Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

MIC Molecules

  • Stefan Holdenrieder
  • Helmut Rainer Salih
  • Alexander Steinle
Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_3705-2

Synonyms

Definition

MICA and MICB are human inducible MHC class I-related glycoproteins expressed by stressed and malignant cells and serve as ligands for the NKG2D receptor (NKG2D receptor) on natural killer (NK) cells (natural killer cell activation) and T cells thereby stimulating innate and adaptive immune responses.

Characteristics

Human MIC molecules are encoded within the MHC on the short arm of chromosome 6. The MIC gene family comprises six genes (MICA to MICF) of which only MICA and MICB are functional, whereas MICC to MICF constitutes pseudogenes. MICA and MICB are tandem genes located between the HLA-Bgene and the BAT1 locus at the transition from the MHC class I to the class III region. The MICA locus is highly polymorphic with 86 alleles known to date. MICA*08 is by far the most frequent allele encoding for a MICA protein with a truncated cytoplasmic domain due to a frameshift mutation. MICA and MICB...

Keywords

Major Histocompatibility Complex Class Imatinib Mesylate Cancer Disease NKG2D Receptor Classical Major Histocompatibility Complex Class 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Holdenrieder S, Stieber P, Peterfi A et al (2006) Soluble MICA in malignant diseases. Int J Cancer 118:684–687CrossRefPubMedGoogle Scholar
  2. Raulet DH, Gasser S, Gowen BG, Deng W, Jung H (2013) Regulation of ligands for the NKG2D activating receptor. Annu Rev Immunol 31:413–441CrossRefPubMedPubMedCentralGoogle Scholar
  3. Salih HR, Rammensee HG, Steinle A (2002) Cutting edge: down-regulation of MICA on human tumors by proteolytic shedding. J Immunol 169:4098–4102CrossRefPubMedGoogle Scholar
  4. Salih HR, Holdenrieder S, Steinle A (2008) Soluble NKG2D ligands: prevalence, release, and functional impact. Front Biosci 13:3448–3456CrossRefPubMedGoogle Scholar
  5. Steinle A, Cerwenka A (2015) Immunology. MULT1plying cancer immunity. Science 348:45–46CrossRefPubMedGoogle Scholar
  6. Ullrich E, Koch J, Cerwenka A, Steinle A (2013) New prospects on the NKG2D/NKG2DL system for oncology. Oncoimmunology 2:e26097CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  • Stefan Holdenrieder
    • 1
  • Helmut Rainer Salih
    • 2
  • Alexander Steinle
    • 3
  1. 1.Institute of Clinical Chemistry and Clinical PharmacologyUniversitatsklinikum BonnBonnGermany
  2. 2.Department of Internal Medicine IIUniversity Hospital of Tuebingen, Eberhard-Karls-UniversityTuebingenGermany
  3. 3.Institute for Molecular Medicine, Centre for Molecular MedicineGoethe UniversityFrankfurt am MainGermany