Subsets of natural killer cells in chronic myeloid leukemia and their relation with some inflammatory cytokines DOI Creative Commons
Yusur Falah Faraj, Khalid Salih, Abderrahim Khélif

et al.

Iraqi Journal of Hematology, Journal Year: 2023, Volume and Issue: 12(2), P. 184 - 189

Published: Jan. 1, 2023

BACKGROUND: As in other malignancies, different subsets of natural killer (NK) cells play a crucial role the recognition and lysing malignant chronic myeloid leukemia (CML). OBJECTIVES: This study aims to identify two NK, cytotoxic (cluster differentiation [CD] 16+ bright ) cytokine-producing NK (CD56+ newly diagnosed CML patients. MATERIALS AND METHODS: is conducted on 20 Iraqi patients (12 males 8 females) with CML, phase, at age range 17–55 years. Along patients, healthy subjects (with matched gender) were enrolled act as control group. To their peripheral blood samples, expression CD45, CD3, CD56, CD16 markers was evaluated by flow cytometry technique. Furthermore, serum level interferon gamma (IFN-γ) interleukin (IL)-18 determined enzyme-linked immunosorbent assay RESULTS: The diagnosis disease (35.6 ± 12.2 years) male: female ratio 1.5:1. IL-18 (30.3 6.5 pg/mL) significantly ( P < 0.0001) higher than those group (18.3 7.8 pg/mL), while levels IFN-γ are = 0.006) dropped down (89.1 7.2 pg/mL from that (109.4 30.3 pg/mL). percentage lower There significant elevation (CD16+ subset, decrease subset when compared CONCLUSION: Although there an first diagnosis, these not able recognize attack cells, which may be due low activating receptors needs more investigation. present results found (CD56+bright) although IL-18, indicates main stimulator so activation pathway this further

Language: Английский

Helper ILCs in the human hematopoietic system DOI
Xiaoyu Su, Zhaoqun Deng, Yu Lan

et al.

Trends in Immunology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

0
Circulating innate lymphoid cells are dysregulated in patients with prostate cancer DOI Creative Commons

Daniela Claudia Maresca,

Evelina La Civita,

Benedetta Romano

et al.

Cellular & Molecular Biology Letters, Journal Year: 2025, Volume and Issue: 30(1)

Published: April 18, 2025

Language: Английский

Citations

0
PGI2 restricts trained ILC2 responses in allergic inflammation DOI
Weisong Zhou, Jian Zhang, Allison E. Norlander

et al.

The Journal of Immunology, Journal Year: 2025, Volume and Issue: unknown

Published: May 7, 2025

Abstract Pulmonary type 2 innate lymphoid cells (ILC2s) exhibit immune memory, termed “trained immunity,” which enhances their activation following exposure to an independent protease-containing allergen. The role of prostaglandin I2 (PGI2), a cyclooxygenase (COX) pathway metabolite, in modulating these trained ILC2 responses remains unclear. PGI2 acts through its G protein–coupled receptor IP. We hypothesized that IP signaling inhibits training. To test this hypothesis, we used mouse training model challenged wild-type (WT) and knockout (KO) mice with Alternaria alternata extract (Alt) induce After 33-d resting period, subsided homeostatic level. Mice were then intranasally papain evaluate unrelated KO displayed significantly heightened interleukin (IL)-13 expression concomitant increased eosinophilia the lungs post–papain challenge compared WT control mice. Notably, neither nor only, devoid training, exhibited lung responses. augmented inflammation observed both Alt challenges correlated numbers percentages IL-13-producing ILC2s greater mean fluorescence intensity IL-13 Furthermore, RNA sequencing sorted from Alt-papain revealed response pathways mitochondrial respiratory IP-deficient ILC2s. These findings reveal inhibitory responses, emphasizing pivotal contribution allergic inflammation.

Language: Английский

Citations

0
Agree to disagree: The contradiction between IL-18 and IL-37 reveals shared targets in cancer DOI Creative Commons
Dongjie Wang,

Bitian Zhang,

Xiaolin Liu

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 200, P. 107072 - 107072

Published: Jan. 19, 2024

IL-37 is a newly discovered member of the IL-1 cytokine family which plays an important role in regulating inflammation and maintaining physiological homeostasis. showed close relationship with IL-18, another key regulation cancer development. affects function IL-18 either by binding to IL-18Rα, subunit both receptor, or drastically neutralizing protein expression protein, natural inhibitory molecule IL-18. Moreover, as receptor IL-37, IL-1R8 can suppress IL-18Rα expression, functioning surveillance mechanism prevent overactivation signaling pathways. While share same subunit, would turn interfere signal transduction IL-18Rα. It also reported that demonstrated opposing effects variety cancers, such glioblastoma, lung cancer, leukemia, hepatocellular cancer. Although mutual their diametrically opposed cancers has been reported, not taken into consideration when interpreting clinical findings conducting investigations related We aim review recent progress research summarize correlation between based on level underlying mechanisms, provide new insights elucidating conflicting roles bring ideas for translational IL-37.

