Journal articles: 'Tcell'

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Schalck, Aislyn, Donastas Sakellariou-Thompson, Marie-Andrée Forget, Emi Sei, Tara Hughes, Shanshan Bai, Min Hu, et al. "Abstract 2847: Simultaneous TCR and transcriptomic sequencing of single Tcells defines biological subtypes in pancreatic cancer for adoptive Tcell therapy." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2847. http://dx.doi.org/10.1158/1538-7445.am2022-2847.

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Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly fatal tumor-type with very few effective treatment strategies. Attempts to improve outcomes using immune checkpoint blockade therapy have also failed, likely because the overall Tcell infiltration in this tumor-type is low. Despite this, the presence of CD3+CD8+ tumor-infiltrating lymphocytes (TIL) in PDAC is associated with improved survival outcomes, suggesting that other immune-based strategies could be more successful. Here, we examine ex vivo tumor-infiltrating Tcell expansion for adoptive Tcell therapy (ACT) as a potential strategy for treating PDAC. The focus of this study is to understand the transcriptional states of Tcells in the pancreas and PDACs and how they change with ex vivo expansion and re-infusion into patients as treatment strategy. We have performed both single cell transcriptome and TCR sequencing (scRNA-TCRseq) on 54,579 Tcells from 8 human PDAC samples and the ex vivo grown TIL from a subset of 6 patients and found 13 purported substates. Through TCR tracking of the Tcell clonotypes, we find that the expansion protocol is able to expand Tcells found in many different Tcell states in the primary tumor. Furthermore, we compared our thirteen tumor-infiltrating substates with 41,935 Tcells from two other independent single cell studies across 71 samples, and confirmed our substates to be present across all datasets. Citation Format: Aislyn Schalck, Donastas Sakellariou-Thompson, Marie-Andrée Forget, Emi Sei, Tara Hughes, Shanshan Bai, Min Hu, Tapsi Kumar, Mark Hurd, Matthew Katz, Chine-Wei Tzeng, Shubham Pant, Milind Javle, Anirban Maitra, Cara Haymaker, Michael Kim, Nicholas Navin, Chantale Bernatchez. Simultaneous TCR and transcriptomic sequencing of single Tcells defines biological subtypes in pancreatic cancer for adoptive Tcell therapy [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2847.

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Florek, Mareike, Emanuela I. Sega, Antonia MS Mueller, Dennis B. Leveson-Gower, Judith A. Shizuru, and Robert S. Negrin. "A Novel Model of Pre-Emptive ECP Treatment Shows Significant Reduction of Gvhd-Related Mortality In Mice,." Blood 118, no. 21 (November 18, 2011): 4025. http://dx.doi.org/10.1182/blood.v118.21.4025.4025.

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Abstract Abstract 4025 Graft versus host disease (Gvhd) remains the major cause of morbidity and mortality after bone marrow transplantation (BMT). To prevent Gvhd the graft has to be rendered tolerant to avoid alloreactivity towards the host. One promising approach to induce tolerance in the graft is to administer apoptotic cells to the host. Apoptosis can be induced by extracorporeal photopheresis (ECP), a therapy based on exposure of cells to photoactivable 8-methoxypsoralen (8MPO) and UVA irradiation. The effect of ECP treatment is at least in part, due to alteration of dendritic cell (DC) maturation, leading to reduced antigen presentation and Tcell activation. Moreover, ECP treatment increases the number of regulatory Tcells (Treg), further reducing Tcell activation. In contrast to clinical practice where ECP is only applied to established Gvhd, we have developed a pre-emptive murine model with the aim of inhibiting the initiation phase of acute Gvhd and improving survival. Here we describe our model and characterization of the mechanisms of action. Apoptotic host-type splenocytes were infused into MHC matched or mismatched recipients 5 and 2 days prior to lethal irradiation and BMT. Apoptotic cells were generated by incubation with 8-MPO and UVA light (UVAR light set, Therakos). Mice were followed for Gvhd score and survival. ECP-treated mice survived longer both across major (median survival 51 versus 26 days, p<0.0001) and minor (median survival 56.5 versus 9 days, p<0.002) histocompatibility barriers. Importantly, even though ECP treatment promoted tolerance against the host it did not impact the graft versus tumor effect in a B-cell lymphoma model. To address the mechanisms of this beneficial outcome we investigated Tcell proliferation in vivo (i), ex vivo (ii) and in vitro (iii). (i) Luciferase-expressing Tcon were used to quantify Tcell proliferation in vivo by bioluminescent imaging. ECP-treated mice showed reduced CD4+Tcell proliferation during the initiation phase of Gvhd (day+4) compared to mice receiving Tcon only. (ii) Re-isolation of CFSE labeled Tcon on day+4 after BMT showed a reduction in CD4+Tcell proliferation. (iii) FACS-sorted DC incubated with apoptotic cells for 2 days in vitro showed a diminished capability to induce Tcell proliferation. To evaluate the impact of ECP treatment on the expression of homing (P-Selectin, α4β7) and activation (CD44, CD69) markers on donor Tcells we performed re-isolation experiments on day+3 and day+7. At day +3 ECP-treated groups showed a reduced expression of these markers in comparison to control groups. These studies demonstrate slower trafficking to Gvhd target organs. Furthermore, at day+7 ECP-treated groups showed increased FoxP3-expressing host Tregs in comparison to control groups whereas donor Treg were similar in both groups. Ongoing experiments will utilize a mouse model in which it is possible to selectively deplete either donor or host Tregs to examine the role of these two subpopulations of Treg in improving Gvhd outcome. In summary, ECP treatment prior to transplantation led to (i) a significant survival benefit with no impact on graft versus tumor effect; (ii) reduced CD4+ Tcell proliferation; (iii) delayed expression of homing and activation markers during the initiation phase of Gvhd and (iv) an increase in host Treg. Overall our work suggests that pre-emptive ECP of host cells prior to BMT may be a clinically relevant strategy to prevent acute Gvhd. Disclosures: No relevant conflicts of interest to declare.

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Kennedy, Steven C., Alison J. Johnson, Alessandro Sette, John Chan, William R. Jacobs, and Steven A. Porcelli. "M. smegmatis vaccination reveals the mycobacterial ribosome as a potential CD4+ Tcell enhancing vaccine target." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 65.10. http://dx.doi.org/10.4049/jimmunol.196.supp.65.10.

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Abstract Mycobacterium tuberculosis(Mtb) is an airborne pathogen that infects one third of the world’s population. To date no vaccine has had major success in reducing the enormous global burden of disease from this infection. Critical to the control of Mtb is the ability of a vaccine to induce a strong CD4+ Tcell response. The currently available vaccine, M. bovis BCG, is of limited efficacy, potentially due to its retention of immune evasion mechanisms that actively inhibit the host presentation of critical antigens to CD4+ Tcells. Examining antigens that are hidden during a BCG immunization may lead to identification of novel vaccine targets. Our lab has previously identified an M. smegmatis based vaccine, IKEPLUS, which elicits a strong CD4+ Tcell response leading to significantly enhanced protection to Mtb over BCG vaccination. M. smegmatis is a non-pathogenic mycobacterium that has not retained the ability to disrupt antigen presentation to the host immune system. Examination of the CD4+ Tcell response to IKEPLUS and BCG has identified the mycobacterial ribosome as a major immunogenic target in the M. smegmatis based IKEPLUS, but not in BCG. This dichotomy in the immune response led us to further characterize the ribosome and evaluate its protein constituents as potential vaccine targets. The ribosome is composed of 57 individual proteins; of these 57 proteins, we have identified 20 as immunogenic, and identified minimal CD4+ Tcell epitopes for 10 of the 20 identified proteins. These findings have led us to begin development of a mycobacterial ribosome based vaccine to enhance the currently existing BCG regimen. This approach will allow us to complement what we believe is a critical flaw of BCG while retaining the widely used BCG vaccination regimen.

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Davidson, Tom, Willy Hugo, Anthony Wang, Jiyoon Kim, Gang Li, and Robert Prins. "IMMU-30. UPREGULATED T CELL AND INTERFERON-Γ-RELATED GENE EXPRESSION IS ASSOCIATED WITH INCREASED SURVIVAL IN RECURRENT PEDIATRIC HIGH-GRADE GLIOMA." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii365—iii366. http://dx.doi.org/10.1093/neuonc/noaa222.384.

