Ablation of T-Helper 1 Cell Derived Cytokines and of Monocyte-Derived Tumor Necrosis Factor-α in Hereditary Hemorrhagic Telangiectasia: Immunological Consequences and Clinical Considerations

2006 ◽  
Vol 12 (10) ◽  
pp. 1201-1208 ◽  
Author(s):  
F. Resta ◽  
V. Triggiani ◽  
E. Jirillo ◽  
C. Sabba ◽  
L. Amati ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Hereditary Hemorrhagic Telangiectasia ◽  
Tumor Necrosis ◽  
T Helper ◽  
T Helper 1 ◽  
Clinical Considerations ◽  
Necrosis Factor

Attenuation of bleomycin-induced pneumopathy in mice by monoclonal antibody to interleukin-12

2001 ◽  
Vol 280 (6) ◽  
pp. L1128-L1137 ◽  
Author(s):  
Takashige Maeyama ◽  
Kazuyoshi Kuwano ◽  
Masayuki Kawasaki ◽  
Ritsuko Kunitake ◽  
Naoki Hagimoto ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Lung Injury ◽  
Lung Tissue ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
T Helper ◽  
Antibody Treatment ◽  
Factor Α ◽  
Necrosis Factor ◽  
Helper Type

We previously demonstrated essential roles of the Fas-Fas ligand (FasL) pathway in bleomycin-induced pneumopathy in mice. T lymphocytes and natural killer cells express FasL on activation and use it as a cytotoxic effector molecule. Because interleukin (IL)-12 is known to play a critical role in cell-mediated immunity, we investigated whether anti-IL-12 antibody treatment suppresses the development of this model. The anti-IL-12 antibody treatment decreased the number of apoptotic cells and the degree of inflammation and fibrosis in lung tissue. The results of RT-PCR showed that IL-12p40, IL-12 receptor (R) β2, interferon-γ, tumor necrosis factor-α and FasL mRNAs were upregulated after bleomycin instillation. The upregulation of FasL, IL-12Rβ2, and tumor necrosis factor-α mRNA expression in lung tissue was suppressed by anti-IL-12 antibody treatment. The results of enzyme-linked immunosorbent assay showed that the levels of IL-12p40, but not of IL-12p70, were increased in lung tissue after bleomycin instillation. Although the increase in IL-12Rβ2 mRNA levels suggests that the T helper type 1 cell response may participate in lung injury, the increase in IL-12p40 supports T helper type 2 cell predominance in the fibrotic process of this model. The administration of anti-IL-12 antibody could be a novel therapy against lung injury and pulmonary fibrosis.

IL-17A, IL-22, and IL-23 as Markers of Psoriasis Activity

2015 ◽  
Vol 19 (6) ◽  
pp. 555-560 ◽  
Author(s):  
Christina Fotiadou ◽  
Elizabeth Lazaridou ◽  
Eleni Sotiriou ◽  
Spiridon Gerou ◽  
Athanasios Kyrgidis ◽  
...  
Keyword(s):  
Th17 Cells ◽  
Tumor Necrosis ◽  
Serum Levels ◽  
Sensitivity Analyses ◽  
T Helper ◽  
T Helper 1 ◽  
Factor Α ◽  
Necrosis Factor ◽  
Active Disease

Introduction: T-helper 1 (Th1), Th17 cells, and their related cytokines are implicated in psoriasis pathogenesis although the contribution of each group of cytokines in psoriasis activity has not been fully clarified. Objectives: To investigate whether Th17-related cytokines are associated with psoriasis activity. Methods: The serum levels of interleukin (IL)-1β, 6, 8, 17Α, 22, 23, and tumor necrosis factor-α (TNFα) were measured with flow cytometry in 35 patients with plaque psoriasis (21 with stable and 14 with active disease) and in 20 healthy controls. Results: Interleukin-6, 8, 17A, 22, 23, and TNFα were significantly elevated in psoriasis patients compared with controls. In the sensitivity analyses, patients with active disease showed significantly increased levels of IL-17A, IL-23, and IL-22 as compared to the group of patients with stable psoriasis. Conclusions: Our study highlights a possible crucial role of IL-17A, IL-22, and IL-23 in the activity of psoriasis and the early stages of the disease.

scholarly journals Evaluation of Th9 lymphocytes in peripheral blood of rheumatoid arthritis patients and correlation with anti-tumor necrosis factor therapy: results from an in vitro pivotal study

Reumatismo ◽  
2016 ◽  
Vol 68 (2) ◽  
pp. 83 ◽  
Author(s):  
R. Talotta ◽  
A. Berzi ◽  
F. Atzeni ◽  
D. Dell'Acqua ◽  
P. Sarzi Puttini ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Peripheral Blood ◽  
Tumor Necrosis ◽  
Mononuclear Cells ◽  
Healthy Controls ◽  
T Helper ◽  
Th9 Cells ◽  
Necrosis Factor