Language: Английский

Citations

1
IL-18, a therapeutic target for immunotherapy boosting, promotes temozolomide chemoresistance via the PI3K/AKT pathway in glioma DOI Creative Commons

Huangyi Ji,

Yufei Lan,

Pengpeng Xing

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Oct. 21, 2024

Interleukin-18, a member of the interleukin − 1 family cytokines, is upregulated in glioma. However, its effects on glioma remain unclear. This study aimed to explore role and underlying mechanisms interleukin-18 expression Here, we demonstrated that enhanced resistance temozolomide by increasing proliferation inhibiting apoptosis cultured cells. Further vivo studies revealed promoted BALB/c nude mice bearing tumor. Mechanical exploration indicated stimulation could activate PI3K/AKT signaling pathway cells, PI3K inhibition reduce interleukin-18. We found CD274 glioma, revealing potential microenvironment. Furthermore, established tumor xenograft model explored therapeutic efficacy anti-interleukin-18 monoclonal antibody. Targeting prolonged survival attenuated Combined treatment with anti-PD-1 antibody showed better suppressing growth than either alone Collectively, these data present promotes chemoresistance cells via PI3K/Akt activation establishes an immunosuppressive milieu modulating CD274. highlights value

Language: Английский

Citations

1
IL-18, a therapeutic target for immunotherapy boosting, promotes temozolomide chemoresistance via the PI3K/AKT pathway in glioma DOI Creative Commons

Huangyi Ji,

Yufei Lan,

Pengpeng Xing

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: April 17, 2024

Abstract Background: Temozolomide (TMZ) resistance is still the urgent topic in treatments of glioma. Recent studies show inflammation involved tumor chemoresistance.Interleukin-18, a proinflammatory cytokine, highly expressed glioma and related with worse prognosis. However, its effects on remain unclear. Methods Results: In this research, we detected that interleukin-18 enhanced growth inhibited apoptosis cultured cells via CCK8 EdU assay. Further, in vivo revealed promoted mice bearing tumors. Mechanical exploration indicated stimulation could activate PI3K/AKT pathway, PI3K inhibition reduce interleukin-18-induced proliferation cells. We found upregulated CD274 expression cells.Furthermore, established xenograft model explored therapeutic efficacy anti-interleukin-18 monoclonal antibodies. Targeting prolonged survival attenuated mice-bearing tumor. Combined application anti-PD-1 antibodies showed better suppressing than either treatment alone Conclusion: Interleukin-18 promotes temozolomide chemoresistance PI3K/Akt activation establishes an immunosuppressive milieu by modulating CD274. This study highlights value

Language: Английский

Citations

0
Subsets of natural killer cells in chronic myeloid leukemia and their relation with some inflammatory cytokines DOI Creative Commons
Yusur Falah Faraj, Khalid Salih, Abderrahim Khélif

et al.

Iraqi Journal of Hematology, Journal Year: 2023, Volume and Issue: 12(2), P. 184 - 189

Published: Jan. 1, 2023

BACKGROUND: As in other malignancies, different subsets of natural killer (NK) cells play a crucial role the recognition and lysing malignant chronic myeloid leukemia (CML). OBJECTIVES: This study aims to identify two NK, cytotoxic (cluster differentiation [CD] 16+ bright ) cytokine-producing NK (CD56+ newly diagnosed CML patients. MATERIALS AND METHODS: is conducted on 20 Iraqi patients (12 males 8 females) with CML, phase, at age range 17–55 years. Along patients, healthy subjects (with matched gender) were enrolled act as control group. To their peripheral blood samples, expression CD45, CD3, CD56, CD16 markers was evaluated by flow cytometry technique. Furthermore, serum level interferon gamma (IFN-γ) interleukin (IL)-18 determined enzyme-linked immunosorbent assay RESULTS: The diagnosis disease (35.6 ± 12.2 years) male: female ratio 1.5:1. IL-18 (30.3 6.5 pg/mL) significantly ( P < 0.0001) higher than those group (18.3 7.8 pg/mL), while levels IFN-γ are = 0.006) dropped down (89.1 7.2 pg/mL from that (109.4 30.3 pg/mL). percentage lower There significant elevation (CD16+ subset, decrease subset when compared CONCLUSION: Although there an first diagnosis, these not able recognize attack cells, which may be due low activating receptors needs more investigation. present results found (CD56+bright) although IL-18, indicates main stimulator so activation pathway this further

Language: Английский

Citations

0