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COVID-19 vaccination produces exercise-responsive SARS-CoV-2 specific t-cells regardless of infection history

Journal of Sport and Health Science 2024年第1期13卷 99-107页

作者： Kyle A.Smith tiffany M.Zúñiga Forrest L.Baker Helena Batatinha Charles R.Pedlar Shane C.Burgess Michael P.Gustafson Emmanuel Katsanis Richard J.Simpson School of Nutritional Sciences and Wellness The University of ArizonaTucsonAZ 85721USA Department of Pediatrics The University of ArizonaTucsonAZ 85724USA Faculty of Sport Allied Health and Performance ScienceSt.Mary's UniversityTwickenham TW14SXUK Institute of Sport Exercise and Health University College LondonLondon WC1E 7HUUK Department of Animal and Comparative Biomedical Sciences The University of ArizonaTucsonAZ 85721USA the University of Arizona Cancer Center The University of ArizonaTucsonAZ 85719USA Laboratory Medicine and Pathology Mayo Clinic ArizonaPhoenixAZ 85054USA Department of Immunobiology The University of ArizonaTucsonAZ 85724USA Department of Medicine The University of ArizonaTucsonAZ 85724USA Department of Pathology The University of ArizonaTucsonAZ 85724USA

Background:the mobilization and redistribution of severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)specific t-cells and neutralizing antibodies(nAbs)during exercise is purported to increase immune surveillance and protect against severe coronavirus disease 2019(COVID-19).We sought to determine if COVID-19 vaccination would elicit exercise-responsive SARS-CoV-2 t-cells and transiently alter nAb titers.Methods:Eighteen healthy participants completed a 20-min bout of graded cycling exercise before and/or after receiving a COVID-19 vaccine.All major leukocyte subtypes were enumerated before,during,and after exercise by flow cytometry,and immune responses to SARS-CoV-2 were determined using whole blood peptide stimulation assays,t-cell receptor(tCR)-βsequencing,and SARS-CoV-2 nAb serology.Results:COVID-19 vaccination had no effect on the mobilization or egress of major leukocyte subsets in response to intensity-controlled graded exercise.However,non-infected participants had a significantly reduced mobilization of CD4+and CD8+naive t-cells,as well as CD4+central memory t-cells,after vaccination(synthetic immunity group);this was not seen after vaccination in those with prior SARS-CoV-2 infection(hybrid immunity group).Acute exercise after vaccination robustly mobilized SARS-CoV-2 specific t-cells to blood in an intensity-dependent manner.Both groups mobilized t-cells that reacted to spike protein;however,only the hybrid immunity group mobilized t-cells that reacted to membrane and nucleocapsid antigens.nAbs increased significantly during exercise only in the hybrid immunity group.Conclusion:these data indicate that acute exercise mobilizes SARS-CoV-2 specific t-cells that recognize spike protein and increases the redistribution of nAbs in individuals with hybrid immunity.

关键词： Anti-viral COVID-19 Exercise immunology SARS-CoV-2 t-cells Vaccine

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Cross-talk between t-cells and gut-microbiota in neurodegenerative disorders

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Neural Regeneration Research 2019年第12期14卷 2091-2092页

作者： Rodrigo Pacheco Departamento de Ciencias Biológicas Facultad de Ciencias de la Vida Universidad Andres Bello Laboratorio de Neuroinmunología Fundación Ciencia & Vida

the emerging role of gut microbiota as a key player in the development of neurodegenerative disorders: Mammals have evolved together with commensal microbiota to establish a symbiotic relationship in which they regulate reciprocally by synthesizing and responding to several common chemical substances. In this regard, gut microbiota constitutes a consortium of bacteria that not only participates in the degradation of nutrients, but also produces metabolites, fatty acids and neurotransmitters that can act on the enzymes and receptors expressed in eukaryotic cells, which considerably affects the physiology of the host and contribute to maintaining homeostasis (Lyte, 2013).