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Abstract Recurrent pediatric high-grade glioma (pHGG) is the leading cause of cancer-related mortality in children. Immunotherapy is a successful treatment approach for a growing number of cancers and is being investigated as a treatment strategy for pHGG. Immunotherapy has shown the most benefit in tumors with increased infiltrating T cells at baseline. Our recently published results revealed that neoadjuvant checkpoint inhibition in recurrent adult glioblastoma was associated with upregulation of a T cell and interferon-γ-related gene expression signature (Tcell-IFNγGES) and was correlated with a significantly extended overall survival (OS). In this study, we examined the immune landscape in recurrent pHGG and the association of Tcell-IFNγGES in the tumor with survival. We analyzed tumor RNAseq data collected at time of recurrence from a historical cohort of 42 pHGG patients from the Children’s Brain Tumor Tissue Consortium. We found a significant transcriptional enrichment of Tcell-IFNγGES in 54% of the tumors. The survival of patients with high Tcell-IFNγGES was observed to be significantly higher than patients with low Tcell-IFNγGES, (log-rank p=0.05). The 3-year OS for patients with low versus high Tcell-IFNγGE was 28.5% (95%, CI:13.7%-59.5%) compared to 50.2% (95%, CI:33.1%-76.1%). When patients were stratified by age, gender and race, low Tcell-IFNγGES was found to be a poor OS prognostic factor (hazard ratio=2.4 (1.14–5.14), p=0.02). This indicates a strong relationship of decreased Tcell-IFNγGES and increased risk of death. Future investigations are necessary to validate these findings, and to explore the value of Tcell-IFNγGES as a predictive biomarker for response to immunotherapy in pHGG.

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Darwiche, Sophie, Yanting Wang, John Brumfield, Sladjana Stratimirovic, Kathryn Vreeland, Ana Botero, Sylvia Martinez, et al. "Heme oxygenase-1/CO protect against post-traumatic suppression of adaptive immune responses (IRC8P.475)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 190.3. http://dx.doi.org/10.4049/jimmunol.192.supp.190.3.

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Abstract Traumatic injury induces a systemic dysregulated immuno-inflammatory response that contributes to mortality. This response includes an upregulation of pro-inflammatory cytokines by innate cells and an independent suppression of adaptive immunity characterized by reduced Th1 responses. Heme oxygenase-1 (HO-1) and its byproduct, carbon monoxide (CO), are protective against injury-induced inflammation and end-organ damage, but their beneficial role in the dysregulation of adaptive responses following trauma is unknown. To investigate this, B6 mice received multiple-trauma or no manipulation, and were given either vehicle or a HO-1 inducer (Cobalt protoporphyrin, CoPP; 5mg/kg) prior to injury. Another cohort received either room air or CO (250ppm) for 4 hours directly post-injury. At 48hr post-trauma, Tcell functions were assessed by ex-vivo mitogen-induced Tcell proliferation and Th1 cytokine release (IL-2 and IFN-γ). As expected after injury, a near 50% reduction in Tcell proliferation was seen in vehicle- or air-treated trauma mice, compared to uninjured controls (p=0.007). A parallel reduction in Tcell IL-2 and IFN-γ release was observed. In clear contrast, CoPP or CO treatment prevented trauma-induced reductions in Tcell proliferation and cytokine release (fold difference 0.90±0.10 and 1.21±0.16 to uninjured controls, respectively). Overall, HO-1 represents an endogenous protective pathway that can be exploited following trauma to preserve normal immune functions & survival.

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Khichade, Monika D., Dr Sameer Shafi, Priyanka S. Nilangekar, Aishwarya S. Gandhle, Mohini A . Gurav, and Vishal B. Phulsundar. "Immunotherapy in Cancer: Biology Therapy." Journal of Biomedical and Pharmaceutical Research 11, no. 5 (November 14, 2022): 62–73. http://dx.doi.org/10.32553/jbpr.v11i5.937.

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Abstract: The relationship between immune system and cancer has progressively increased in the last few years. Recent advancement in treating cancer immunotherapy includes monoclonal antibodies, adaptive cancer therapy; monoclonal antibodies have came into force. General therapies include surgery, radiation and chemotherapy etc... Beyond that the immunotherapy in treating cancer helps our immune system to fight against tumor forming cell, which acts as an example of precision medicine .It mainly targets tumor in filtering lymphocytes, CAR Tcells, TCR Tcell etc…. Personalized combination therapy stands as promising stratergy for upcoming cancer treatment, personalized medicines includes patient derived tumor cell DNA oncolytic viruses dendritic cells etc.

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Heald, Peter, Jo-Ann Latkowski, Lynn D. Wilson, and Lawrence A. Mark. "Successful therapy of cutaneous Tcell lymphoma." Expert Review of Dermatology 3, no. 1 (February 2008): 99–110. http://dx.doi.org/10.1586/17469872.3.1.99.

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Nguyen, Vy Tuong, Nhung Thi Tuyet Do, Thuong Thi Thuong Nguyen, and Trung Lap Huynh. "Effect of the reduced-graphene oxide on the structure and thermal properties of compoiste PMMA/micro-cellulose fibers from petioles of Vietnamese nipa palm tree." Science and Technology Development Journal 19, no. 4 (December 31, 2016): 202–11. http://dx.doi.org/10.32508/stdj.v19i4.682.

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This study separated and treated successfully micro-cellulose fibers from petioles of Vietnamese nipa palm tree (tCell) by simple mechanical and chemical methods. The combination of the treated micro-cellulose fibers and reduced-graphene oxide by hydrazine hydrate (tCell-RGO) increases the thermal stability and the glass transition temperature of polymethylmathacrylat (PMMA) in synthesis composite by in situ emulsion method. The study improves the environmental friendliness of PMMA and overcome the disadvantages of low thermal decomposition of cellulose in preparation of polymer composites, especially kinds of heat-stable polymers as PMMA.

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Santamaria, P. "Transgenic animal expressing diabetogenic Tcell receptor transgenes." Biofutur 1997, no. 167 (May 1997): 48. http://dx.doi.org/10.1016/s0294-3506(99)80369-x.

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Faulkner, Matthew F., and Jeannine M. Durdik. "Age-associated defects in Tcell metabolism (46.10)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 46.10. http://dx.doi.org/10.4049/jimmunol.182.supp.46.10.

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Abstract Aging at the cellular and molecular level causes a decline in immune function. We are characterizing the responses of naïve T-cells to activation. Activated T-cells of aged mice initiate proliferation as well as their young counterparts, but have increased apoptotic rates. However, the mechanisms behind this post- activation death are not completely understood. We will show alterations in metabolic activities in T-cells of aged mice through differences in the expression of glucose transporter (Glut 1), glucose uptake and lactate production. Additionally, we will correlate these findings with autophagocytic vesicle formation by analyzing microtubule-associated protein -1 light chain 3 (LC3) as well as comparing relative amounts of actively respiring mitochondria using Mitotracker Red CM-H2XRos, a membrane potential dependant dye, and total mitochondrial mass by staining with the mitochondrial-selective fluorescence label Mitotracker Green. Levels of reactive oxygen species will be then quantified by staining with ROS specific dye DCF-DA and correlated to the ratio of mitochondrial mass to membrane potential.

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Nishioka, Kensuke, and Yasuyuki Ota. "Impact of Spectral Irradiance Distribution and Temperature on Concentrator Photovoltaic System." Advanced Materials Research 893 (February 2014): 773–76. http://dx.doi.org/10.4028/www.scientific.net/amr.893.773.

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The output characteristics of concentrator photovoltaic (CPV) system were analyzed in the data period of a year from November 2010 to October 2011. Characteristics of CPV are more sensitive to environmental factors as compared to flat-plate PV system. Especially, solar spectrum distribution has considerable influence on the output of CPV because CPV uses multi-junction solar cells. In this study, we analyzed the influence of environmental factors using average photon energy (APE) and temperature of solar cell (Tcell). Most frequent condition during operation was APE = 1.87 ± 0.005 eV and Tcell = 65 ± 2.5 °C. Performance ratio at the most frequent condition was 83.9%. These results indicated the importance of the understanding of the behavior of the outdoor performance and the accurate data of environmental conditions where the PV systems were installed.

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Solé-Marcé, C., T. Moline, and J. Cortés-Hernández. "POS0463 REENGINEERING CHIMERIC ANTIGEN RECEPTOR T CELLS FOR TARGETED THERAPY OF LUPUS NEPHRITIS." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 485–86. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4281.

