of the Ladies Auxiliary, Veterans of Foreign Wars. Fig. 1 was reprinted by permission from the Journal of Immunology.
Funding Information:
ACKNOWLEDGEMENTS The excellent technical assistance o f Ms. Elizabeth Mayhew and Ms. Beverly Fischer i s greatly appreciated. We are indebted t o Dr. Martha W. Luckenbach for assistance i n the interpretation and photography of the histopathological specimens. This work supported i n part by NIH grants EY05631, CA09083 and CA30276 and an
PY - 1988
Y1 - 1988
N2 - Spontaneous rejection of syngeneic intraocular P91 mastocytoma occurred by a T cell-dependent immune process that produced extensive, irreparable damage to normal ocular tissues indicative of a delayed-type hypersensitivity (DTH) lesion. We investigated the contribution of other effector modalities in this tumor resolution. Antibody was not responsible for either tumor rejection or phthisis of the tumor-containing eye since passively transferred hyperimmune serum failed to produce either tumor rejection or the characteristic ocular lesions. Moreover, the destructive pattern of tumor rejection occurred in splenectomized hosts which had depressed anti-P91 serum antibody and in a congenic strain (B10-.D2oSn) lacking the C5 complement component. The likelihood that tumor necrosis factor (TNF) was involved in this pathogenesis was also ruled out by the observation that P91 tumor cells were not susceptible to lysis by recombinant TNF. A different pattern of tumor resolution was observed when the opposite eye was challenged with tumor. In this case, the tumor was rejected without damaging any major ocular structures. Histological analysis demonstrated a mononuclear cellular infiltrate which was identified by immuno-histology to be Thy 1+, Lyt 2+. Thus, although both forms of cell-mediated immunity are available to the host, only one predominated in each eye. These results suggest that unique immuno-logical control mechanisms influence the outcome of tumor resolution in the eye.
AB - Spontaneous rejection of syngeneic intraocular P91 mastocytoma occurred by a T cell-dependent immune process that produced extensive, irreparable damage to normal ocular tissues indicative of a delayed-type hypersensitivity (DTH) lesion. We investigated the contribution of other effector modalities in this tumor resolution. Antibody was not responsible for either tumor rejection or phthisis of the tumor-containing eye since passively transferred hyperimmune serum failed to produce either tumor rejection or the characteristic ocular lesions. Moreover, the destructive pattern of tumor rejection occurred in splenectomized hosts which had depressed anti-P91 serum antibody and in a congenic strain (B10-.D2oSn) lacking the C5 complement component. The likelihood that tumor necrosis factor (TNF) was involved in this pathogenesis was also ruled out by the observation that P91 tumor cells were not susceptible to lysis by recombinant TNF. A different pattern of tumor resolution was observed when the opposite eye was challenged with tumor. In this case, the tumor was rejected without damaging any major ocular structures. Histological analysis demonstrated a mononuclear cellular infiltrate which was identified by immuno-histology to be Thy 1+, Lyt 2+. Thus, although both forms of cell-mediated immunity are available to the host, only one predominated in each eye. These results suggest that unique immuno-logical control mechanisms influence the outcome of tumor resolution in the eye.
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U2 - 10.3109/02713688809031806
DO - 10.3109/02713688809031806
M3 - Article
C2 - 3409718
AN - SCOPUS:0023893954
SN - 0271-3683
VL - 7
SP - 515
EP - 526
JO - Current Eye Research
JF - Current Eye Research
IS - 5
ER -