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Increased T cell immunoglobulin mucin‐3 and its ligand in acquired aplastic anemia
Author(s) -
Zhang Jian,
Gu Yan,
Xu Conggao,
Qu Xun
Publication year - 2008
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2008.01095.x
Subject(s) - peripheral blood mononuclear cell , pathogenesis , immunology , aplastic anemia , antibody , mucin , immune system , biology , t cell , medicine , bone marrow , in vitro , biochemistry
T cell immunoglobulin mucin‐3 (TIM‐3) is recently described as a T helper 1 (Th)1‐specific molecule, participating in the regulation of immune responses and the pathogenesis of Th1‐driven diseases. The TIM‐3 pathway, however, has not been investigated in acquired aplastic anemia (AA). In this study, we examined the expression of TIM‐3 and interferon‐γ (IFN‐γ) at both transcript and protein levels in 29 acquired AA patients and in 31 controls. Increased mRNA expression of TIM‐3 and IFN‐γ were observed in both peripheral blood mononuclear cells (PBMCs) and bone marrow mononuclear cells from AA patients and controls using quantitative real‐time reverse transcriptase‐polymerase chain reaction. An increase of TIM‐3 expression on PBMCs was detected increased in AA patients by flow cytometry. An overproduction of IFN‐γ was determined in the sera from AA patients by enzyme‐linked immunoassay. In addition, the expression of TIM‐3 ligand, galectin‐9, increased in PBMCs from AA patients. The results are the first human data to demonstrate the increase of TIM‐3 expression in AA. The enhanced TIM‐3 engagement by its ligand in AA patients may play an important role in the pathogenesis of this disease.