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BackgroundAlthough the pathogenesis of lupus nephritis (NL) is not completely clear, it is known that the production of anti-dsDNA or anti-C1q antibodies is related to its activity [1]. Despite treatment, approximately 30-40% of patients continue to present a significant number of renal outbreaks [2]. Therefore, there is a growing interest in the development of more specific drugs. As B cells play a central role in the pathogenesis of SLE, the therapy CAR-T cells has been studied reporting good results for the prevention and also for as treatment in murine lupus models [3,4]. Recently, a new selective immunotherapy for autoimmune diseases has been demonstrated by modifying the T cells with a chimeric autoantigen receptor (CAAR) [5]. This novel therapeutic approach could be beneficial in NL with the aim of depleting only anti-DNA producing B cells. In this way, the benefits of anti-CD20 biologics would be obtained, but it would be much more specific, personalized and, surely, effective since only the self-reactive B cells would be destroyed.ObjectivesTo study CAAR-Tcell anti-dsDNA and anti-C1q therapy in NL through in vitro experiments (primary cells and kidney organoids).MethodsSynthesis of 6 CAAR anti-dDNA that will be transfected in the primary T cells extracted from patients with NL and healthy controls (N = 10 per group). Through in vitro experiments their ability to lyse the B cells that produce anti-dsDNA or anti-C1q will be evaluated. The two CAAR-Tcell models that is most effective will be evaluated using kidney organoid models obtained from human samples.ResultsWe engineered six human T cells models to express a chimeric autoantibody receptor (CAAR), consisting lupus nephritis autoantigen. As antigens for anti-DNA produced B cells, we designed Heparanase1/2, Histone1 and alpha actinin 1/2 CAAR-Tcells. For anti-C1q produced B cells, we used C1q protein fused to CD19-CD3 signaling domains. The CAAR-Tcells models that exhibited specify cytotoxicity in vitro againts B cells producing anti-dDNA were Heparanase2 and alpha actinin1 CAAR-Tcells (selectivity of 75% vs 45%). C1q CAAR-T cells also presented specificy cytotoxicity for anti-C1q B cells (selectivity of 80%). In vivo imaging assay reveals that C1q or Heparanase2 CAAR-Tcells depleted completly B cells at 48 hours (ratio 1:10, Bcells:CAAR T-cells). We developed 3D in vitro organoid culture using human kidney organoid and B cells from lupus nephritis patients. We evaluated Heparanase2 and C1q CAAR-Tcells using them and we demostrated that C1q CAAR-Tcells could resolved better local kidney inflammation (reduction of IL6, TNF and INF cytokines levels).ConclusionTaken together, these results show that C1q CAAR-Tcells could be an effective and selective immune therapy for treatment of lupus nephritis. Currently, we are evaluated this therapy using NZWB/F1 murine models.References[1]Rekvig OP, Thiyagarajan D, Pedersen HL, Horvei KD, Seredkina N. Future Perspectives on Pathogenesis of Lupus Nephritis: Facts, Problems, and Potential Causal Therapy Modalities. Am J Pathol. 2016;186:2772-2782[2]Liu Z, Davidson A. Taming lupus-a new understanding of pathogenesis is leading to clinical advances. Nat Med 2012;18:871–82.[3]Kansal R et al. Sustained B cell depletion by CD19-targeted CAR T cells is a highly effective treatment for murine lupus. Sci Transl Med. 2019; 11:eaav1648.[4]Jin X et al. Therapeutic efficacy of anti-CD19 CAR-T cells in a mouse model of systemic lupus erythematosus. Cell Mol Immunol. 2021;18:1896-1903.[5]Christoph T et al. Reengineering chimeric antigen receptor T cells for targeted therapy of autoimmune disease. Science. 2016; 353:179-84.AcknowledgementsI have acknowledgement Instituto de Salud Carlos III for their kind financial support (grant PI18/01917)Disclosure of InterestsNone declared.

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NAKAHARA, Yoshiaki, and Tomoya OGAWA. "Recent progress in complex glycans synthesis; Plan tcell wall oligogalacuturonic acids." Journal of the agricultural chemical society of Japan 62, no. 8 (1988): 1259–63. http://dx.doi.org/10.1271/nogeikagaku1924.62.1259.

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Correa, Luis O., Rich Lee, Alexander Dils, Aditi I. Vijendra, and Shannon A. Carty. "Sel1L, an Endoplasmic Reticulum Associated Degradation Adaptor, Regulates CD8+ Tcell Fate." Blood 140, Supplement 1 (November 15, 2022): 5508–9. http://dx.doi.org/10.1182/blood-2022-170207.

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De Cock, D., P. Durez, V. Badot, R. Westhovens, and P. Verschueren. "POS0694 WHAT TREATMENT GIVES THE BEST CLINICAL RESPONSE AFTER CESSATION OF JAKi THERAPY IN PATIENTS WITH RA? DATA OF THE TARDIS-RA REGISTRY, A NATIONWIDE BELGIAN BIOLOGIC REGISTRY." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 626.2–627. http://dx.doi.org/10.1136/annrheumdis-2022-eular.2779.

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BackgroundJAKi represent a new important class in Rheumatoid Arthritis (RA) treatment options. It is unknown which specific bDMARD or mode of action should be selected after stopping a JAKi.ObjectivesTo study if clinical response differs between advanced therapies that are initiated after stopping a JAKi.MethodsPatients were included from the electronic platform “Tool for Administrative Reimbursement Drug Information Sharing” (TARDIS). Data from all Belgian RA patients on biologic and targeted therapy are collected here for drug reimbursement. Patients were selected for this analysis if they had stopped JAKi therapy and initiated a subsequent therapy. Patients were grouped by TNFi, T/B cell therapy, IL6i or JAKi therapy. The DAS28 response and proportion of patients in remission at the first follow-up (between 3 and 6 months) were compared between groups. Remission was defined as DAS28<2.6. Analyses were repeated in patients who were prescribed the stopped JAKi as first-line or as subsequent line therapy. Data were compared via χ2, Anova and t-tests.ResultsIn total, 1238 patients who had stopped JAKi therapy were included. TNFi, T/B cell therapy, IL6i or JAKi therapy was initiated in 36% (441/1238), 19% (233/1238), 18% (227/1238) and 27% (337/1238) respectively. Most baseline demographic and clinical characteristics differed between groups (Table 1).Table 1.TNFiB/T cellIL6iJAKip-valueNumber441 (36%)233 (19%)227 (18%)337 (27%)Age (years)55 ± 1457 ± 1355 ± 1459 ± 12<0.001Gender (women)323 (73%)177 (76%)186 (82%)257 (76%)0.100Weight (kg)74 ± 1579 ± 1775 ± 1575 ± 150.111Disease duration (years)9 ± 810 ± 911 ± 911 ± 90.002HAQ (0-3)1.6 ± 0.71.8 ± 0.61.5 ± 0.71.5 ± 0.80.353PGA (0-100)65 ± 2068 ± 2167 ± 2157 ± 24<0.001CRP (mg/l)10 ± 1614 ± 2016 ± 2811 ± 170.003ESR (mm/h)22 ± 2124 ± 1927 ± 2125 ± 220.117TJC288 ± 68 ± 69 ± 67 ± 60.001SJC285 ± 46 ± 56 ± 45 ± 50.006DAS284.7 ± 1.14.8 ± 1.14.9 ± 1.24.4 ± 1.3<0.0012nd line of therapy after initial JAKi therapy211 (48%)56 (24%)52 (23%)112 (33%)<0.001Numbers given are mean ± SD or number, proportion. TNFi = tumour necrosis factor inhibitor, ts= targeted synthetic, HAQ= health assessment questionnaire, PGA= Patient Global assessment; CRP= C-reactive protein; ESR= erythrocyte sedimentation rate; TJC= tender joint count; SJC= Swollen joint Count; DAS28 = disease activity score based on the 28jointsThe clinical response could be studied in 577 patients. Patients on rituximab were excluded as these were retreated on flare, following Belgian reimbursement criteria. TNFi, Tcell therapy, IL6i or JAKi therapy was initiated in 37% (211/577), 13% (76/577), 18% (102/577) and 33% (188/577) of these patients respectively. DAS28 decreased on average with 1.7 ± 1.5, 1.6 ± 1.4, 2.4 ± 1.6* and 1.3 ± 1.6 for patients on TNFi, T cell therapy, IL6i or JAKi therapy respectively (*p<0.001). Remission was reached in 42%, 41%, 56%* and 39% for patients on TNFi, T cell therapy, IL6i or JAKi therapy respectively (*p=0.045).Before switching, JAKi therapy was the first advanced therapy in 35% (204/577). In this “naïve” subgroup, DAS28 decreased on average with 1.9 ± 1.5, 1.9 ± 1.3, 2.4 ± 1.8 and 1.0 ± 1.7* for patients on TNFi, Tcell therapy, IL6i or JAKi therapy respectively (*p=0.001). Remission was reached in 44%, 48%, 58% and 35% for patients on TNFi, Tcell therapy, IL6i or JAKi therapy respectively (p=0.279).In the “experienced” subgroup, who started JAKi therapy as subsequent line therapy in 65% (373/577), DAS28 decreased on average with 1.5 ± 1.6, 1.5 ± 1.4, 2.3 ± 1.6* and 1.4 ± 1.6 for patients on TNFi, Tcell therapy, IL6i or JAKi therapy respectively (*p<0.001). Remission was reached in 40%, 38%, 55% and 41% for patients on TNFi, Tcell therapy, IL6i or JAKi therapy respectively (p=0.118).ConclusionOur results show clearly that IL6 inhibitors have a better clinical response after JAKi cessation compared to other mode of actions, including other JAKi. However, considerable baseline differences existed, that could influence our results.Disclosure of InterestsNone declared

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Tsukamoto, Yuka, Yoshioka Katsunobu, Yoko Omura, Isseki Maeda, Manabu Hirai, Hirofumi Teshima, Yoshio Konishi, Takeshi Inoue, and Toshihiko Sato. "Subcutaneous Panniculitislike Tcell Lymphoma: Successful Initial Treatment with Prednisolone and Cyclosporin A." Internal Medicine 45, no. 1 (2006): 21–24. http://dx.doi.org/10.2169/internalmedicine.45.1433.

