Journal of cellular immunology最新文献

{"title":"Evaluating the Role of the Renin-angiotensin System in COVID-19: Implications for ACE Inhibitor and ARB Use During SARS-CoV-2 Infection.","authors":"Sarah R Tritsch, Evelyn Mendoza-Torres, Mónica Gómez-Pulido, Jairo Castellar-López, Rebecca Lynch, Carlos Herrera Gomez, Hana Akselrod, Adrienne Poon, Sam Simmens, Christopher N Mores, Gary Simon, Lauren C Ray, Sarah Conway, Aileen Y Chang","doi":"10.33696/immunology.6.213","DOIUrl":"10.33696/immunology.6.213","url":null,"abstract":"<p><p>This study aimed to investigate the role of the renin-angiotensin system (RAS) in COVID-19, particularly focusing on key components such as ACE, ACE2, and their related peptides, angiotensin-(1-7) and angiotensin-(1-9). Using serum samples from healthy controls and both non-severe and severe COVID-19 patients, ELISA assays revealed no significant differences in these RAS components between the groups. In addition, <i>in vitro</i> studies showed no impact of ACE inhibitors or Angiotensin Receptor Blockers (ARB) on cell viability during SARS-CoV-2 infection. These clinical findings suggest that RAS alterations may not be a major factor in COVID-19 severity and the <i>in vitro</i> data support current guidelines, indicating the safety of continuing ACE inhibitors and ARBs in COVID-19 patients without evidence of increased SARS-CoV-2 infectivity in the presence of these compounds. This study highlights the lack of significant changes in key RAS components during COVID-19 in a clinical cohort and provides critical <i>in vitro</i> evidence supporting the continued use of ACE inhibitors and ARBs in treating patients.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"6 6","pages":"255-265"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epidemiology, Symptoms and Pathophysiology of Long Covid Complications.","authors":"Chongyang Zhang, Chiung-Yu Hung, Chia George Hsu","doi":"10.33696/immunology.6.209","DOIUrl":"https://doi.org/10.33696/immunology.6.209","url":null,"abstract":"<p><p>Long COVID, or post-acute sequelae of SARS-CoV-2 infection, reports to affect a significant proportion of COVID-19 survivors, leading to persistent and multi-organ complications. This review examines the epidemiology, symptoms of long COVID complications, including cardiac, hematological, vascular, pulmonary, neuropsychiatric, renal, gastrointestinal, musculoskeletal, immune dysregulation, and dermatological issues. By synthesizing the latest research, this article provides a comprehensive overview of the prevalence and detailed pathophysiological mechanisms underlying these complications. The purpose of this review is to enhance the understanding of diverse and complex nature of long COVID and emphasize the need for ongoing research, seeking to support future studies for better management of long COVID.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"6 5","pages":"219-230"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12021439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144054834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of Neutrophil Elastase Inhibitors as Potential Therapies for <i>ELANE</i> Associated Neutropenia.","authors":"Vahagn Makaryan, Merideth Kelley, Audrey Anna Bolyard, Gobind Chugh, David C Dale","doi":"10.33696/immunology.6.208","DOIUrl":"10.33696/immunology.6.208","url":null,"abstract":"<p><p>Neutrophil elastase (<i>ELANE</i>) mutations are the most common cause of cyclic (CyN) and congenital neutropenia (SCN), two autosomal dominant disorders causing recurrent infections due to impaired neutrophil production. Granulocyte colony-stimulating factor (G-CSF) corrects neutropenia but has adverse effects, including bone pain and in some cases, an increased risk of myelodysplasia (MDS) and acute myeloid leukemia (AML). Hematopoietic stem cell transplantation is an alternative but is limited by its complications and donor availability. Alternative therapies are needed, particularly for patients with poor responses to G-CSF and those at higher risk of MDS/AML. We previously reported that cell-permeable neutrophil elastase (NE) inhibitors are a potential treatment for <i>ELANE</i> neutropenia, based on studies using HL-60 cells. Our hypothesis was that mutant NE was not properly stored to the neutrophil granules and thereby caused cytoplasmic damage, activation of apoptotic pathways and neutropenia. We have extended this work using CD34⁺ cells from patients with <i>ELANE</i> mutations and several selective NE inhibitors, i.e., MK0339, sivelestat, BAY-678, and GW311616, as well as the DDP1 inhibitor, brensocatib. Only MK0339 restored neutrophil differentiation with an increase in the proportion of neutrophil marker-positive cells (CD66b⁺/CD14⁺ and CD11b⁺/CD15⁺). In contrast, other NE inhibitors, i.e., sivelestat, BAY-678, and GW311616 and the DPP1 inhibitor, brensocatib, showed no effect on neutrophil differentiation. Molecular docking studies showed that MK0339 binds to an alternative site on the NE protein compared to other inhibitors with greater inhibitor-NE protein stability, suggesting a unique mechanism of action and supporting further investigation of MK0339 as a therapy for <i>ELANE</i> associated neutropenia.