Identification of highly expressed genes in peripheral blood T cells from patients with atopic dermatitis.
BACKGROUND
Analysis of genes that are differentially expressed in patients with atopic dermatitis (AD) and normal individuals will provide important information on the underlying molecular pathogenetic mechanisms of AD.


METHODS
Transcript of freshly isolated peripheral blood T cells from 59 individuals were analyzed with a fluorescent differential display (FDD) method. Ninety-two differentially expressed genes were identified in this manner. Additionally, real-time quantitative RT-PCR was employed to investigate the expression of the FDD-selected genes and also genes related to T cell function.


RESULTS
A number of genes, including CC chemokine receptor 4, T cell-specific tyrosine kinase (Emt/Itk), integrin beta1, integrin alpha6, IQGAP1 and MAR/SAR DNA-binding protein (SATB1), were shown to be more highly expressed in patients with moderate and/or severe AD than in controls or patients with mild AD. Because the products of these upregulated genes influence chemotaxis, adhesion, migration and Th2 polarization, it is suggested that in more severe AD, circulating T cells may function differently in this regard. Several other genes, the role of which in T cell function is currently unknown, were also found to be differentially expressed in AD. These included the heat shock protein 40 and vasopressin-activated calcium-mobilizing receptor 1.


CONCLUSIONS
The upregulated genes identified in this work may serve as useful markers for moderate to severe AD as opposed to normal or mild AD and also as markers indicating progression to more severe AD. Further functional characterization will provide a better understanding of the pathophysiology of circulating T cells in AD.
Matsumoto
Yoshiko
Y
Genox Research, Inc., Teikyo University Biotech Center, Kawasaki, Kanagawa, Japan.
Oshida
Tadahilo
T
Obayashi
Izumi
I
Imai
Yukiho
Y
Matsui
Keiko
K
Yoshida
Ning Lu
NL
Nagata
Naoko
N
Ogawa
Kaoru
K
Obayashi
Masaya
M
Kashiwabara
Tomoko
T
Gunji
Shigemichi
S
Nagasu
Takeshi
T
Sugita
Yuji
Y
Tanaka
Toshio
T
Tsujimoto
Gozoh
G
Katsunuma
Toshio
T
Akasawa
Akira
A
Saito
Hirohisa
H
D000293:Adolescent; D000328:Adult; D001249:Asthma / Q000235:genetics / Q000276:immunology; D002352:Carrier Proteins / Q000235:genetics; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000235:genetics* / Q000276:immunology*; D015870:Gene Expression; D020869:Gene Expression Profiling; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D036961:Matrix Attachment Region Binding Proteins / Q000235:genetics; D008875:Middle Aged; D011505:Protein-Tyrosine Kinases / Q000235:genetics; D054398:Receptors, CCR4; D019707:Receptors, Chemokine / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism*; D020703:ras GTPase-Activating Proteins
C515354:CCR4 protein, human; D002352:Carrier Proteins; C101203:IQ motif containing GTPase activating protein 1; D036961:Matrix Attachment Region Binding Proteins; D054398:Receptors, CCR4; D019707:Receptors, Chemokine; C076189:SATB1 protein, human; D020703:ras GTPase-Activating Proteins; D011505:Protein-Tyrosine Kinases; C080813:emt protein-tyrosine kinase