scholarly journals Pain Relief Dependent on IL-17–CD4+ T Cell–β-Endorphin Axis in Rat Model of Brachial Plexus Root Avulsion After Electroacupuncture Therapy

2021 ◽  
Vol 14 ◽  
Author(s):  
Zihang Xu ◽  
Yangzhuangzhuang Zhu ◽  
Jun Shen ◽  
Lin Su ◽  
Yifei Hou ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
T Lymphocytes ◽  
Brachial Plexus ◽  
Signaling Pathway ◽  
T Lymphocyte ◽  
Analgesic Effect ◽  
Critical Role ◽  
Root Avulsion ◽  
Immunological Mechanism ◽  
Complementary And Alternative Therapy

Background and purposeNeuropathic pain is the typical symptom of brachial plexus root avulsion (BPRA), and no effective therapy is currently available. Electroacupuncture (EA), as a complementary and alternative therapy, plays a critical role in the management of pain-associated diseases. In the present study, we aimed to reveal the peripheral immunological mechanism of EA in relieving the pain of BPRA through the IL-17–CD4+ T lymphocyte–β-endorphin axis.MethodsAfter receiving repeated EA treatment, the pain of BPRA in rats along with the expressions of a range of neurotransmitters, the contents of inflammatory cytokines, and the population of lymphocytes associated were investigated. CD4+ T lymphocytes were either isolated or depleted with anti-CD4 monoclonal antibody. The titers of IL-17A, interferon-γ (IFN-γ), and β-endorphin were examined. The markers of T lymphocytes, myeloid-derived suppressor cells (MDSCs), dendritic cells (DCs), macrophages, and natural killer (NK) cells were assessed. The activation of the nuclear transcription factor κB (NF-κB) signaling pathway was tested.ResultsThe pain of BPRA was significantly relieved, and the amount of CD4+ T lymphocytes was increased after EA treatment. The release of β-endorphin was up-regulated with the up-regulation of IL-17A in CD4+ T lymphocytes. The titer of IL-17A was enhanced, leading to an activated NF-κB signaling pathway. The release of β-endorphin and the analgesic effect were almost completely abolished when CD4+ T lymphocytes were depleted.ConclusionWe, for the first time, showed that the neuropathic pain caused by BPRA was effectively relieved by EA treatment via IL-17–CD4+ T lymphocyte–β-endorphin mediated peripheral analgesic effect, providing scientific support for EA clinical application.

scholarly journals Immune Checkpoint Receptors Tim-3 and PD-1 Regulate Monocyte and T Lymphocyte Function in Septic Patients

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Qi Xia ◽  
Li Wei ◽  
Yuntao Zhang ◽  
Jifang Sheng ◽  
Wei Wu ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Immune Response ◽  
T Lymphocytes ◽  
Signaling Pathway ◽  
T Lymphocyte ◽  
Receptor Blockade ◽  
Lymphocyte Function ◽  
Significant Elevation ◽  
Programmed Cell Death 1 ◽  
Checkpoint Receptors

We aim to investigate the effects of Tim-3 and programmed cell death-1 (PD-1) on the monocytes and T lymphocytes in septic patients. Expression of Tim-3 and PD-1 on the CD3, CD4, and CD8 lymphocytes and monocytes was determined using flow cytometry. CBA technique was utilized to determine the expression of cytokines in the lymphocyte supernatant in addition to the IL-10 and TNF-αpositivity in monocytes in the presence of Tim-3 and/or PD-1 receptor blockade. Compared with the normal control, significant elevation was observed in the expression of PD-1 on CD3 (P=0.004), CD4, and CD8 monocytes. Blockade of the Tim-3 signaling pathway contributed to the significant elevation of IL-10 and TNF-αin the supernatant of T lymphocytes in the septic patients, while the PD-1 signaling pathway blockade only triggered the obvious elevation of TNF-αin the T lymphocytes. Blockade of Tim-3 and PD-1 induced the positivity of IL-10- and TNF-α-expressing cells in the peripheral monocytes. Significant changes were noticed in the Tim-3 and PD-1 in the T lymphocytes and monocytes. Blockade of Tim-3 and PD-1 contributed to the function of lymphocytes and monocytes. In the septic process, Tim-3 and PD-1 played crucial roles in the immune response of T lymphocytes and monocytes.