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"6 5","pages":"211-218"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143049027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Essentials of CAR-T Therapy and Associated Microbial Challenges in Long Run Immunotherapy.","authors":"Muhammad Kalim, Rui Jing, Xin Li, Zhiwu Jiang, Ningbo Zheng, Ziyu Wang, Guo Wei, Yong Lu","doi":"10.33696/immunology.6.189","DOIUrl":"10.33696/immunology.6.189","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR)-T cell therapy has shown potential in improving outcomes for individuals with hematological malignancies. However, achieving long-term full remission for blood cancer remains challenging due to severe life-threatening toxicities such as limited anti-tumor efficacy, antigen escape, trafficking restrictions, and limited tumor invasion. Furthermore, the interactions between CAR-T cells and their host tumor microenvironments have a significant impact on CAR-T function. To overcome these considerable hurdles, fresh methodologies and approaches are needed to produce more powerful CAR-T cells with greater anti-tumor activity and less toxicity. Despite advances in CAR-T research, microbial resistance remains a significant obstacle. In this review, we discuss and describe the basics of CAR-T structures, generations, challenges, and potential risks of infections in CAR-T cell therapy.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"6 1","pages":"22-50"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11172397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141332652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Natural History of Post-Chikungunya Viral Arthritis Disease Activity and T-cell Immunology: A Cohort Study.","authors":"Aileen Yu-Hen Chang, Alfonso Sucerquia Hernández, Jose Forero Mejía, Sarah Renee Tritsch, Evelyn Mendoza-Torres, Liliana Encinales, Andres Cadena Bonfanti, Abigale Marie Proctor, Gary Leonard Simon, Samuel Joseph Simmens, Gary Steven Firestein","doi":"10.33696/immunology.6.191","DOIUrl":"10.33696/immunology.6.191","url":null,"abstract":"<p><strong>Background: </strong>Chikungunya virus (CHIKV) is an alphavirus spread by mosquitos that causes arthralgias and arthritis that may last for years. The objective of this study was to describe the arthritis progression and T cell immunology over a two-year period.</p><p><strong>Methods: </strong>A cohort of 40 cases of serologically confirmed CHIKV from Magdalena and Atlántico, Colombia were followed in 2019 and again in 2021. Arthritis disease severity, disability, pain, stiffness, physical function, mobility, fatigue, anxiety, sleep disturbances and depression were assessed. Serum cytokines and T-cell subsets were measured and tested for change. Correlations within each of the 2 time periods for laboratory parameters were also examined.</p><p><strong>Results: </strong>Although, arthritis disease severity, as measured by the Disease Activity Score-28 (DAS-28) did not change significantly over a two-year period, a new metric- the Chikungunya Disease Activity Score (CHIK-DAS)- was more sensitive to detect changes in disease severity than the Disease Activity Score-28 (DAS-28) and showed some improvement in average disease severity from moderate to mild over two years. Cases were characterized by moderate disability, pain, and stiffness with mild alterations of physical function, mobility, fatigue, anxiety, sleep disturbances and depression that did not change significantly over time. Small joints including the fingers and wrists were most affected without significant change over time. The percentage of effector T cells (Teffs) and regulatory T cells (Tregs) of CD4⁺ T cells both decreased over time. Teff percentages decreased more significantly resulting in a halving of the Teff/Treg ratio two years later. Furthermore, markers of Treg immunosuppressive function such as CTLA4, Helios, CD28, CD45RA and 41bb decreased over time. Cytokines did not change significantly over time.</p><p><strong>Conclusions: </strong>The presented data suggest that arthritis persists almost seven years after chikungunya infection in some patients with waning Teff and Treg numbers and activation markers over time. Treg activation may be a promising therapeutic target for further investigation.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"6 2","pages":"64-75"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11172407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141319169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyamines: Key Players in Immunometabolism and Immune Regulation.","authors":"Shanmuga S Mahalingam, Pushpa Pandiyan","doi":"10.33696/immunology.6.206","DOIUrl":"10.33696/immunology.6.206","url":null,"abstract":"<p><p>Polyamines are small organic molecules ubiquitously present in all living organisms and function as crucial regulators of biological processes ranging from fundamental cellular metabolism to immune regulation. Dysregulation of polyamine metabolism has been implicated in numerous diseases, including neurodegenerative disorders, inflammatory conditions, autoimmune diseases, and cancer. This review provides an overview of pathophysiology of these conditions, highlighting polyamines' role in immunometabolic alterations in the context of immune regulation. Exploring the intricate mechanisms of polyamine metabolism holds promise for advancing our understanding of disease processes and developing potential innovative therapeutic interventions.