关键词： Cross-talk t-cells neurodegenerative disorders

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Cytotoxic t-cells as imaging probes for detecting glioma

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World Journal of Clinical Oncology 2010年第1期1卷 3-11页

作者： Ali Syed Arbab Cellular and Molecular Imaging Laboratory Department of RadiologyHenry Ford HospitalDetroitMI 48202United States

tumor vaccination using tumor-associated antigenprimed dendritic cells(DCs)is in clinical trials.Investigators are using patients’own immune systems to activate t-cells against recurrent or metastatic tumors.Following vaccination of DCs or attenuated tumor cells,clinical as well as radiological improvements have been noted due to migration and accumulation of cytotoxic t-cells(CtLs).CtLs mediated tumor cell killing resulted in extended survival in clinical trails and in preclinical models.Besides administration of primed DCs or attenuated or killed tumors cells to initiate the generation of CtLs,investigators have started making genetically altered t-cells(CtLs)to target specific tumors and showed in vivo migration and accumulation in the implanted or recurrent tumors using different imaging modalities.Our groups have also showed the utilization of both in vivo and in vitro techniques to make CtLs against glioma and used them as imaging probes to determine the sites of tumors.In this short review,the current status of vaccination therapy against glioma and utilization of CtLs as in vivo imaging probes to determine the sites of tumors and differentiate recurrent glioma from radiation necrosis will be discussed.

关键词： Cellular magnetic resonance imaging Cytotoxic t-cells Glioma Glioma associated antigen Imaging probes Magnetic resonance imaging tumor vaccine

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Impaired t-cell differentiation in diabetic foot ulceration

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Cellular & Molecular Immunology 2017年第9期14卷 758-769页

作者： João Moura João Rodrigues Marta Gonçalves Cláudia Amaral Margarida Lima Eugénia Carvalho Center for Neuroscience and Cell Biology(CNC) University of Coimbra3004-517 CoimbraPortugal Hospital de Santo Antonio(HSA) Centro Hospitalar do Porto(CHP)4099-001 PortoPortugal Unidade Multidisciplinar de Investigação Biomédica(UMIB/ICBAS/UP) PortoPortugal Department of Geriatrics University of Arkansas for Medical Sciences(UAMS)Little RockAR 72202USA Arkansas Children's Hospital Research Institute(ACHRI) Little RockAR 72202USA

Foot ulceration is one of the most debilitating complications associated with diabetes,but its cause remains poorly understood.Several studies have been undertaken to understand healing kinetics or find possible therapies to enhance healing.However,few studies have been directed at understanding the immunological alterations that could influence wound healing in diabetes.In this study,we analysed the t-cell receptor(tCR)repertoire diversity in tCR-αβ^(+)t cells.We also analysed the distribution and phenotype of t cells obtained from the peripheral blood of healthy controls and diabetic individuals with or without foot ulcers.Our results showed that diabetic individuals,especially those with foot ulcers,have a significantly lower naive t-cell number and a poorer tCR-Vβrepertoire diversity.We also showed that the reduced tCR-Vβrepertoire diversity in diabetic individuals was mainly owing to the accumulation of effector t cells,the major source of tumour necrosis factor-αproduction,which was even more pronounced in patients with acute foot ulceration.Moreover,the expression of several inflammatory chemokine receptors was significantly reduced in diabetic patients.In conclusion,effector t-cell accumulation and tCR repertoire diversity reduction appear to precede the development of foot ulcers.this finding may open new immunological therapeutic possibilities and provide a new prognostic tool in diabetic wound care.

关键词： diabetes t-cells t-cell repertoire diversity wound healing

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Immune mechanisms of vaccine induced protection against chronic hepatitis C virus infection in chimpanzees

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World Journal of Hepatology 2015年第1期7卷 53-69页

作者： Babs E Verstrepen André Boonstra Gerrit Koopman Department of Virology Biomedical Primate Research Centre2280GH RijswijkThe Netherlands Department of Gastroenterology and Hepatology Erasmus University Medical Center Rotterdam3015 CE RotterdamThe Netherlands

Hepatitis C virus(HCV) infection is characterized by a high propensity for development of life-long viral persistence. An estimated 170 million people suffer from chronic hepatitis caused by HCV. Currently,there is no approved prophylactic HCV vaccine available.With the near disappearance of the most relevant animal model for HCV,the chimpanzee,we review the progression that has been made regarding prophylactic vaccine development against HCV. We describe the results of the individual vaccine evaluation experiments in chimpanzees,in relation to what has been observed in humans. the results of the different studies indicate that partial protection against infection can be achieved,but a clear correlate of protection has thus far not yet been defined.