Trehalose protects motorneuron after brachial plexus root avulsion by activating autophagy and inhibiting apoptosis mediated by the AMPK signaling pathway

Gene ◽  
2021 ◽  
Vol 768 ◽  
pp. 145307
Author(s):  
Bohan Li ◽  
Ping Li ◽  
Ricong Weng ◽  
Zichao Wu ◽  
Bengang Qin ◽  
...  
Keyword(s):  
Brachial Plexus ◽  
Signaling Pathway ◽  
Root Avulsion ◽  
Ampk Signaling

scholarly journals Identification of Ny-Eso-1 Epitopes Presented by Human Histocompatibility Antigen (Hla)-Drb4*0101–0103 and Recognized by Cd4+T Lymphocytes of Patients with Ny-Eso-1–Expressing Melanoma

2000 ◽  
Vol 191 (4) ◽  
pp. 625-630 ◽  
Author(s):  
Elke Jäger ◽  
Dirk Jäger ◽  
Julia Karbach ◽  
Yao-Tseng Chen ◽  
Gerd Ritter ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Immune Responses ◽  
Cancer Patients ◽  
T Lymphocyte ◽  
Tumor Antigens ◽  
Cytotoxic T Lymphocyte ◽  
Critical Role ◽  
Class Ii ◽  
Hla Class Ii ◽  
Hla Class Ii Alleles

NY-ESO-1 is a member of the cancer-testis family of tumor antigens that elicits strong humoral and cellular immune responses in patients with NY-ESO-1–expressing cancers. Since CD4+ T lymphocytes play a critical role in generating antigen-specific cytotoxic T lymphocyte and antibody responses, we searched for NY-ESO-1 epitopes presented by histocompatibility leukocyte antigen (HLA) class II molecules. Autologous monocyte-derived dendritic cells of cancer patients were incubated with recombinant NY-ESO-1 protein and used in enzyme-linked immunospot (ELISPOT) assays to detect NY-ESO-1–specific CD4+ T lymphocyte responses. To identify possible epitopes presented by distinct HLA class II alleles, overlapping 18-mer peptides derived from NY-ESO-1 were synthetized and tested for recognition by CD4+ T lymphocytes in autologous settings. We identified three NY-ESO-1–derived peptides presented by DRB4*0101–0103 and recognized by CD4+ T lymphocytes of two melanoma patients sharing these HLA class II alleles. Specificity of recognition was confirmed by proliferation assays. The characterization of HLA class II–restricted epitopes will be useful for the assessment of spontaneous and vaccine-induced immune responses of cancer patients against defined tumor antigens. Further, the therapeutic efficacy of active immunization using antigenic HLA class I–restricted peptides may be improved by adding HLA class II–presented epitopes.

TGF-β1 in SP-A preparations influence immune suppressive properties of SP-A on human CD4+ T lymphocytes

2006 ◽  
Vol 291 (4) ◽  
pp. L747-L756 ◽  
Author(s):  
Steffen Kunzmann ◽  
Jo Rae Wright ◽  
Wolfram Steinhilber ◽  
Boris W. Kramer ◽  
Kurt Blaser ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
T Lymphocyte ◽  
Lymphocyte Proliferation ◽  
Chinese Hamster Ovary Cells ◽  
Smad Signaling ◽  
T Lymphocyte Proliferation ◽  
Smad Signaling Pathway ◽  
Tgf Β1

Surfactant protein A (SP-A) and transforming growth factor-β1 (TGF-β1) have been shown to modulate the functions of different immune cells and specifically to inhibit T lymphocyte proliferation. The aim of the present study was to elucidate whether the Smad signaling pathway, which is activated by TGF-β1, also plays a role in SP-A-mediated inhibition of CD4+ T lymphocyte activation. Recombinant human SP-A1 expressed in Chinese hamster ovary cells [rSP-A1m (mammalian)], but not recombinant Baculovirus-derived rSP-A1hyp (hydroxyproline-deficient), suppressed T lymphocyte proliferation and IL-2 mRNA expression. To test whether SP-A induced Smad signaling, a Smad3/4-specific reporter gene was transfected in primary human CD4+ T lymphocytes. Only rSP-A1m, but not rSP-A1hyp, induced Smad-specific reporter genes, Smad2 phosphorylation, and Smad7 mRNA expression. The effect of rSP-A1m was mediated through the TGF-βRII and could be antagonized by anti-TGF-β1 neutralizing antibodies and sTGF-βRII. Western blot and ELISA analysis revealed that rSP-A1m, but not rSP-A1hyp, contained TGF-β1. TGF-β1 was responsible for the differences in inhibition of CD4+ T lymphocyte proliferation and activation of the Smad signaling pathway between rSP-A1m and rSP-A1hyp. After acidification, native SP-A, obtained from patients with alveolar proteinosis, also induced Smad signaling in human CD4+ T lymphocytes leading to an increased inhibition of T lymphocyte proliferation, thus indicating the presence of inactive, latent TGF-β1 in native SP-A samples. Association between SP-A and latent TGF-β1 provides a possible novel mechanism to regulate TGF-β1-mediated inflammation and fibrosis reactions in the lung but also leads to possible misinterpretation of immune-modulator functions of SP-A. Monitoring of SP-A preparations for possible TGF-β1 is essential.