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Tzelepis, Fanny, Joshua Gillard, Joanna Jaworska, Tomoyasu Nishimura, Mark Verway, Kymia Hassani-Ardakani, Heinz Remold, Hojattolah Vali, and Divangahi Maziar. "Critical role of Annexin A1 in protection against pulmonary Mycobacterium tuberculosis infection. (P3320)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 134.13. http://dx.doi.org/10.4049/jimmunol.190.supp.134.13.

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Abstract Annexin1 is a 37kDa protein with wide spectrum of biological activity. Although there are data emphasizing on anti-inflammatory role of Annexin1 in inflammatory diseases, little is known about its role in pathogenesis of tuberculosis. Recently, it has been described the involvement of Annexin1 in the formation of apoptotic envelope, generation of “eat me” signal and activation of Tcells. As phagocytosis of apoptotic vesicles from Mycobacterium tuberculosis (Mtb) infected macrophages is one of the main sources of antigens for CD8T cells via cross-presentation, we hypothesized that impaired capacity of Annexin1-/-DC in cross-presentation increases host susceptibility to Mtb infection. We found that Annexin1-/-mice were severely susceptible to Mtb infection. High levels of pulmonary bacterial burden and mortality in Annexin1-/-mice were associated with reduced antigen-specific CD8T cell response in the lungs. This reduced response was not due to an intrinsic role of Annexin1 in macrophage apoptosis or T cell activation as generation of chimeric mice in which only T cells were deficient in Annexin1 did not show impairment in Tcell mediated immunity or protection against Mtb infection. Interestingly, both in vitro and in vivo, Annexin1-/-DC demonstrated a significantly reduced capacity to cross-present antigens to CD8Tcells. Together, these data identify Annexin1 as a central player in protective immunity against Mtb infection, by regulating the power of DC in cross-presentation.

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Ernst, P., M. Worthington, J. Linden, and M. Naganuma. "Oral treatment of mice with adenosine A2A receptor agonist inhibits Tcell mediated colitis." Inflammatory Bowel Diseases 13, supplement (May 2007): 643. http://dx.doi.org/10.1097/00054725-200705001-00001.

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Gold, Doria M., Philippa Hillyer, Nataly Raviv, Melissa A. Heuer, B. Chi, and Ronald L. Rabin. "PS2-71 Differential effects of human interferon-alpha subtypes on CD4 Tcell function." Cytokine 52, no. 1-2 (October 2010): 65. http://dx.doi.org/10.1016/j.cyto.2010.07.276.

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Бордаков, М. М. "ВИЗНАЧЕННЯ КОЕФІЦІЄНТІВ ТЕПЛОВІДДАЧІ UC ТА UV ДЛЯ МОДЕЛЮВАННЯ ФЕС В ПРОГРАМІ PVSYST." Vidnovluvana energetika, no. 2(65) (June 28, 2021): 47–52. http://dx.doi.org/10.36296/1819-8058.2021.2(65).47-52.

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У наш час розповсюдженим програмним продуктом для розрахунку планової роботи сонячних станцій є PVsyst. Цей програмний продукт використовує для розрахунків такі погодні дані: рівень сонячної радіації; температура навколишнього середовища; середня швидкість вітру. Погодні дані програма отримує з баз даних метеостанцій. Історичні метеодані накопичуються в базах протягом багатьох років; для виконання розрахунків програма використовує середньозважені дані для одного року (середньозважений рік). Також програма враховує особливості конкретного обладнання, що планується встановити на майбутній фотоелектричній станції (ФЕС). Погодні дані програма обирає відповідно до географічних координат об’єкта. Для отримання даних в конкретній точці програма використовує алгоритми апроксимації даних. Відомо, що в процесі роботи сонячна панель нагрівається. Даний нагрів призводить до того, що потужність панелі падає з ростом температури при сталій сонячній радіації. Рівень зменшення потужності залежно від температури характеризується коефіцієнтом gPmax, що відповідає зменшенню потужності при підвищенні температури на 1 ºС (Температурний коефіцієнт потужності). Наприклад, для панелей із полікристалічного кремнію (Si-poly) він дорівнює 0,4 %/ ºC. Але температурний коефіцієнт зменшення потужності характеризує зменшення потужності ФЕМ від температури робочої поверхні модуля, далі Cell Temperature або Tcell (ºC). Для розрахунку Tcell використовується температура навколишнього середовища (TAmb), швидкість вітру (VWind). Ці величини пов’язуються між собою через сонячну радіацію, що потрапляє на модуль (IPoa, Вт/м2), та коефіцієнти тепловіддачі Uc та Uv [1]. Величина цих коефіцієнтів суттєво впливає на розрахунок температури сонячного модуля. Програма рекомендує обирати стандартні значення, але не завжди такі значення правильно описують процес теплообміну. Тому, ця стаття присвячена визначенню даних параметрів на ФЕС, яка вже працює, і переоцінки планових показників її роботи. Бібл. 8, рис. 2.

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Safari, Anahid, Rasool Safari, and Afshin Borhani-Haghighi. "Immunology of stroke." Galen Medical Journal 5 (May 24, 2016): 10–17. http://dx.doi.org/10.31661/gmj.v5is1.592.

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Stroke, a multifactorial disease, has distinct pathophysiologic mechanisms, among which inflammation plays a pivotal role. Various types of inflammatory cells, substances, and molecules emerge in the ischemic stroke. Neutrophils, Tcell subtypes, macrophages, microglial cells, dendritic cell, mast cells, asrocytes, as influential cell, tumor necrosis factor_α, interleukin-17, interleukin-10, as released substances, and vascular cell adhesion molecule-1 (VCAM-1), leukocyte very late antigen-4 (VLA-4), and glial fibrillary acidic protein (GFAP), as cellular adhesion molecules. Lymphocytes' invasion to the ischemic brain tissue occurs as the result of VLA-4 ̶ VCAM-1 interaction. Regarding Tcell subtypes, CD4+ cells have known detrimental effects in the ischemic area, while natural killer T cells (NKT cells) and γδ T cells have minor importance in the early stage of ischemia. While some studies proved the cerebroprotective impact of T regulatory cells, others refuted this by presenting a prominent harmful role of them. Bcells have important protective function by releasing IL-10. Neutrophils along with microglial cell, appearing as the first inflammatory cell in the ischemic tissue, and also macrophages deteriorate ischemia. Mast cells and dendritic cells are of great value in stroke progression. The resting astrocytes are neuroprotective, whereas the activated ones present detrimental function in the ischemic region by expression of GFAP. Hence, stroke consequences occur as the result of systemic inflammatory response. The more activation of this system, the poorer neurological outcomes would be observed. As expected, anti-inflammatory interventions in the experimental stroke in animals, have revealed successful results as less infarct size and attenuated neurological damages.

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Contreras, N., M. Smithey, and J. Nikolich-Zugich. "THE ROLE OF ANTI-CYTOMEGALOVIRUS CD8 TCELL RESPONSES IN ADIPOSE METABOLIC DYSREGULATION AND DIABETES." Innovation in Aging 1, suppl_1 (June 30, 2017): 1391. http://dx.doi.org/10.1093/geroni/igx004.5121.

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Hameed, Rabia. "Diarylheptanoids: Potent Anticancer Agents." Clinical Cancer Drugs 8, no. 1 (December 30, 2021): 18–26. http://dx.doi.org/10.2174/2212697x08666210930185846.

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Abstract: Diarylheptanoids are widely distributed among species belonging to the family Betulaceae. Being highly polar in nature, they can either be isolated from plants by using sophisticated chromatographic techniques or can be synthesized in the laboratory. They are found to exhibit a wide range of activities, from very simple analgesics to anticancer agents. Recently, they have gained considerable attention due to inhibitory activity against NF-κB activation, NO and TNF-α production, reduction in NO and COX-2 levels in a dose-dependent manner, and suppression of Tcell activation. The current review article highlights the role of diarylheptanoids as potent anticancer agents in a variety of cancers.

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K., Hariharan, Bharathraj S., Riches Immanuel, and Shanmugam Kirubanandan. "Implanting Decellularized Plant Tissue Containing CAR-T Cells at Debulked Tumor Sites." BOHR International Journal of Biocomputing and Nano Technology 1, no. 1 (2021): 42–45. http://dx.doi.org/10.54646/bijbnt.009.

