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Review
. 1993 Oct;14(3):182-90.
doi: 10.1097/00002371-199310000-00004.

Molecular mechanisms used by tumors to escape immune recognition: immunogenetherapy and the cell biology of major histocompatibility complex class I

N P Restifo  1 , Y Kawakami, F Marincola, P Shamamian, A Taggarse, F Esquivel, S A Rosenberg
Affiliations
Review

Molecular mechanisms used by tumors to escape immune recognition: immunogenetherapy and the cell biology of major histocompatibility complex class I

N P Restifo et al. J Immunother Emphasis Tumor Immunol. 1993 Oct.

Abstract

In this article, we explore the hypothesis that tumor cells can escape recognition by CD8+ T cells via deficiencies in antigen processing and presentation. Aspects of the molecular and cellular biology of major histocompatibility complex class I are reviewed. Evidence for histology-specific molecular mechanisms in the antigen-processing and -presentation deficiencies observed in some human and murine tumors is presented. Mechanisms identified include down-regulation of antigen processing, loss of functional beta 2-microglobulin, and deletion of specific alpha-chain alleles. Finally, we discuss studies using an antigen-presentation-deficient mouse tumor as a model for the immunogenetherapy of an antigen-presentation deficiency.

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Figures

FIG. 1
FIG. 1
Screening of human tumor lines for antigen-processing defects. Cell lines studied were cultured human tumor cells tested for their capacity to present vaccina virus (VV) antigens to Kd-restricted, VV-specific TCD8+. The tumor cell lines were provided by J. Minna (University of Texas, Southwestern). H1155, H28, and H460 are all non-small-cell lung cancers. H146, H1092, and H82 are all small-cell lung cancers. In the representative experiment shown, all tumor cell lines processed and presented endogenous antigens poorly.
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