Faculty Opinions recommendation of A critical control element for interleukin-4 memory expression in T helper lymphocytes.

2005 ◽  
Author(s):  
Santa Jeremy Ono
Keyword(s):  
Interleukin 4 ◽  
Control Element ◽  
T Helper ◽  
T Helper Lymphocytes

scholarly journals A Critical Control Element for Interleukin-4 Memory Expression in T Helper Lymphocytes

2005 ◽  
Vol 280 (31) ◽  
pp. 28177-28185 ◽  
Author(s):  
Lars-Oliver Tykocinski ◽  
Petra Hajkova ◽  
Hyun-Dong Chang ◽  
Torsten Stamm ◽  
Osman SÖzeri ◽  
...  
Keyword(s):  
Interleukin 4 ◽  
Control Element ◽  
T Helper ◽  
T Helper Lymphocytes

scholarly journals Alteration of Interleukin 4 Production Results in the Inhibition of T Helper Type 2 Cell–Dominated Inflammatory Bowel Disease in T Cell Receptor α Chain–Deficient Mice

1999 ◽  
Vol 190 (5) ◽  
pp. 607-616 ◽  
Author(s):  
Hideki Iijima ◽  
Ichiro Takahashi ◽  
Daisuke Kishi ◽  
Jin-Kyung Kim ◽  
Sunao Kawano ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
T Cells ◽  
T Cell ◽  
T Cell Receptor ◽  
Bowel Disease ◽  
Cell Receptor ◽  
Interleukin 4 ◽  
T Helper ◽  
Inflammatory Bowel ◽  
Α Chain

T cell receptor α chain–deficient (TCR-α−/−) mice are known to spontaneously develop inflammatory bowel disease (IBD). The colitis that develops in these mice is associated with increased numbers of T helper cell (Th)2-type CD4+TCR-ββ (CD4+ββ) T cells producing predominantly interleukin (IL)-4. To investigate the role of these Th2-type CD4+ββ T cells, we treated TCR-α−/− mice with anti–IL-4 monoclonal antibody (mAb). Approximately 60% of TCR-α−/− mice, including those treated with mock Ab and those left untreated, spontaneously developed IBD. However, anti–IL-4 mAb–treated mice exhibited no clinical or histological signs of IBD, and their levels of mucosal and systemic Ab responses were lower than those of mock Ab–treated mice. Although TCR-α−/− mice treated with either specific or mock Ab developed CD4+ββ T cells, only those treated with anti–IL-4 mAb showed a decrease in Th2-type cytokine production at the level of mRNA and protein and an increase in interferon γ–specific expression. These findings suggest that IL-4–producing Th2-type CD4+ββ T cells play a major immunopathological role in the induction of IBD in TCR-α−/− mice, a role that anti–IL-4 mAb inhibits by causing Th2-type CD4+ββ T cells to shift to the Th1 type.

scholarly journals APOPTOSIS, MEMORY CELL, AND T-HELPER LYMPHOCYTES BALANCE BETWEEN SEVERE AND MILD BRONCHIAL ASTHMA

2015 ◽  
Vol 21 (4) ◽  
pp. 1-13
Author(s):  
Maha Abd El-wahed ◽  
Ebtesam Ahmed ◽  
Mohamed Mohamed ◽  
Nora Said
Keyword(s):  
Bronchial Asthma ◽  
Memory Cell ◽  
T Helper ◽  
T Helper Lymphocytes ◽  
Mild Bronchial Asthma

scholarly journals Interactions of thymic stromal lymphopoietin with interleukin-4 in adaptive immunity during Aspergillus fumigatus keratitis

2021 ◽  
Vol 14 (10) ◽  
pp. 1473-1483
Author(s):  
Chen Chen ◽  
◽  
Fang Han ◽  
Jia-Yin Wu ◽  
Lin Sun ◽  
...  
Keyword(s):  
Aspergillus Fumigatus ◽  
Adaptive Immunity ◽  
Post Infection ◽  
Thymic Stromal Lymphopoietin ◽  
Interleukin 4 ◽  
Enzyme Linked Immunosorbent Assay ◽  
T Helper ◽  
Cytokine Levels ◽  
Pretreated Group ◽  
Helper Type