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Surgical treatment of cancer includes the removal of the entire tumor. Sometimes, surgery removes some, but not all, of cancer tumors regarding the safety of the organ. This is called debulking. The debulked site contains some cancer cells. CAR-Tcell therapy is a cancer immunotherapy that uses T cells of patients toﬁght against cancer cells.Tcellscollectedfrompatients’bloodaregeneticallymodiﬁedusingchimericantigenreceptor(CAR)gene. The modiﬁed T cells are grown in a culture medium. Decellularization is the process of sterilizing a preexisting natural organ to the extent that only the extracellular matrix scaffold base remains. The CAR-T cells injected decellularized plant tissues are used as an effective treatment against cancer cells present at debulked tumor sites.

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Wang, Yuan, Tao Li, Jiahua Lv, and Ling Xiao. "Irradiated esophageal squamous cell carcinoma cells induced the increase of Treg by TGF-beta." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e16092-e16092. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e16092.

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e16092 Background: The infiltration of CD4+CD25+Foxp3+ regulatory T cells (Treg) in the tumor microenvironment is one of the main reasons for radiation resistance and tumor recurrence after radiotherapy. It has been established that Treg is more resistant to radiation than other T cells, but the proliferation of immune cells after radiotherapy is affected by other factors, including tumor cells. Treg frequency in the tumor microenvironment after radiotherapy has not been defined. We studied the effect and mechanism of esophageal squamous cell carcinoma on Treg cells after radiation. Methods: After 2Gy irradiation, TE-1 cells were co-cultured with normal peripheral blood lymphocytes for 48 hours. Flow cytometry was used to detect Treg/CD4+T cell frequency. The mRNA expression of TGF-β1/2 in TE-1 was detected by qPCR, and the protein content of TGF-β1/2 in the medium was detected by ELISA. Results: Compared with non-irradiation group, the expression of TGF-β1 and TGF-β2 in TE-1 cells of irradiation group increased, and the protein content of TGF-β1 and TGF-β2 in culture medium increased, the difference was statistically significant(P < 0.001). Flow cytometry showed that CD4+CD25+/CD4+Tcell and CD4+CD25+Foxp3+/CD4+Tcell were increased in the radiotherapy group after co-culture, and the difference was statistically significant(P < 0.001). Conclusions: The expression of TGF-β1 and TGF-β1 in esophageal squamous cell carcinoma cells increased after irradiation, and the frequency of Treg induced by co-culture increased, suggesting that esophageal squamous cell carcinoma cells after radiotherapy can induce the increase of Treg cells, which may be achieved mainly through the mechanism of increasing the secretion of TGF-β1/2.

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Young, Jessica S., Kazuaki Takabe, Mariko Asaoka, and Stephen B. Edge. "Comparing the American Joint Committee on Cancer (AJCC) breast cancer staging eighth versus seventh edition and breast cancer biology in large databases." Journal of Clinical Oncology 37, no. 15_suppl (May 20, 2019): e12077-e12077. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.e12077.

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e12077 Background: The AJCC 8th edition Breast Cancer Staging system includes biomarkers (estrogen receptor, progesterone receptor, Her2), grade and a genomic assay, to better reflect outcomes, compared to the 7th edition. We used databases with anatomic, biomarker and genomic information to determine if the 8th edition reflects biology better than the 7th edition. Methods: 696 breast cancer patients in The Cancer Genome Atlas (TCGA) and Text Information Extraction System (TIES) were staged both with 7th and 8th edition. Results: From the 7th to 8th editions, 66% of stage 2 patients migrated (64% to stage 1, 1.5% to stage 3). 36% of stage 3 patients migrated (22% to stage 1, 13% to stage 2). We analyzed the differences between stage 1 and 2 in both editions, and the overall survival hazard ratio calculated using Cox regression was greater in the 8th edition than the 7th (HR=1.50, HR=1.22 respectively). We performed Gene Set Enrichment Analysis (GSEA) and found that gene sets related to cell cycle and cell proliferation (E2F targets, G2M checkpoint) were significantly enriched in higher stage in 8th edition but not 7th. Mutant Allele Tumor Heterogeneity (MATH) and Homologous Recombination Defects (HRD) were elevated in higher stages in the 8th edition (p=0.022, p<0.001 respectively), but not the 7th. Immune cells (CD8 Tcell, NK cell) as well as CYT (Immune cytolytic activity score), and Tcell exhaustion markers (PD1, PDL1) were all found to be elevated in higher stage in 8th edition, but not 7th. Conclusions: The 8th edition AJCC Breast Cancer Staging system categorizes cancers by aggressive biology better than the 7th edition. We also found that higher stage tumors trigger an enhanced immune response, but are unable to overcome the aggressive cancer biology.

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KASAJIMA, Takeshi, Akihiro MASUDA, Noriko YAMASITA, and Yuriko NAKAGAMI. "An Autopsy Case of Smoldeing Adult Tcell Leukemia/Lymphoma with Intestinal Perforation and Hemophagocytic Histiocytosis." Journal of the Japan Society of the Reticuloendothelial System 27, no. 4 (1987): 403–13. http://dx.doi.org/10.3960/jslrt1961.27.403.

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Tsai, Y. K., and T. H. Lin. "Sequence, organization, transcription and regulation of lactose and galactose operons in Lactobacillus rhamnosus TCELL-1." Journal of Applied Microbiology 100, no. 3 (March 2006): 446–59. http://dx.doi.org/10.1111/j.1365-2672.2005.02790.x.

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Gombert, Jean-Marc, Emmanuelle Trancrède-Bohn, Agathe Hameg, Maria do Carmo Leite-de-Moraes, Alain Vicari, Jean-François Bach, and André Herbelin. "IL-7 reverses NK1+ Tcell-defective IL-4 production in the non-obese diabetic mouse." International Immunology 8, no. 11 (1996): 1751–58. http://dx.doi.org/10.1093/intimm/8.11.1751.

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Wali, Shradha, Jose R. Flores, David Goldblatt, Michael Tuvim, Burton F. Dickey, and Scott E. Evans. "Inducible epithelial resistance protects against acute viral infection and subsequent CD8+Tcell dependent lethal Immunopathology." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 66.3. http://dx.doi.org/10.4049/jimmunol.202.supp.66.3.

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Abstract Viral pneumonia leads to significant morbidity and mortality worldwide, demanding better understanding of the host immune response to infections for development of novel strategies to prevent respiratory infections. Our group has shown that mice treated with combination of Toll-like receptor (TLR) 2/6 and 9 agonists (Pam2-ODN) are protected against wide range of respiratory pathogens, including viruses. Mice challenged intra-pharyngeally with Sendai virus showed peak viral burden on day 5 and peak mortality on day 11, overlapping with increased lung CD8+Tcells. We hypothesized that mortality is associated with immunopathology caused by CD8+T cells. Pam2-ODN aerosolization one day prior to Sendai challenge reduced lung viral burden and reduced lung CD8+T cells on day 11 and enhanced mouse survival. Depletion of CD8+T cells before infection increased baseline virus susceptibility and enhanced viral replication in vivo, congruent with the known antiviral function of CD8+T cells. Pam2-ODN pre-treatment protected mice against death following viral challenge, even in the absence of CD8+T cells, reflecting antiviral responses induced directly from epithelial cells. Notably, depletion of CD8+T cells eight days after viral challenge also significantly enhanced survival of sham pre-treated mice, indicating rescue from CD8+T cell-mediated lethal immunopathology. Our findings definitively prove that CD8+T cells, although anti-viral in nature, promote lethal immunopathology that can be prevented by Pam2-ODN pre-treatment. Importantly, Pam2-ODN pre-treatment benefitted survival regardless of when CD8+T cells were depleted and may provide an opportunity to protect vulnerable populations against respiratory infections.

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Singh, Harshit, Narayan Prasad, Vikas Agarwal, Saurabh Chaturvedi, and Akhilesh Jaiswal. "MO042PGLYCOPROTEIN AND MULTIDRUG RESISTANCE-ASSOCIATED PROTEIN1 ON DIFFERENT TCELL SUBSETS IN IDIOPATHIC NEPHROTIC SYNDROME IN CHILDREN." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii60. http://dx.doi.org/10.1093/ndt/gfx121.mo042.

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Florek, M., E. I. Sega, A. M. S. Mueller, D. B. Leveson-Gower, J. A. Shizuru, and R. S. Negrin. "Infusion of Syngeneic Apoptotic Cells Prior to Bone Marrow Transplantation Decreases Tcell Proliferation and Increases Survival." Biology of Blood and Marrow Transplantation 18, no. 2 (February 2012): S221. http://dx.doi.org/10.1016/j.bbmt.2011.12.054.

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Sakkas, L. I., A. G. Demaine, K. I. Welshy, and G. S. Panayi. "Restriction fragment length polymorphism for the Tcell receptor Lα and /β chain genes in rheumatoid arthritis." Arthritis & Rheumatism 30, no. 2 (February 1987): 231–32. http://dx.doi.org/10.1002/art.1780300218.

