Roles of tumour localization, second signals and cross priming in cytotoxic T-cell induction

Adrian F. Ochsenbein (), Sophie Sierro, Bernhard Odermatt, Marcus Pericin, Urs Karrer, Jan Hermans, Silvio Hemmi, Hans Hengartner and Rolf M. Zinkernagel ()
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Adrian F. Ochsenbein: Institute of Experimental Immunology, University Hospital
Sophie Sierro: Institute of Experimental Immunology, University Hospital
Bernhard Odermatt: Institute of Experimental Immunology, University Hospital
Marcus Pericin: Institute of Experimental Immunology, University Hospital
Urs Karrer: Institute of Experimental Immunology, University Hospital
Jan Hermans: Malaghan Institute of Medical Research
Silvio Hemmi: Institute of Molecular Biology, University of Zurich
Hans Hengartner: Institute of Experimental Immunology, University Hospital
Rolf M. Zinkernagel: Institute of Experimental Immunology, University Hospital

Nature, 2001, vol. 411, issue 6841, 1058-1064

Abstract: Abstract The vertebrate immune system has evolved to protect against infections that threaten survival before reproduction. Clinically manifest tumours mostly arise after the reproductive years and somatic mutations allow even otherwise antigenic tumours to evade the attention of the immune system1,2,3. Moreover, the lack of immunological co-stimulatory molecules on solid tumours could result in T-cell tolerance4,5,6,7,8; that is, the failure of T cells to respond. However, this may not generally apply9,10. Here we report several important findings regarding the immune response to tumours, on the basis of studies of several tumour types. First, tumour-specific induction of protective cytotoxic T cells (CTLs) depends on sufficient tumour cells reaching secondary lymphatic organs early and for a long enough duration. Second, diffusely invading systemic tumours delete CTLs. Third, tumours that stay strictly outside secondary lymphatic organs, or that are within these organs but separated from T cells by barriers, are ignored by T cells but do not delete them. Fourth, co-stimulatory molecules on tumour cells do not influence CTL priming but enhance primed CTL responses in peripheral solid tumours. Last, cross priming of CTLs by tumour antigens, mediated by major histocompatibility complex (MHC) class I molecules of antigen-presenting host cells, is inefficient and not protective. These rules of T-cell induction and maintenance not only change previous views but also rationales for anti-tumour immunotherapy1,2.

Date: 2001
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DOI: 10.1038/35082583

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