scholarly journals A critical role for the autophagy gene Atg5 in T cell survival and proliferation

2006 ◽  
Vol 204 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Heather H. Pua ◽  
Ivan Dzhagalov ◽  
Mariana Chuck ◽  
Noboru Mizushima ◽  
You-Wen He
Keyword(s):  
T Lymphocytes ◽  
Cell Survival ◽  
T Lymphocyte ◽  
Critical Role ◽  
Degradation Process ◽  
Microbial Pathogens ◽  
Lymphocyte Development ◽  
Cell Clearance ◽  
Primary Mouse ◽  
T Cell Survival

Macroautophagy (hereafter referred to as autophagy) is a well-conserved intracellular degradation process. Recent studies examining cells lacking the autophagy genes Atg5 and Atg7 have demonstrated that autophagy plays essential roles in cell survival during starvation, in innate cell clearance of microbial pathogens, and in neural cell maintenance. However, the role of autophagy in T lymphocyte development and survival is not known. Here, we demonstrate that autophagosomes form in primary mouse T lymphocytes. By generating Atg5−/− chimeric mice, we found that Atg5-deficient T lymphocytes underwent full maturation. However, the numbers of total thymocytes and peripheral T and B lymphocytes were reduced in Atg5 chimeras. In the periphery, Atg5−/− CD8+ T lymphocytes displayed dramatically increased cell death. Furthermore, Atg5−/− CD4+ and CD8+ T cells failed to undergo efficient proliferation after TCR stimulation. These results demonstrate a critical role for Atg5 in multiple aspects of lymphocyte development and function and suggest that autophagy may be essential for both T lymphocyte survival and proliferation.

scholarly journals Microarray Analysis of Potential Biomarkers for brachial plexus avulsion caused neuropathic pain

2021 ◽  
Author(s):  
Le Wang ◽  
Jie Lao
Keyword(s):  
Neuropathic Pain ◽  
Brachial Plexus ◽  
Signaling Pathway ◽  
Quantitative Polymerase Chain Reaction ◽  
Control Group ◽  
Rt Pcr ◽  
Pain Group ◽  
Brachial Plexus Avulsion ◽  
Neurotrophin Signaling ◽  
Potential Biomarkers

Nerve injury-induced neuropathic pain remains a challenging clinical problem due to a lack of satisfactory treatment. Pain after BPA (Brachial Plexus Avulsion) is resistant to most traditional pain relief treatments due to the lack of understanding of the cellular or molecular mechanism of pain development. The present study aimed to investigate the expression of mRNA in the brachial plexus avulsion neuropathic pain model and analyze biological functions. Sprague-Dawley rats were treated with complete brachial plexus avulsion. An animal behavior test was carried out to distinguish the pain group from the control group. In this study, a microarray mRNA assay and reverse transcriptase quantitative polymerase chain reaction (RT-PCR) was conducted. The whole blood was collected from two groups for Microarray mRNA analysis. The predicted mRNA targets were studied by gene ontology analysis and pathway analysis. The PIK3CB, HRAS, and JUN genes were verified by RT-PCR. In total, differentially expressed genes(DEGs) were identified between individuals with or without neuropathic pain (case and control), and A biological processes were enriched. We identified 3 targeted mRNAs, including PIK3CB, HRAS, and JUN, which may be potential biomarkers for BPA-caused NP. The results showed that PIK3CB, HRAS, and JUN gene expression was increased in the control group but decreased in the neuropathic pain group. The PIK3CB gene was part of the Neurotrophin signaling pathway. The function of the HRAS gene was synergetic in the aspect of axon guidance and the Neurotrophin signaling pathway. The JUN gene participates in axon regeneration. These results suggest that PIK3CB, HRAS, and JUN genes might become potential biomarkers for the prediction of and new targets for the prevention and treatment of neuropathic pain after BPA. These findings indicate that mRNA expression changes in the blood may play an important role in the development of NP after BPA, which is of theoretical and clinical importance for future research and clinical-treatment strategies.