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Doherty, Peter C. "The terminology problem for T cells: a discussion paper." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, no. 1395 (March 29, 2000): 361–62. http://dx.doi.org/10.1098/rstb.2000.0574.

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The school of thought that owes allegiance to Ludwig Wittgenstein teaches that language conditions perceptions. When we use the term ‘cytotoxic T lymphocyte’ or ‘helper Tcell’ we tend to orientate our own thinking processes, and those of listeners or readers, down particular paths. Part of the problem is that we are often describing cell populations by functions that may either be a property of only a proportion of those that are being assayed, or are simply inferred from the expression of various cell–surface markers. The consequence can be a measure of confusion that might be avoided if we could communicate with greater clarity. Is it possible to achieve a better terminology that will be accepted generally? The following are some examples of why there may be some value in thinking about this.

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Tsirogianni, Maria, Eirini Grigoriou, Kleopatra Dagla, Vassiliki Pappa, Evi Konsta, Violetta Kapsimali-Vaiopoulou, Nora-Athina Viniou, Katerina Psarra, and Panagiotis Tsirigotis. "NK Cytotoxicity in Vitro and NK/ MDSCs/Tcell Subpopulations in AML/MDS Patients on 5-Azacytidine Treatment." Blood 128, no. 22 (December 2, 2016): 5123. http://dx.doi.org/10.1182/blood.v128.22.5123.5123.

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Abstract 5-Azacytidine is a cytosine analog and a potent DNA methyltransferase inhibitor, previously shown to induce DNA demethylation. 5-Azacytidine is indicated for the treatment of adult patients with intermediate-2 and high-risk myelodysplastic syndrome (MDS) and acute myeloid leukaemia (AML) with <30 % blasts or of patients aged ≥65 years with AML who are not eligible for HSCT. NK cells are an important component of immunological tumor surveillance and their role in MDS pathogenesis is of rising interest. The role of immunosuppressive myeloid derived suppressor cells (MDSCs) in NK cell cytotoxicity and their correlation with lymphocyte subpopulations, is currently under investigation. With regard to MDS, increased NK-cell mediated cytotoxicity was found in one study, while several other studies reported impaired NK cell function ( Chamuleau ME et al. Hematologica 2009;94(4):496-50, Kiladjian JJ et al. Leukemia 2006;20(3):463-470, Epling-Burnette PK et al., Blood 2007;109(11):4816-482. We investigated 5-Azacytidine's impact on human in vitro NK cell cytotoxicity and in parallel its impact on frequencies of peripheral blood T, NKT, NK, Tregs and MDSCs cell subpopulations. To elucidate the immunological effects of 5-Azacytidine , we collected blood samples from 17 AML/MDS patients (age: 40-86y, median: 76y) and 9 healthy donors (age: 34-58y, median: 54y). Informed consent was obtained from all patients and donors according to the Declaration of Helsinki. Eleven patients suffered from MDS-RAEB II, three from secondary AML (MDS related) and three from AML. All patients had received at least 3 5-Azacytidine cycles (median 10, ranged from 3 -32). Complete remission was achieved by 47% of patients. Peripheral blood mononuclear cells (PBMC) were isolated from patients and healthy donors using density gradient centrifugation. CD56+/CD3- NK cells were purified from PBMCs by negative immunomagnetic selection. Purified NK cells were tested against the NK resistant Raji cell line and the NK sensitive K562 cell line, at a ratio of effector to target cells 5:1 . Cytotoxicity was measured in duplicate samples using a 4-h cytotoxicity assay at 37°C. Target cells were labeled with PKH-67stain and the analysis of cell viability was determined by staining with 7-AAD and was restricted to the PKH-67+ fraction. The mean proportion of 7AAD positive cells from the duplicate samples was determined. Background target cell death was determined from cells incubated in the absence of effector cells. Cell-mediated cytotoxicity was reported as the percentage of killing over background cell death averaged from the two samples. Frequencies of T, NKT, NK, Tregs and MDSCs cell populations were measured by flow cytopetry the same day as the cytotoxicity test was performed. MDSCs were phenotypically defined as CD33+/CD11b+/CD14-/HLA-DR lo/- . Statistical significance was determined by two-tailed unpaired t-test. Grouped data were expressed as mean ± standard error of the mean. The in vitro cytolytic capacity of AML/MDS-NK cells was investigated first against the erythroleukemia cell line K562, which represents a highly susceptible NK cell target and was presented significantly decreased compared with healthy donors (19,3±3,33 vs 38,3±5,68, p=0,0051)(graph 1.). In vitro cytotoxicity of AML/MDS-NK cells against NK resistant Raji cell line didn't show any difference between the two studied cohorts (patients:1,93±0,44 vs healthy donors:3,41±0,83, p=0,1). Overall frequencies of T, NKT, NK, TRegs and MDSCs cells were comparable among AML/MDS patients and healthy controls as it is presented in table 1, while CD3+/CD4+ subpopulation showed significant reduction in the patient's cohort. Natural Killer cell, well known to mediate anti-leukemic responses, showed defective in vitro cytoxicity in patient's cohort on 5'Azacytidine treatment , implying further in vivo impaired immune surveillance. Notably no reduced NK levels were found, nor any alterations in frequencies of MDSCs and Tregs were noted in patient's cohort. As it is already presented, MDS patients show a significant increase in MDSCs that negatively correlates with lymphocyte populations (Michelle K. Gleason et al.Blood, 2014; 123 (19):3016-3026). 5-Azacytidine treatment may confer to restitution of this impairment, conferring to meliorate antitumor immunity. Figure Figure. Disclosures No relevant conflicts of interest to declare.

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Geskin, Larisa J. "Vorinostat in combination therapy for cutaneous Tcell lymphoma: a first year of clinical experience at a single center." Community Oncology 7, no. 1 (January 2010): 31–36. http://dx.doi.org/10.1016/s1548-5315(11)70386-2.

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Mihaljevic, Biljana, Aleksandra Sretenovic, Ljubomir Jakovic, Maja Perunicic-Jovanovic, Dragana Kovacevic, Dejan Rasic, and Zoran Latkovic. "A case of primary peripheral T-cell type non-Hodgkin lymphoma originating in the iris: Clinico-pathological findings." Vojnosanitetski pregled 67, no. 12 (2010): 1025–28. http://dx.doi.org/10.2298/vsp1012025m.

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Background. The ocular adnexal region is the primary localization of extranodal lymphoma in 5% to 15% of all Non-Hodgkin lymphoma. Intraocular lymphoma of T-cell origin is extremely rare and such sites of infiltration have been rarely observed in clinical examination. Case report. We presented a 56-year-old man with iris infiltration by primary intraocular peripheral T-cell lymphoma. The patient was in clinical stage I BE and the treatment was initiated according to cyclophosphamide, hydroxydaunorubicin, oncovin, prednisone (CHOP) regimen. When the second course of the therapy was scheduled, the patient developed central nervous system lymphoma infiltration. Although De Angelis regimen was used, 3 months after the diagnosis was established, lethal outcome ensued due to disease progression. Conclusion. According to our experience we can conclude that further therapeutical approach to patients with primary intraocular Tcell lymphoma requires modification of conventional treatment regimens. The lower median survival in these patients suggests that the disease may be of more aggressive course.

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Odeyemi, A. O., A. O. Odeyemi, O. F. Awopeju, O. O. Adewole, M. O. Tanimowo, M. O. Tanimowo, and G. E. Erhabor. "Community-acquired lower respiratory tract infections in an adult population with HIV infection in a Nigerian tertiary hospital." Research Journal of Health Sciences 9, no. 2 (April 13, 2021): 150–57. http://dx.doi.org/10.4314/rejhs.v9i2.5.

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Objective: Lower respiratory tract infections (LRTI) are 25-fold more common in people with HIV than in the general population. This study aimed to determine the prevalence of community-acquired LRTI and its associated factors in an adult population of people living with HIV (PLWH) in a Nigerian tertiary Hospital.Methodology: This was a prospective study done at the HIV clinic of Ladoke Akintola University of Technology (LAUTECH) Teaching Hospital Osogbo, Nigeria. It involved 130 randomly selected adult participants with a confirmed HIV-positive serology. The participants were followed up for a period of one year while looking out for symptoms and signs suggestive of LRTI.Results: The participants had a mean age of 41.9±10.02 years and a male to female ratio of 0.4:1. Seventeen (13.9%) of the participants developed LRTI during the study period and this was significantly associated with CD4 count and cigarette smoking history.Conclusion: LRTI is common among PLWH in Osogbo, and it occurs more commonly in those with low CD4 Tcell count and those with a history of cigarette smoking. Keywords: Lower respiratory tract infection, HIV, pneumonia.

