The Localized Primary Cytotoxic T‐cell Response to Cells Expressing Minor Histocompatibility Differences

Korngold, Robert; Doherty, Peter C.

doi:10.1111/j.1365-3083.1984.tb00914.x

Cited by 8 publications

(2 citation statements)

References 20 publications

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“…The BALB/c effectors and the P815 cells are both H-2 d but differ at minor histocompatibility loci27. In the allogeneic system, these IL-4 induced cells displayed higher cytotoxic activity toward P815s when lipid was present (Figure 4C).…”

Section: Resultsmentioning

confidence: 98%

Lipid‐dependent cytotoxicity by the lipase PLRP2 and by PLRP2‐positive cytotoxic T lymphocytes (CTLs)

Alves

Marshall

Tamang

et al. 2009

Cell Biochemistry & Function

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IL-4 induces a lipase, pancreatic lipase related protein 2 (PLRP2), in cytotoxic T lymphocytes (CTLs). Because PLRP2 in semen can mediate lipid-dependent toxicity to sperm, we questioned whether CTL-derived PLRP2 could support similar cytotoxicity towards tumor cells. Recombinant PLRP2 was toxic to P815 tumor cells in 48 hours when lipid and another protein, colipase, were present. However, PLRP2-positive CTLs (induced with many lots of IL-4) were unable to mediate lipid-dependent cytotoxicity. Notably, CTLs induced with only one lot of IL-4 had lipiddependent cytotoxicity. The exceptional lot of IL-4 was effective in multiple experiments at inducing lipid-dependent cytotoxicity. The lipid-dependent cytotoxicity it induced was determined to be perforin-independent. CTLs induced with IL-4 that was unable to induce lipid-dependent cytotoxicity had mRNA for PLRP2 but not mRNA for colipase. Therefore, we added exogenous colipase to the CTL assays but still cytotoxicity was unchanged. We conclude (1) that lipiddependent cytotoxicity, promoted by the lipase PLRP2 and colipase, will kill tumor cells and (2) that more than PLRP2 alone is required for lipid-dependent cytotoxicity mediated by CTLs.

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Section: Resultsmentioning

confidence: 98%

Lipid‐dependent cytotoxicity by the lipase PLRP2 and by PLRP2‐positive cytotoxic T lymphocytes (CTLs)

Alves

Marshall

Tamang

et al. 2009

Cell Biochemistry & Function

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show abstract

“…The model presented in this report for localization of an inflammatory process, particularly that of CTL in the CSF of mice inoculated i.c. with antigen, has been used previously to study the response to lymphocyte choriomeningitis virus (43), ectromelia virus (21), Semliki Forest virus (10), vaccinia virus (11), and tumor cells (14,15,31). With vaccinia virus, reasonably large volumes (>20 ,ul) of CSF could be aspirated from the cisterna magna of mice (11) on day 7 after i.c.…”

Section: Discussionmentioning

confidence: 99%

Treatment of mice with polyinosinic-polycytidilic polyribonucleotide reduces T-cell involvement in a localized inflammatory response to vaccinia virus challenge

Korngold¹,

Doherty²

1985

J Virol

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Role of the major histocompatibility complex in targeting effector T cells into a site of virus infection

Doherty¹,

Allan²

1986

Eur J Immunol

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Bone marrow radiation chimeras have been used as virus-infected, cyclophosphamide-suppressed recipients to analyze the major histocompatibility complex (MHC) restriction constraints on the adoptive transfer of lymphocytic choriomeningitis by immune T cells. The basic protocol employed [(A X B)F1----(A X C)F1] chimeras, where A, B, C are different MHC haplotypes, and the establishment of appropriate chimerism was measured by the capacity of, for instance, the transferred A, T cells to generate MHC-restricted, virus-specific cytotoxic T lymphocytes (CTL) in the spleen of the [(A X B)F1----(B X C)F1] recipients. The experiments show quite clearly that maximal inflammatory process is only induced when donor bone marrow, irradiated recipient and transferred T cells share at least one MHC haplotype. Compatibility of the T cells and the radiation-resistant phenotype alone in, for instance, transfer of C immune lymphocytes into [(A X B)F1----(B X C)F1] recipients produced little inflammation if the chimeras had been established for at least 10 weeks. These results are compatible with a model which proposes that the transferred T cells first replicate in MHC-compatible lymphoid tissue and are then targeted onto the appropriate MHC plus virus expressed on cells in the blood-cerebrospinal fluid (CSF) barrier. An alternative postulate, that all that is required for the development of inflammatory process is MHC-restricted T cell replication in lymphoid tissue, with subsequent nonspecific localization to the central nervous system (CNS), was explored by transferring B, immune T cells into [(A X B)F1----A] recipients. The finding was that H-2b effectors did not cause any meningitis in [H-2kXb F1----H-2k] recipients, though potent H-2b-restricted CTL were generated in the spleens of comparable chimeras. However, in the H-2k immune----[H-2kXbF1----H-2b] transfer there was evidence of moderate inflammation that was about 9 times less severe than that caused by the H-2b effectors in comparable recipients. This indicates that, for maximal inflammatory process to occur, the T cells must encounter MHC-compatible, virus-infected cells in the CNS, with the effect being absolute in one strain combination and partial in another. Possible mechanisms underlying this divergence are discussed.

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The Localized Primary Cytotoxic T‐cell Response to Cells Expressing Minor Histocompatibility Differences

Cited by 8 publications

References 20 publications

Lipid‐dependent cytotoxicity by the lipase PLRP2 and by PLRP2‐positive cytotoxic T lymphocytes (CTLs)

Lipid‐dependent cytotoxicity by the lipase PLRP2 and by PLRP2‐positive cytotoxic T lymphocytes (CTLs)

Treatment of mice with polyinosinic-polycytidilic polyribonucleotide reduces T-cell involvement in a localized inflammatory response to vaccinia virus challenge

Role of the major histocompatibility complex in targeting effector T cells into a site of virus infection

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