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Upregulated mRNA expression of major histocompatibility complex class I chain‐related gene A in colon and activated natural killer cells of Chinese patients with ulcerative colitis
Author(s) -
GE Liu Qing,
JIANG Ting,
ZHAO Jie,
CHEN Zhi Tao,
ZHOU Feng,
XIA Bing
Publication year - 2011
Publication title -
journal of digestive diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.684
H-Index - 51
eISSN - 1751-2980
pISSN - 1751-2972
DOI - 10.1111/j.1751-2980.2010.00464.x
Subject(s) - nkg2d , major histocompatibility complex , microbiology and biotechnology , flow cytometry , intestinal mucosa , natural killer cell , pathology , medicine , immunology , biology , immune system , cytotoxic t cell , biochemistry , in vitro
OBJECTIVE: To explore the expression of major histocompatibility complex class I chain‐related gene A (MICA) and its ligand in colonic mucosa and the role of MICA‐natural killer (NK) group 2D (NKG2D) interaction in activating NK cells in ulcerative colitis (UC) patients. METHODS: Intestinal mucosal biopsies were obtained from patients with UC and the controls. The expression of major histocompatibility complex class I‐related gene (MIC) genes was determined by a reverse transcription polymerase chain reaction (RT‐PCR) and the imaging of MICA expressed on colonic mucosa was measured by confocal microscopy resonance scanning. NKG2D and intracellular interferon (IFN)‐γ expressions on NK cells were assayed by flow cytometry. RESULTS: The relative amount of MICA mRNA in the colonic mucosa of UC patients was significantly higher than in that of the controls (3.5408 ± 2.6658 vs 1.0477 ± 0.7201, P = 0.001), as were the major histocompatibility complex class I chain‐related gene B (MICB) (8.9879 ± 3.2893 vs 4.6293 ± 1.2616, P < 0.001) and NKG2D mRNA expression (2.4395 ± 0.8147 vs 1.1624 ± 0.3954, P < 0.001). Confocal microscopy resonance scanning had shown that MICA was localized predominantly on the basolateral membranes of the epithelium. Further flow cytometry confirmed that the percentage of IFN‐γ producer NK cells that expressed NKG2D in peripheral blood lymphocytes was higher in UC patients than in the healthy controls (45.36% ± 12.47% vs 27.45% ± 9.30%, P < 0.001). CONCLUSION: MICA, MICB and NKG2D were upregulated in the colonic mucosa of UC and were associated with activating NK cells with promoted NKG2D and IFN‐γ production.