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Bunnell, Stephen C., David I. Hong, Julia R. Kardon, Tetsuo Yamazaki, C. Jane McGlade, Valarie A. Barr, and Lawrence E. Samelson. "T cell receptor ligation induces the formation of dynamically regulated signaling assemblies." Journal of Cell Biology 158, no. 7 (September 23, 2002): 1263–75. http://dx.doi.org/10.1083/jcb.200203043.

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Tcell antigen receptor (TCR) ligation initiates tyrosine kinase activation, signaling complex assembly, and immune synapse formation. Here, we studied the kinetics and mechanics of signaling complex formation in live Jurkat leukemic T cells using signaling proteins fluorescently tagged with variants of enhanced GFP (EGFP). Within seconds of contacting coverslips coated with stimulatory antibodies, T cells developed small, dynamically regulated clusters which were enriched in the TCR, phosphotyrosine, ZAP-70, LAT, Grb2, Gads, and SLP-76, excluded the lipid raft marker enhanced yellow fluorescent protein–GPI, and were competent to induce calcium elevations. LAT, Grb2, and Gads were transiently associated with the TCR. Although ZAP-70–containing clusters persisted for more than 20 min, photobleaching studies revealed that ZAP-70 continuously dissociated from and returned to these complexes. Strikingly, SLP-76 translocated to a perinuclear structure after clustering with the TCR. Our results emphasize the dynamically changing composition of signaling complexes and indicate that these complexes can form within seconds of TCR engagement, in the absence of either lipid raft aggregation or the formation of a central TCR-rich cluster.

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Khazaee, I. "Analytical Investigation and Improvement of Performance of a Proton Exchange Membrane (Pem) Fuel Cell in Mobile Applications." International Journal of Applied Mechanics and Engineering 20, no. 2 (May 1, 2015): 319–28. http://dx.doi.org/10.1515/ijame-2015-0021.

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Abstract In this study, the performance of a proton exchange membrane fuel cell in mobile applications is investigated analytically. At present the main use and advantages of fuel cells impact particularly strongly on mobile applications such as vehicles, mobile computers and mobile telephones. Some external parameters such as the cell temperature (Tcell ) , operating pressure of gases (P) and air stoichiometry (λair ) affect the performance and voltage losses in the PEM fuel cell. Because of the existence of many theoretical, empirical and semi-empirical models of the PEM fuel cell, it is necessary to compare the accuracy of these models. But theoretical models that are obtained from thermodynamic and electrochemical approach, are very exact but complex, so it would be easier to use the empirical and smi-empirical models in order to forecast the fuel cell system performance in many applications such as mobile applications. The main purpose of this study is to obtain the semi-empirical relation of a PEM fuel cell with the least voltage losses. Also, the results are compared with the existing experimental results in the literature and a good agreement is seen.

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Herz, Jasmin, Khalil Alves de Lima, Andrea Francesca Salvador, Mackenzie Lemieux, Taitea Dykstra, Igor Smirnov, and Jonathan Kipnis. "MENINGES HARBOR IMMUNE MEMORIES OF LIFE EXPERIENCES." Innovation in Aging 6, Supplement_1 (November 1, 2022): 347. http://dx.doi.org/10.1093/geroni/igac059.1373.

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Abstract The adaptive immune system relies on formation of the memory of past microbial challenges to accelerate protective immune responses in the event of reinfection. This memory is accomplished in part by the retention of antigen-specific B and T cells within barrier tissues. As the healthy central nervous system parenchyma is virtually devoid of adaptive immune cells, the meningeal spaces carry out the vital function of coping with environmental threats during aging. We conducted an extensive molecular and functional analysis of meningeal T cells to test the hypothesis that the meninges in the brain sense and respond to internal and external cues throughout life, and that alterations in the meningeal T cell repertoire alter brain function. We found presumably self-reactive tissue-resident T cells in the meninges of naive mice. Using models of pathogen exposure, we describe a neuroimmune axis in which antigen experienced resident Tcell subsets dynamically record immune perturbations, which resulted in behavioral abnormalities that were exacerbated with aging. Our findings elucidate molecular properties of T cells that survey the brain borders under both homeostatic and pathological conditions and provide insights linking CNS immune privilege with memory.

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Bellanger, Anne-Pauline, Tony Labaigt, Anne-Sophie Brunel, Emeline Scherer, Frédéric Grenouillet, and Ana Berceanu. "Acute disseminated candidiasis due to Candida tropicalis with skin and muscular lesions in a patient with Tcell acute lymphocytic leukemia (T-ALL)." Journal of Medical Mycology 32, no. 2 (May 2022): 101243. http://dx.doi.org/10.1016/j.mycmed.2021.101243.

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Phan, Chin Lee, Siew Ngoh Tan, Sen Mui Tan, Sharifah Shahnaz Syed Abd Kadir, Nur Liyana Mohd Ramli, Teck Onn Lim, and Ching Ching Ng. "A variant e13a3 BCR-ABL1 fusion transcript in refractory adult B-cell acute lymphoblastic leukemia achieving complete remission with CAR-Tcell therapy." Cancer Genetics 250-251 (January 2021): 20–24. http://dx.doi.org/10.1016/j.cancergen.2020.11.003.

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von Bergwelt-Baildon, Michael S., Alexey Popov, Tomo Saric, Jens Chemnitz, Sabine Classen, Marc S. Stoffel, Francesca Fiore, et al. "CD25 and indoleamine 2,3-dioxygenase are up-regulated by prostaglandin E2 and expressed by tumor-associated dendritic cells in vivo: additional mechanisms of T-cell inhibition." Blood 108, no. 1 (July 1, 2006): 228–37. http://dx.doi.org/10.1182/blood-2005-08-3507.

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Immune tolerance is a central mechanism counteracting tumor-specific immunity and preventing effective anticancer immunotherapy. Induction of tolerance requires a specific environment in which tolerogenic dendritic cells (DCs) play an essential role deviating the immune response away from effective immunity. It was recently shown that maturation of DCs in the presence of PGE2 results in upregulation of indoleamine 2,3-dioxygenase (IDO) providing a potential mechanism for the development of DC-mediated Tcell tolerance. Here, we extend these findings, demonstrating a concomitant induction of IDO and secretion of soluble CD25 after DC maturation in the presence of PGE2. While maturation of DCs induced IDO expression on transcriptional level, only integration of PGE2 signaling led to up-regulation of functional IDO protein as well as significant expression of cell-surface and soluble CD25 protein. As a consequence, T-cell proliferation and cytokine production were significantly inhibited, which was mediated mainly by IDO-induced tryptophan depletion. Of importance, we demonstrate that different carcinoma entities associated with elevated levels of PGE2 coexpress CD25 and IDO in peritumoral dendritic cells, suggesting that PGE2 might influence IDO expression in human DCs in the tumor environment. We therefore suggest PGE2 to be a mediator of early events during induction of immune tolerance in cancer. (Blood. 2006;108:228-237)

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Marx, Alexander, Anja Schultz, Annette Wilisch, Markus Helmreich, Regina Nenninger, and Hans Konrad Müller-Hermelink. "Paraneoplastic Autoimmunity in Thymus Tumors." Developmental Immunology 6, no. 1-2 (1998): 129–40. http://dx.doi.org/10.1155/1998/49484.

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Autoimmune phenomena are more frequent in thymic epithelial tumors (TET) than in any other human tumor. Mysthenia gravis (MG) is by far the most common autoimmune disease in thymoma patients. MG is characterized by muscle weakness due to autoantibodies against the acetylcholine receptor (AChR), and CD4+AChR-specific T cells play a pivotal role for the production of these autoantibodies. About 10% of MG patients have a thymoma and, interestingly, only such thymomas exhibit an MG association that maintains thymuslike morphological and functional features with respect to the homing and differentiation of immature T cells. Since AChR protein is not expressed in thymomas, the specificity of the autoimmunity in thymoma-associated MG is thought to be determined by nonreceptor proteins with AChR epitopes. Such proteins are overexpressed in cortical-type MG-associated thymomas, and medullary thymomas express these proteins at barely detectable levels. Aside from this quantitative difference, the pathogenesis of anti-AChR autoimmunity might be qualitatively different in these thymoma subtypes. Our findings suggest that an antigen-specific abnormal Tcell selection by cortical-type TET may contribute to the pathogenesis of paraneoplastic MG. In contrast, an abnormal (intratumorous) activation of autoreactive T cells may be operative in medullary thymomas.

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Du, Xin, Yangqiu Li, Shuxia Geng, Jianyu Weng, Zesheng Lu, and Rong Guo. "T Cell Receptor Excision Circles (TRECs) Decrease in Patients after Allogeneic Stem Cell Transplantation." Blood 106, no. 11 (November 16, 2005): 5357. http://dx.doi.org/10.1182/blood.v106.11.5357.5357.