The aim of this study was to determine the prevalence of T helper 9 (Th9) lymphocytes in rheumatoid arthritis (RA) patients and to identify a possible association between the percentage of Th9 and the discontinuation of a biological treatment with an anti-tumor necrosis factor (TNF) (infliximab). We collected peripheral blood mononuclear cells (PBMCs) from 55 consecutive RA outpatients and 10 healthy controls. Among RA patients, 15 were not receiving any immunosuppressive drug, 20 were successfully treated with infliximab and 20 discontinued infliximab because of adverse events or inefficacy and were treated with other biological agents. PBMCs were cultured with/without infliximab 50 mg/L for 18 h, and the percentage of Th9 cells was assessed by means of flow cytometry. Th9 lymphocytes were identified as interferon gamma, interleukin (IL)4-, IL17-, IL9-secreting cluster of differentiation 4 (CD4)+ T cells. Cytometric analysis revealed no significant decrease in the percentage of Th9 cells after infliximab exposure in any of the groups, although it was lower in healthy controls than RA patients either before and after the infliximab stimulation assay. Th9 cells are IL-9-secreting T helper lymphocytes whose role in RA is still poorly known. IL-9 levels are increased in RA patients, in whom this cytokine plays a crucial role. Th9 cells are the major producers of IL-9, and their prevalence is higher in RA patients than in healthy subjects; however our experiment <em>in vitro</em> does not demonstrate an association between Th9 lymphocytes and the response to infliximab. Further studies are required to evaluate the real involvement of Th9 population in the immunogenicity of anti-TNF agents.

Altered Immune Responses in Patients with Chuvash Polycythemia

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4582-4582
Author(s):  
Xiaomei Niu ◽  
Galina Y Miasnikova ◽  
Adelina I Sergueeva ◽  
Daniel J Okhotin ◽  
Mehdi Nouraie ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Peripheral Blood ◽  
T Helper Cells ◽  
Tumor Necrosis ◽  
T Helper ◽  
Blood Concentrations ◽  
Altered Expression ◽  
Suspension Array ◽  
Helper Cells ◽  
Necrosis Factor

Abstract Chuvash polycythemia results from a homozygous 598 C&gt;T mutation in exon 3 of the von Hippel-Lindau (VHL) gene. This disrupts the normoxia pathway for degrading hypoxia inducible factor (HIF)-1a and HIF-2a causing altered expression of HIF-1 and HIF-2 regulated genes. As hypoxia induces expression of pro-inflammatory cytokines, we hypothesized that there might be an elevation of Th1 cytokines in the setting of Chuvash polycythemia. Concentrations of Th1 (interleukins-2 and 12, interferon-g, GM-CSF, tumor necrosis factor-a) and Th2 cytokines (interleukins-4, 5, 10 and 13) were measured in plasma using the Bio-Plex multiplex suspension array system. Concentrations of all of these cytokines were elevated in patients with Chuvash polycythemia 598C&gt;T homozygous compared to the control wild type participants. In parallel, peripheral blood concentrations of CD3 positive T-helper cells and CD-4 positive T-helper cells were lower in patients with Chuvash polycythemia compared to controls. The ratios of interferon-g and tumor necrosis factor-a to interleukin-10 did not differ by genotype. Thus, although the upregulated hypoxic response in Chuvash polycythemia is associated with increased plasma products of the Th1 and Th2 pathways, the peripheral blood concentrations of T-helper cells are reduced, perhaps as part of a feed-back mechanism, and the balance between the two pathways may be preserved. Such countervailing responses to unregulated hypoxia sensing may explain why patients with Chuvash polycythemia do not present clinically with immunologic disorders.

scholarly journals Disruption of Tumor Necrosis Factor Receptor-Associated Factor 5 Exacerbates Murine Experimental Colitis via Regulating T Helper Cell-Mediated Inflammation

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Jian Shang ◽  
Lixia Li ◽  
Xiaobing Wang ◽  
Huaqin Pan ◽  
Shi Liu ◽  
...  
Keyword(s):  
T Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Mrna Levels ◽  
Tnf Receptor ◽  
T Helper ◽  
Associated Factor ◽  
Cell Immunity ◽  
Th Cell ◽  
Necrosis Factor

Tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) is a key mediator of TNF receptor superfamily members and is important in both T helper (Th) cell immunity and the regulation of multiple signaling pathways. To clarify TRAF5’s influence on inflammatory bowel diseases (IBDs), we investigated TRAF5 deficiency’s effect on dextran sulfate sodium- (DSS-) induced colitis. Colitis was induced in TRAF5 knockout (KO) mice and their wild-type (WT) littermates by administering 3% DSS orally for 7 days. The mice were then sacrificed, and their colons were removed. Our data suggested that KO mice were more susceptible to DSS-induced colitis. TRAF5 deficiency significantly enhanced IFN-γ, IL-4, and IL-17a mRNA and protein levels in the colons of DSS-fed mice, and the mRNA expression of T-bet and GATA-3 was also markedly elevated. However, ROR-αand ROR-γt mRNA levels did not differ between DSS-induced KO and WT mice. Flow cytometry showed increased frequencies of Th2 and IFN-γ/IL-17a-coproducing CD4+T cells in the colons of DSS-induced KO mice. Additionally, TRAF5 deficiency significantly enhanced the activation of NF-κB in CD4+T cells after DSS administration. These results indicated that TRAF5 deficiency significantly aggravated DSS-induced colitis, most likely by regulating Th cell-mediated inflammation.