关键词： Hepatitis C virus Vaccines Chimpanzees Review Prophylactic Antibodies t-cells

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A two-hit model of autoimmunity： lymphopenia and unresponsiveness to tGF-β signaling

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Cellular & Molecular Immunology 2012年第5期9卷 369-370页

作者： Andrew L'Huillier Guangwen Ren Yufang Shi Jimin Zhang Dr YF Shi Child Health Institute of New Jersey Robert Wood Johnson Medical School University of Medicine and Dentistry of New Jersey New Brunswick NJ Institute of Health Sciences Shanghai Institutes for Biological Sciences Chinese Academy of Sciences and Shanghai Jiaotong University School of Medicine Shanghai China

he immune system can robustly respond to pathogens, while it is capableor malntaining Itolerance to self and innocu- ous antigens, so that the body is not jeopar- dized by autoimmune reactivity. Under certain circumstances, nonetheless, control of homeostasis of the immune system is sus- pended, and the body subsequently fails to recognize its own constituent parts as self, which contributes to homeostatic peripheral expansion and autoimmune diseases. Although autoimmunity is extensively studied, the ori- gins of this increasing public health challenge remain not well understood.

关键词： GROWtH-FACtOR-BEtA t-cells HOMEOStASIS

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Suppressing autoimmunity by tGF-β： not just through treg cells

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Cellular & Molecular Immunology 2012年第5期9卷 371-372页

作者： Ming-Xiao He You-Wen He Department of Immunology Duke University MedicalCenter Durham NC USA

Cellular ＆ Molecular Immunology （2012） 9,371-372; doi： 10.1038/cmi.2012.24; published online 13 August 2012transforming growth factor-β （tGF-β） is a pleiotropic factor. It regulates manyaspects of t-cell biology including thymocyte development, t cell differentiation and effector t cell function.1 Previous work has shown that the loss of tGF-β signaling in the t-cell lineage leads to severe lymphopro- liferafive autoimmunity.2.3 Until now, it has been unclear to what extent the autoimmunity observed in those mice is driven by tGF- unresponsive conventional t cells, as tGF- is also crucial for the maintenance and function of regulatory t cells （treg）. A recent study pub- lished in Nature Immunology revealed a novel role of tGF-β signaling in non-regulatory naive t cells. It was found that tGF-β controls lym- phopenia-driven t-ceU proliferation in neonatal mice, thereby preventing the development of autoimmtmity.

关键词： t-cells HOMEOStASIS MECHANISMS

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Interleukin 4-induced neuroprotection and regulation of microglia activation as a therapeutic approach in the MPtP model of Parkinson's disease

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Neural Regeneration Research 2017年第9期12卷 1433-1434页

作者： Bjorn Spittau Institute for Anatomy and Cell Biology Department of Molecular Embryology Faculty of Medicine University of Freiburg Institute of Anatomy University of Rostock

Parkinson＇s disease （PD） has been described as one of the most common neurodegenerative diseases affecting up to 2% of the worldwide population over 60 years of age. the hallmarks of PD are progressive loss of midbrain dopaminergic （mDA） neurons and a decrease in striatal dopamine levels, which result in typ- ical clinical motor symptoms such as akinesia, resting tremor, rigidity, and gait impairments. Although the causes for PD are only partially understood and seem to be very heterogeneous, one of the common phenomenons observed in toxin-based an- imal models of PD as well as PD patients is a microglia-driven neuroinflammatory response,

关键词： t-cells NEURONS BRAIN CYtOKINE

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Lack of correlation between treg quantification assays in inflammatory bowel disease patients

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World Journal of Gastroenterology 2015年第11期21卷 3325-3329页

作者： Gunnar Brandhorst Darinka todorova Petrova Sebastian Weigand Christoph Eberle Nicolas von Ahsen Jessica Schmitz Frank Christian Schultze Dirk Raddatz Michael Karaus Michael Oellerich Philip D Walson Department of Clinical Chemistry University Medical Center Department of Clinical Pharmacology University Medical Center Chronix Biomedical Clinics of Gastroen-terology and Endocrinology University Medical Center Department of Internal Medicine Evangelisches Krankenhaus G?ttingen--Weende