AIM: To investigate the potential interactions of thymic stromal lymphopoietin (TSLP) with interleukin-4 (IL-4) in adaptive immunity during fungal keratitis (FK). METHODS: An FK mouse model was induced with Aspergillus fumigatus (AF) hyphal infection. Mice were divided into several groups: untreated, phosphate buffer saline (PBS), infected with AF, and pretreated with a scrambled siRNA, a TSLP-specific siRNA (TSLP siRNA), murine recombinant TSLP (rTSLP), immunoglobulin G (IgG), murine recombinant IFN (rIFN-γ), murine recombinant IL-4 (rIL-4), rIL-13, murine recombinant IL-17A (rIL-17A), and murine recombinant IL-17F (rIL-17F) groups. Quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) or Western blot were performed to determine mRNA and protein levels in the inflamed cornea. Cytokine locations were observed by immunofluoresence staining after AF hyphal infection. RESULTS: Compared to those in the untreated group, TSLP and T helper type 1 (Th1) cytokine levels in the AF group were upregulated at 24h post infection (hpi), and those of T helper type 2 (Th2) and T helper type 17 (Th17) cytokines were increased at 5d post infection (dpi). Th2 cytokine levels were decreased in the TSLP siRNA-pretreated group and increased in the rTSLP-pretreated group compared with the AF group. The TSLP level was increased in the rIL-4-pretreated group, but there were no significant changes among the other groups. Immunofluorescence staining showed cytokine locations after AF hyphal infection. CONCLUSION: TSLP induces a Th2 immune response and promots Th2 T cell differentiation in vivo. IL-4 promotes TSLP secretion. Therefore, TSLP with IL-4 regulates adaptive immunity in FK.

Altered Expressions of CXCR4 and CD26 On T-Helper Lymphocytes in Hereditary Hemorrhagic Telangiectasia

2021 ◽  
Author(s):  
Alexandre GUILHEM ◽  
Pierre Portalès ◽  
Sophie Dupuis-Girod ◽  
Sophie Rivière ◽  
Thierry Vincent
Keyword(s):  
Hereditary Hemorrhagic Telangiectasia ◽  
Severe Infection ◽  
Intravenous Iron ◽  
Surface Expression ◽  
T Helper ◽  
Membrane Expression ◽  
Susceptibility To Infection ◽  
T Helper Lymphocytes ◽  
Infectious Risk ◽  
Healthy Control

Abstract Background: Hereditary hemorrhagic telangiectasia (HHT) is a rare genetic disease characterized by a deregulated neo-angiogenesis. Besides a mainly vascular phenotype (telangiectasia, arteriovenous malformations), patients exhibit a specific infectious risk and a deficit of T and natural killer (NK) lymphocytes. As the CXCR4/CXCL12 chemotactic axis is dysregulated in HHT endothelial cells, we hypothesized that a similar phenomenon could occur on lymphocytes.Results: Eighteen HHT patients with history of severe infection (HSI) were matched in age and sex with 18 HHT without HSI and 18 healthy control subjects (HC). We assessed the cell count and the surface expression of CXCR4 and CD26 (CXCL12 inactivating peptidase) of circulating helper and cytotoxic T lymphocytes (including naive, memory and activated subsets) and NK cells.The overall HHT group of 36 patients exhibited a reduction of circulating T-helper lymphocytes compared to HC (median: 517 vs 1026 cells/mm3, p<0.0001), correlated with age (r=-0.46, p=0.005), requirement of intravenous iron or blood transfusions (median: 291 vs 627 cells/mm3, p=0.03) and CXCR4 surface expression (r=0.353, p=0.0345). CXCR4 and CD26 membrane expression were both decreased on HHT T-helper lymphocytes (median MFI ratio: 4.49 vs 5.74 for CXCR4 and 3.21 vs 4.33 for CD26, p=0.03 and 0.0018 respectively) with an unchanged CXCR4/CD26 ratio. The HHT group with HSI had a higher CXCR4/CD26 ratio on the naive T-helper lymphocytes (median: 2.34 vs 1.32, p=0.0002), also observed on the T and T-helper populations.Conclusions: Our findings support a dysregulation of the CXCL12/CXCR4 chemotaxis of T-helper lymphocytes in HHT patients, potentially linked to their T-helper lymphopenia and susceptibility to infection.

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