DREZotomy in the management of post brachial plexus root avulsion neuropathic pain: fMRI correlates for pain relief

2021 ◽  
pp. 1-10
Author(s):  
Satyakam Baruah ◽  
Dhananjaya Ishwar Bhat ◽  
Bhagavatula Indira Devi ◽  
Alok Mohan Uppar ◽  
Komal Bharti ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Pain Relief ◽  
Brachial Plexus ◽  
Root Avulsion

Induction of insulitis by adoptive transfer with L3T4+Lyt2- T-lymphocytes in T-lymphocyte-depleted NOD mice

Diabetes ◽  
1988 ◽  
Vol 37 (2) ◽  
pp. 204-208 ◽  
Author(s):  
T. Hanafusa ◽  
S. Sugihara ◽  
H. Fujino-Kurihara ◽  
J. Miyagawa ◽  
A. Miyazaki ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
T Lymphocyte ◽  
Adoptive Transfer ◽  
Nod Mice

PROTEIN 24 HIV DAN LIMFOSIT T-CD4+ DI INFEKSI HIV TAHAP I

2016 ◽  
Vol 21 (3) ◽  
pp. 273
Author(s):  
I Made Sila Darmana ◽  
Endang Retnowati ◽  
Erwin Astha Triyono
Keyword(s):  
T Lymphocytes ◽  
Hiv Infection ◽  
T Lymphocyte ◽  
Negative Correlation ◽  
Stage I ◽  
Cross Sectional ◽  
Protein Levels ◽  
P24 Protein ◽  
Persistent Generalized Lymphadenopathy ◽  
Spearman Test

Measuring HIV p24 protein is a test which is more practical than determination of CD4+ T-lymphocyte counts and viral load, as it does not require a very sophisticated instrument and requires a lower cost. Independent predictive value of p24 to the decline of CD4+ T-lymphocytes, clinical progression and survival in HIV-infected patients have been reported. In this study, HIV-infected patients were found to have HIV p24 protein levels inversely proportional to CD4+ T-lymphocyte counts by using Spearman test (R2=0.225; p=0.0331). Studies on the correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIV infection have not yet been reported. The aim of this study was to prove the correlation between HIV p24 protein levels and CD4+ T-lymphocytes in stage I HIV infection. Research issue was whether a correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIVinfection existed ? The hypothesis was that a correlation between HIV p24 protein levels and CD4+ T-lymphocyte counts in stage I HIV infection existed. The study design was cross sectional observational. Subjects consisted of 30 stage I HIV-infected patients treated at the Infectious Disease Intermediate Care Unit, Dr. Soetomo Hospital and VCT Clinic of the Dr. Ramelan Naval Hospital, Surabaya from May to July 2014. Stage I HIV infection is an asymptomatic HIV infection or with persistent generalized lymphadenopathy and the patient is able to perform normal activities. Levels of p24 were measured by ELISA method and CD4+ T-lymphocyte counts using flowcytometry(BD FACSCaliburTM). The results were statistically analyzed using Pearson’s correlation test. HIV p24 protein levels in stage I of HIV infection ranged from 1.8 to 10.8 pg/mL, mean of 5.14 pg/mL and a standard deviation of 2.08 pg/mL. CD4+ T-lymphocyte counts decreased with a range of 49-559 cells /uL for absolute values and 4.42–26.02% for percentage values Correlations between blood p24 levels and CD4+ T-lymphocyte counts either absolute (r=–0.392, p=0.032) or percentage (r=–0.363, p=0.049) were found. In stage I HIV-infected patients, a negative correlation was found between p24 levels and CD4+ T-lymphocyte counts, in both CD4+T-lymphocyte counts as absolute and as well as percentage values. This negative correlation showed that the p24 HIV levels were inversely proportional to the CD4+ T-lymphocyte counts. HIV p24 protein levels have a possibility to be used predicting CD4+ T-lymphocyte counts

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