AIM:to compare the number of regulatory t-cells( tregs) measured by flow cytometry with those obtained using a real-time quantitative PCR(q PCR) method in patients suffering from inflammatory bowel disease(IBD).MEtHODS:tregs percentages obtained by both flow cytometry and q PCR methods in 35 adult IBD patients,18 out of them with Crohn′s disease(CD)and 17 with ulcerative colitis(UC)were compared to each other as well as to scores on two IBD activity questionnaires using the Harvey Bradshaw Index(HBI)for CD patients and the Simple Colitis Clinical Activity Index(SCCAI)for UC patients.the treg percentages by flow cytometry were defined as CD4+CD25highCD127lowFOXP3+cells in peripheral blood mononuclear cells,whereas the treg percentages by q PCR method were determined as FOXP3 promoter demethylation in genomic DNA.RESULtS:We found an average of 1.56%±0.78%tregs by using flow cytometry,compared to 1.07%±0.53%tregs by using q PCR in adult IBD patients.there were no significant correlations between either the percentages of tregs measured by flow cytometry or q PCR and the HBI or SCCAI questionnaire scores in CD or UC patients,respectively.In addition,there was no correlation between treg percentages measured by q PCR and those measured by flow cytometry(r=-0.06,P=0.73;Spearman Rho).these data suggest that,either treg-related immune function or the clinical scores in these IBD patients did not accurately reflect actual disease activity.Until the cause(s)for these differences are more clearly defined,the resultssuggest caution in interpreting studies of tregs in various inflammatory disorders.CONCLUSION:the two methods did not produce equivalent measures of the percentage of total tregs in the IBD patients studied which is consistent with the conclusion that tregs subtypes are not equally detected by these two assays.

关键词： Regulatory t-cells Inflammatory bowel disease Croh

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Molecular mechanisms of triggering,amplifying and targeting RANK signaling in osteoclasts

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World Journal of Orthopedics 2012年第11期3卷 167-174页

作者： Yukiko Kuroda Koichi Matsuo Laboratory of Cell and tissue Biology School of MedicineKeio UniversityTokyo 160-8582Japan

Osteoclast differentiation depends on receptor activator of nuclear factor-κB(RANK) signaling,which can be divided into triggering,amplifying and targeting phases based on how active the master regulator nuclear factor of activated t-cells cytoplasmic 1(NFAtc1) is. the triggering phase is characterized by immediateearly RANK signaling induced by RANK ligand(RANKL) stimulation mediated by three adaptor proteins,tumor necrosis factor receptor-associated factor 6,Grb-2-associated binder-2 and phospholipase C(PLC)γ2,leading to activation of IκB kinase,mitogen-activated protein kinases and the transcription factors nuclear factor(NF)-κB and activator protein-1(AP-1). Mice lacking NF-κB p50/p52 or the AP-1 subunit c-Fos(encoded by Fos) exhibit severe osteopetrosis due to a differentiation block in the osteoclast lineage. the amplification phase occurs about 24 h later in a RANKLinduced osteoclastogenic culture when Ca2+ oscillation starts and the transcription factor NFAtc1 is abundantly produced. In addition to Ca2+ oscillation-dependent nuclear translocation and transcriptional auto-induction of NFAtc1,a Ca2+ oscillation-independent,osteoblastdependent mechanism stabilizes NFAtc1 protein in dif-ferentiating osteoclasts. Osteoclast precursors lacking PLCγ2,inositol-1,4,5-trisphosphate receptors,regulator of G-protein signaling 10,or NFAtc1 show an impaired transition from the triggering to amplifying phases. the final targeting phase is mediated by activation of numerous NFAtc1 target genes responsible for cell-cell fusion and regulation of bone-resorptive function. this review focuses on molecular mechanisms for each of the three phases of RANK signaling during osteoclast differentiation.

关键词： Receptor activator of nuclear factor-κB ligand tumor necrosis factor receptor-associated factor 6 c-Fos Nuclear factor of activated t-cells cytoplasmic 1 Immunoreceptor tyrosine-based activation motif Ca2+oscillation

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