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Cited by 51Systemic Lupus Erythematosus ResearchT-cell and B-cell ImmunologySystemic Sclerosis and Related Diseases

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Gene profiling involved in immature CD4+ T lymphocyte responsible for systemic lupus erythematosus

Deng, Y.J., Huang, Z.X., Zhou, C.J., Wang, J.W., You, Y., Song, Z.Q., Xiang, M.M., Zhong, B.Y., Hao, F.·2006·Molecular Immunology
DOI 10.1016/j.molimm.2005.07.039
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Abstract

We attempted to characterize the genes expression of CD4+ T lymphocytes for the pathogenesis of systemic lupus erythematosus (SLE). Genomewide gene expression profiles of CD4+ T cells, which were isolated from the disease severe activity (T4-1s) and nonactivity (T4-2s) with an SLE patient by using long serial analysis of gene expression (LongSAGE). We picked out 289 genes matching to Unigene cluster with different expression more than four copies between T4-1s and T4-2s libraries and analyzed their roles from the collectedly published articles of PubMed by genes functional clustering. The genes functions were related to a diverse cellular process including: (1) most of these genes were associated with CD4+ T cells functions, particularly related to cellular developments; (2) Ras pathway genes as RANBP10, GMIP, RASGRP2 and ARL5 might be responsible for the abnormal development of CD4+ T cells of SLE; (3) HIG2, TCF7, KHSRP, WWP1, SMAD3, TLK2, AES, CCNI and PIM2 belong to Wnt/beta-catenin way, they could play roles in modulating proliferation and differentiation of T lymphocytes; (4) uncertain viral infections may initiate autoimmunity because high levels expression genes were detected in T4-1s such as TRIM22, IER2, ABCE1, DUT, G1P2, G1P3, HNRPUL1, EVER2, IFNAR1, TNFSF14, TMP21 and PVRL2; and (5) apoptosis relating genes as EIF3S8, SH3BGRL3, GPX4, TOSO, PFDN5, BIN1, XIAPAF1, TEGT and CUGBP2 may contribute to over uploading of selfantigens in SLE cells. Abnormalities findings of multiple genes expression involving with a variety of CD4+ T cells process might be meaningful to understanding the pathogenesis of SLE, and immature CD4+ T cells may be responsible for SLE.

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Cited by

Sorted by citations

Metadata

Authors
Deng, Y. J., Huang, Z. X., Zhou, C. J., Wang, J. W., You, Y., Song, Z. Q., Xiang, M. M., Zhong, B. Y., & Hao, F.
Affiliations
  • Army Medical University (CN)
  • Southern Medical University (CN)
Corresponding author
Hao, F.
ORCID
Venue
Molecular Immunology
Publisher
Elsevier BV
Published
2006-03
Volume
43
Issue
9
Pages
1497-1507
ISSN
0161-5890 (ISSN-L)
DOI
10.1016/j.molimm.2005.07.039
OpenAlex
W1965949659
Cited by
51
References
3
Citations by year
2026: 1 · 2025: 1 · 2024: 4 · 2023: 7 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 4 · 2017: 2 · 2016: 2 · 2015: 2 · 2013: 3 · 2012: 4
FWCI
0.81
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Molecular Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China
Topics
  • Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Rheumatology › Systemic Sclerosis and Related Diseases
Keywords
systemic lupus erythematosus, CD4+ T cells, gene expression profiling, T cell development, Ras signaling, Wnt/β-catenin signaling, viral infection, autoimmunity, apoptosis, autoantigen presentation, disease activity
MeSH terms
Adult, Base Sequence, Cell Differentiation, DNA, Female, Multigene Family, Humans, Immunosuppressive Agents, Lupus Erythematosus, Systemic, CD4-Positive T-Lymphocytes, Gene Library, Gene Expression Profiling

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