Cancer Immunology, Immunotherapy

, Volume 61, Issue 8, pp 1327–1341

The expression, function, and clinical relevance of B7 family members in cancer

Focussed Research Review

DOI: 10.1007/s00262-012-1293-6

Cite this article as:
Seliger, B. & Quandt, D. Cancer Immunol Immunother (2012) 61: 1327. doi:10.1007/s00262-012-1293-6

Abstract

The modulation and suppression of anti-tumor immune responses is a characteristic feature of tumor cells to escape immune surveillance. Members of the B7 family are involved in this process, since the level of activation of the anti-tumor immune response depends on the balance between co-stimulatory and co-inhibitory signals. Some molecules are often overexpressed in tumors, which has been associated with the pathogenesis and progression of malignancies as well as their immunological and non-immunological functions. The B7 homologs play a key role in the maintenance of self-tolerance and the regulation of both innate and adaptive immunity in tumor-bearing hosts. Furthermore, the blockade of negative signals mediated by the interaction of co-inhibitory ligands and counter-receptors of the B7 family is currently being studied as a potential immunotherapeutic strategy for the treatment of cancer in humans.

Keywords

CancerCo-stimulationB7 familyPIVAC11Therapy

Abbreviations

ALL

Acute lymphoblastic leukemia

BTLA

B and T lymphocyte attenuator

CTL

Cytotoxic T lymphocyte

CTLA4

Cytotoxic T lymphocyte-associated antigen 4

CR

Complete remission/response

CTL

Cytotoxic T lymphocyte

HLA

Human leukocyte antigen

ICOS

Inducible co-stimulatory molecule

IFN

Interferon

JAK

Janus kinase

mAb

Monoclonal antibody

MAPK

Mitogen-activated protein kinase

MDS

Myelodysplastic syndrome

MDSC

Myeloid-derived suppressor cell

MHC

Major histocompatibility complex

MZL

Marginal zone lymphoma

NK

Natural killer cell

NSCLC

Non-small cell lung cancer

OR

Objective response

PR

Partial response

PTEN

Phosphatase and tensin homolog

RCC

Renal cell carcinoma

STAT

Signal transducer and activator of transcription

T-ALL

T cell lymphoblastic leukemia

TAM

Tumor-associated macrophage

TCR

T cell receptor

TLR

Toll-like receptor

TNF

Tumor necrosis factor

Treg

Regulatory T cell

SD

Stable disease

Copyright information

© Springer-Verlag 2012

Authors and Affiliations

  1. 1.Institute of Medical ImmunologyMartin Luther University Halle-WittenbergHalle (Saale)Germany
  2. 2.Section of Rheumatology, Institute for Gastroenterology and RheumatologyUniversity of LeipzigLeipzigGermany