Contact Inhibition Causes Strong Downregulation of Expression of MICA in Human Fibroblasts and Decreased NK Cell Killing

Yizhou Zou, Fariba Mirbaha, Peter Stastny

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

The polymorphic MICA gene encodes glycoproteins that activate T cells and NK cells through the NKG2D receptor and may costimulate immune functions. We found that MICA was expressed on freshly isolated human fibroblasts and was markedly decreased when fibroblasts were grown to confluency in culture dishes. MICA surface protein was measured by flow cytometry with the MICA-specific monoclonal antibody (mAb) 6B3, and HLA class I-specific protein was determined with mAb w6/32. In these experiments, after culture for 120 hours, the staining for MICA in fibroblasts decreased to about 20% of the initial amount and MICA mRNA fell in parallel, while HLA class I staining was maintained or even became somewhat stronger. In other experiments, MICA expression was not decreased when fibroblast contact was prevented by the addition of 1 μM Rottlerin, a specific inhibitor of protein kinase C delta known to prevent contact inhibition of fibroblasts. In the NK cell cytotoxicity assay, blocking MICA by antibody or downregulation by cell contact resulted in a decrease of specific killing by 30%. Increased MICA expression during proliferation of fibroblasts may support the host response to injury.

Original languageEnglish (US)
Pages (from-to)183-187
Number of pages5
JournalHuman Immunology
Volume67
Issue number3
DOIs
StatePublished - Mar 1 2006

Keywords

  • Fibroblasts
  • MICA
  • NK cells
  • contact inhibition

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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