scholarly journals Tumor Necrosis Factor Receptor–Associated Factor (Traf)2 Represses the T Helper Cell Type 2 Response through Interaction with Nfat-Interacting Protein (Nip45)

2001 ◽  
Vol 194 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Rebecca Lieberson ◽  
Kerri A. Mowen ◽  
Kathryn D. McBride ◽  
Veronica Leautaud ◽  
Xiankui Zhang ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
T Helper Cell ◽  
Cell Type ◽  
T Helper ◽  
Interacting Protein ◽  
Helper Cell Type ◽  
Necrosis Factor

Recently we have identified a novel protein NIP45 (nuclear factor of activated T cells [NFAT]-interacting protein) which substantially augments interleukin (IL)-4 gene transcription. The provision of NIP45 together with NFAT and the T helper cell type 2 (Th2)-specific transcription factor c-Maf to cells normally refractory to IL-4 production, such as B cells or Th1 clones, results in substantial IL-4 secretion to levels that approximate those produced by primary Th2 cells. In studies designed to further our understanding of NIP45 activity, we have uncovered a novel facet of IL-4 gene regulation. We present evidence that members of the tumor necrosis factor receptor–associated factor (TRAF) family of proteins, generally known to function as adapter proteins that transduce signals from the tumor necrosis factor receptor superfamily, contribute to the repression of IL-4 gene transcription and that this effect is mediated through their interaction with NIP45.

scholarly journals Kadar IL-17 dan TNF alfa pada pasien Dermatitis Fase Akut dan Fase Kronik

2020 ◽  
Vol 2 (1) ◽  
pp. 57-61
Author(s):  
Mia Yasmina Andarini ◽  
Oki Suwarsa ◽  
Hendra Gunawan
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
T Helper ◽  
Consecutive Sampling ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Sitokin sel T helper (Th)2 lebih berperan dalam patogenesis dermatitis atopik (DA) fase akut, sedangkan sitokin sel Th1 lebih berperan pada fase kronik.Patogenesis DA dipengaruhi pula oleh interleukin (IL)-17 yang dihasilkan sel Th17, sel Th1, sel Th2, dan sel B. Ekspresi IL-17 meningkat pada lesi kulit DA fase akut dibandingkan fase kronik. Tumor necrosis factor-α (TNF-α) merupakan sitokin proinflamasi yang dapat dihasilkan sel Th1 dan Th17. Tujuan penelitian ini adalah untuk mengetahui kadar IL-17 dan TNF-α dalam serum pasien DA fase akut dibandingkan fase kronik.     Penelitian dilaksanakan selama periode Januari-Februari 2013 di Poliklinik Alergi dan Imunologi Departemen Ilmu Kesehatan Kulit dan Kelamin RSUP Dr. Hasan Sadikin Bandung. Penelitian ini merupakan penelitian klinis secara potong lintang, berdasarkan studi analitik observasional. Subjek penelitian berjumlah 31 pasien, terdiri dari 15 pasien DA fase akut dan 16 fase kronik yang didapatkan melalui consecutive sampling. Terhadap subjek penelitian dilakukan anamnesis, pemeriksaan fisik, dan diagnosis ditegakkan sesuai dengan kriteria Hanifin dan Rajka, kemudian dilakukan pengambilan serum untuk pemeriksaan IL-17 dan TNF-α.     Hasil penelitian memperlihatkan kadar IL-17 dan TNF-α dalam serum pasien DA fase akut secara berurutan adalah 16,50 pg/ml dan 7,70 pg/ml, sedangkan pada fase kronik secara berurutan adalah 14,84 pg/ml dan 7,69 pg/ml. Berdasarkan uji beda kadar IL-17 dan TNF-α pada fase akut dan fase kronik didapatkan nilai p > 0,05.       Simpulan penelitian ini adalah kadar IL-17 dan TNF-α dalam serum pasien DA fase akut tidak berbeda dibandingkan fase kronik. 

Anti‐tumor necrosis factor treatment increases both the Th17 and Th22 T helper subsets in spondyloarthritis

Apmis ◽  
2019 ◽  
Vol 127 (12) ◽  
pp. 789-796
Author(s):  
Thomas Andersen ◽  
René Drage Østgård ◽  
Maithri Prasad Aspari ◽  
Tue Wenzel Kragstrup ◽  
Henning Glerup ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
T Helper ◽  
T Helper Subsets ◽  
Necrosis Factor ◽  
Tumor Necrosis Factor Treatment
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