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CD8 + cell activation to a major mastocytoma rejection antigen, P815AB: requirement for tum − or helper peptides in priming for skin test reactivity to a P815AB‐related peptide
Author(s) -
Grohmann Ursula,
Bianchi Roberta,
Fioretti Maria C.,
Fallarino Francesca,
Binaglia Lucia,
Uyttenhove Catherine,
van Pel Aline,
Boon Thierry,
Puccetti Paolo
Publication year - 1995
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830251013
Subject(s) - mastocytoma , antigen , biology , priming (agriculture) , immunology , cd8 , immunogenicity , sensitization , adoptive cell transfer , t cell , cytotoxic t cell , immune system , microbiology and biotechnology , in vitro , biochemistry , botany , germination
Abstract Delayed‐type hypersensitivity (DTH) responses, mediated by CD8 + cells and detected by skin test assay, occur in sensitized mice in response to challenge with class I‐restricted antigenic peptides of mutagenized (tum − ) P815 mastocytoma cells. In contrast, a nonapeptide related to a tumor rejection antigen, P815AB, failed in this study to elicit DTH after sensitization of mice with irradiated tumor cells or adoptive transfer of P815AB‐pulsed dendritic cells. Unresponsiveness, however, could be overcome by immunization with tumor cells co‐expressing P815AB and tum − antigens. When used for cell pulsing in vitro , a mixture of P815AB and tum − peptides was also highly effective in inducing anti‐P815AB reactivity, as was the combined use of P815AB and class II‐restricted peptides of tetanus toxin or Plasmodium berghei circumsporozoite protein. While the effector phase of the CD8 + cell‐mediated DTH to P815AB was unaffected by the ablation of CD4 + cells, the same treatment, or neutralization of IFN‐γ, negated the induction of reactivity if it occurred at the time of sensitization. Thus, defective activation of CD4 + cells may contribute to the poor immunogenicity of P815AB. Besides providing an insight into the mechanisms of anti‐tumor protection induced by tum − cells, these data offer useful information for the design of vaccination strategies against identified tumor antigens.