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Abstract Human thymus is required for establishment of a T-cell pool in fetal life, T-cell emigration from thymus (thymic recent emigrants [TRECs]) is a continuous thymic-dependent process. To analyze the content of signal joint Tcell receptor excision DNA circles signal joint T cell receptor excision DNA circles(sjTRECs) within peripheral blood mononuclear cells (PBMCs), thereby to infer the level of naive T cells and the recent thymic output function in patients with allogeneic stem cell transplantation. We used real-time polymerase chain reaction (PCR) to quantify SjTRECs in 5 patients with chronic myeloid leukemia-chronic phase. Five patients(4 males, 1 females; median age 37 years,) who underwent HLA-matching sibling BMT and/or peripheral blood stem cell transplantation (PBSCT) at our department. Quantitative detection of sjTRECs in DNA of peripheral blood mononuclear cells from 13 normal individuals. The median value of sjTRECs copies P1 000 PBMCs was 4.37±3.64 in normal individuals whereas it was 0.57±0.51 copies P1 000 PBMCs in patients at least two years after allogeneic stem cell transplantation (P < 0. 03). We conclude that these Patients decrease in recent thymic output function,. Therefore, measurement of sjTREC may provide an important tool for predicting thymus-dependent T-cell reconstitution after transplantation.

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Kennedy, Steven, Alison Johnson, Ronald Seidel, John Chan, William Jacobs, and Steven Porcelli. "Assessing the capability of the mycobacterial ribosome to elicit a CD4+ T cell response (APP5P.115)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 183.17. http://dx.doi.org/10.4049/jimmunol.194.supp.183.17.

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Abstract Mycobacterium tuberculosis (Mtb) infects one third of the world’s population, and an effective vaccine is desperately needed to curb the spread of disease. We have identified that the CD4+ T cell response is critical in combating Mtb. Using an attenuated version of Mycobacterium smegmatis, IKEPLUS, our lab previously identified the mycobacterial ribosome as a potential target to enhance CD4+ T cell responses to Mtb in mice. To directly assess the CD4+ T cell response mounted against the individual mycobacterial ribosomal proteins, we used an E. coli expression system to express and purify all fifty-seven proteins that make up the Mtb ribosome. This Mtb ribosomal library was then used to identify which proteins of the mycobacterial ribosome elicited a CD4+ T cell response in IKEPLUS infected animals by IFN-γ ELISPOT. When CD4+T cells of infected animals were isolated and restimulated with the Mtb ribosomal protein library, twenty-five of the fifty-seven total proteins elicited significant CD4+ Tcell responses. These ELISPOT results indicate that the Mtb ribosome is a highly immunogenic structure with the ability to stimulate strong T cell responses in mice. Further studies will focus on the use of the mycobacterial ribosome and isolated ribosomal proteins as potential components of vaccination regimens for inducing protective immunity against Mycobacterium tuberculosis.

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Rossi, Valentina, Chiara Cattaneo, Alessandro Re, Giulia Quaresmini, Davide Bertelli, Ottorino Barozzi, Benvenuto Antonini, Mario Luppi, and Giuseppe Rossi. "Adult Onset of Hemophagocytic Syndrome: Report of 13 Cases from a Single Institution." Blood 106, no. 11 (November 16, 2005): 3880. http://dx.doi.org/10.1182/blood.v106.11.3880.3880.

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Abstract Hemophagocytic syndrome (HLH) is a rare disorder usually of early infancy characterized by fever, hepatosplenomegaly, cytopenia, hypertriglyceridemia, hypofibrinogenemia and hemophagocytosis. Impaired natural killer activity has been demonstrated in these patients (pts). The persistent antigen driven T-cell activation results in the hyperproduction of cytokines and secondary tissue damage caused by macrophages’ activation. Mutations in the perforin 1 gene (PRF1) are known and may be considered the most frequent genetic defect underlying familial HLH. Two distinct forms of HLH are recognized: familial (autosomal recessive disorder) and secondary (in association with systemic infection, underlying malignancy or autoimmune disorder). The diagnosis of adult HLH is often overlooked because of its rarity and heterogeneous clinical presentation. Aim, patients and methods: to clarify common clinical characteristics and underlying disease, we describe 13 cases (M/F 7/6, median age 64, range 31–71) fulfilling the diagnostic criteria for HLH, according to guidelines of the histiocyte society, admitted to our Institution since February 2003. Results: at presentation 12/13 pts had fever, 9/13 splenomegaly, 13/13 cytopenia, 11/13 hypertriglyceridemia and/or hypofibrinogenemia, 8/13 histological hemophagocytosis. Median hemoglobin level was 8.6 g/dl (range 7.7–11.7), platelets 25 x109/L (4–166), ANC 0.76 x109/L (0.09–17.1); ferritin > 40000 mg/L (1687->40000). In 9/13 pts an underlying disease was diagnosed: 2 autoimmune haemolytic anemia [AHA], 1 Still disease, 1 Castleman disease, 4 Non-Hodgkin lymphoma (2 diffuse large B cell, 1 anaplastic null lymphoma, 1 peripheral unspecified T cell lymphoma, 1 small B-lymphocyte lymphoma). Both B-cell lymphoma had marked accompanying Tcell infiltration. Twelve pts were screened for viral infection, which was positive in 5/12 (41.7%). In 4 of 9 evaluated pts HHV8 DNA was detected, in three of whom without any other manifestation of infection. In 2/3 pts the viral load, determined by real time PCR for orf26, showed an extremely high number of viral copies. Two of the 11 evaluated pts were positive for CMV-DNA (1 Tcell lymphoma, 1 AHA); 3/6 pts had detectable EBV-DNA (1 Castleman, 2 AHA). Three of 3 pts studied, showed low NK activity, using K562 cells as target or perforin expression (two without concomitant haematological disease, one pts with a small B-lymphocyte lymphoma). In spite of aggressive treatment (steroid, immunoglobulin, rituximab, cyclosporine A), eleven of 13 pts died of multiorgan failure few days after diagnosis (median survival of 9 days range 2–24); two patients are still alive (one without underlying haematological disease and one with diffuse large B cell lymphoma), after steroid therapy and anthracycline containing chemotherapy respectively. Conclusion: HLH in adults is a not-uncommon disorder often associated with systemic viral infection, underlying malignancy or autoimmune disorder. Mutations in the perforin 1 gene (PRF1) or acquired abnormal perforin or NK function may have a pathogenic role. Its earlier recognition by haematologists in the setting of unexplained pancytopenia may allow more effective treatment of this highly fatal disease.

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Mohan, Nishant, Salman Hosain, Jun Zhao, Yi Shen, Xiao Luo, Jiangsong Jiang, Yukinori Endo, and Wen Jin Wu. "Atezolizumab potentiates Tcell-mediated cytotoxicity and coordinates with FAK to suppress cell invasion and motility in PD-L1+ triple negative breast cancer cells." OncoImmunology 8, no. 9 (June 6, 2019): e1624128. http://dx.doi.org/10.1080/2162402x.2019.1624128.

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Jung, Jae Wook, Ae Rin Lee, Jaesung Kim, Young Rim Kim, Jassy Mary S. Lazarte, Jung Suk Lee, Kim D. Thompson, Hyeongsu Kim, and Tae Sung Jung. "Elucidating the Functional Roles of Helper and Cytotoxic T Cells in the Cell-Mediated Immune Responses of Olive Flounder (Paralichthys olivaceus)." International Journal of Molecular Sciences 22, no. 2 (January 15, 2021): 847. http://dx.doi.org/10.3390/ijms22020847.

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In higher vertebrates, helper and cytotoxic T cells, referred to as CD4 and CD8 T lymphocytes, respectively, are mainly associated with adaptive immunity. The adaptive immune system in teleosts involves T cells equivalent to those found in mammals. We previously generated monoclonal antibodies (mAbs) against olive flounder (Paralichthys olivaceus) CD4 T cells, CD4-1 and CD4-2, and used these to describe the olive flounder’s CD4 Tcell response during a viral infection. In the present study, we successfully produced mAbs against CD8 T lymphocytes and their specificities were confirmed using immuno-blotting, immunofluorescence staining, flow cytometry analysis andreverse transcription polymerase chain reaction (RT-PCR). The results showed that these mAbs are specific for CD8 T lymphocytes. We also investigated variations in CD4 and CD8 T cells populations, and analyzed the expression of immune-related genes expressed by these cells in fish infected with nervous necrosis virus or immunized with thymus dependent and independent antigens. We found that both CD4 and CD8 T lymphocyte populations significantly increased in these fish and Th1-related genes were up-regulated compared to the control group. Collectively, these findings suggest that the CD4 and CD8 T lymphocytes in olive flounder are similar to the helper and cytotoxic T cells found in mammals, and Th1 and cytotoxic immune responses are primarily involved in the early adaptive immune response against extracellular antigens.

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Journal articles on the topic 'Tcell'

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