</p>","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"6 5","pages":"196-208"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11666123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142883763","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Can Vaccines Stop Cancer Before It Starts? Assessing the Promise of Prophylactic Immunization Against High-Risk Preneoplastic Lesions","authors":"T. Addissouky, Ibrahim El Tantawy El Sayed, Majeed M. A. Ali, Yuliang Wang, Ayman El Baz, Ahmed A. Khalil, N. Elarabany","doi":"10.33696/immunology.5.178","DOIUrl":"https://doi.org/10.33696/immunology.5.178","url":null,"abstract":"Background: Cancer remains a leading cause of mortality with modest declines, highlighting the need for more efficacious prevention strategies like early immunological intervention against premalignant disease. Main body of abstract: Oncogenic viruses demonstrate prophylactic vaccines can successfully reduce malignancy by blocking precipitating infections. However, most cancers lack viral etiology, requiring novel approaches targeting sporadic precancerous states to enable early immunoprevention. Preneoplastic tissues exhibit biological changes making them appealing targets for stimulating immune surveillance before additional mutations cause unconstrained proliferation. High-risk precancers also provide sources of dysregulated self-antigens. Yet challenges exist in lesion identification, overcoming tolerance, and avoiding inflammation potentially worsening progression. Multidisciplinary insights into precancer immunology, predictive biomarkers, antigen discovery, and combinatorial vaccination strategies are illuminating rational vaccine design. Despite obstacles, prophylactic immunization against early dysplastic changes holds disruptive potential if key steps advance this approach. Elucidating preneoplasia immunobiology and progression risk modeling will be critical to guide productive immune targeting while mitigating immunotherapy hazards. Thoughtful translation could eventually shift paradigms by priming immunosurveillance against peak vulnerability lesions. Short Conclusion: Advancements in precancer vaccines may profoundly expand prevention horizons. Cautious immune targeting of premalignant states could intercept progression toward widely disseminated malignancies. This warrants methodical efforts to unravel the promise of thwarting lethal cancers before they start.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"234 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139212732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Type 1 Diabetes: A Disorder of the Exocrine and Endocrine Pancreas","authors":"Brittany S. Bruggeman, Desmond A. Schatz","doi":"10.33696/immunology.5.177","DOIUrl":"https://doi.org/10.33696/immunology.5.177","url":null,"abstract":"Type 1 diabetes has historically been described as an endocrine (β-cell) specific autoimmune disease. However, a substantial reduction (20-50%) in pancreas organ size and subclinical to symptomatic exocrine pancreatic insufficiency are present at diagnosis and may begin even prior to the development of islet autoimmunity. The mechanisms of exocrine loss in type 1 diabetes are not well understood, but leading hypotheses include developmental defects, β-cell loss resulting in exocrine atrophy, or autoimmune or inflammatory destruction of exocrine cells. Inflammatory changes including acute and chronic pancreatitis, exocrine T cell infiltration and classical complement activation, and serum exocrine autoantibodies within type 1 diabetes individuals suggest that an autoimmune or inflammatory process may contribute to exocrine pancreatic dysfunction. Exocrine pancreas atrophy primarily occurs prior to the onset of clinical disease. Indeed, recent work implicates exocrine-specific alterations in gene and protein expression as key in type 1 diabetes development. Measures of exocrine size and function could be useful additions in the prediction of disease onset and in identifying potential therapeutic responders to disease therapies, however, this is an underdeveloped area of research. Additionally, exocrine pancreatic insufficiency is underdiagnosed in individuals with type 1 diabetes and individualized treatment protocols are lacking. Much work remains to be done in this area, but we can definitively say that type 1 diabetes is a disorder of both the exocrine and endocrine pancreas likely from the start.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"904 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139242226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Commentary on Updated Insight into the Role of Th2-Associated Immunity in Systemic Lupus Erythematosus","authors":"Xinyue Hou, Jinjin Chu, Shuhao Liu, Shuyu Jin, Jiamei Sun, Hui Wang, Haibo Li, Wei Liu, Chunxiang Chai, Sue Zhang, Donghua Xu","doi":"10.33696/immunology.5.176","DOIUrl":"https://doi.org/10.33696/immunology.5.176","url":null,"abstract":"Systemic lupus erythematosus (SLE) is a common autoimmune disease caused by multiple factors. The pathogenesis of SLE remains unclear. Helper T cell 2 (Th2 cell) is essential for humoral immunity, which participates in regulating type 2 immune response by producing typical cytokines of interleukin (IL)-4, IL-5, and IL-13. It is well known that Th2-associated immunity plays a vital role in autoimmune diseases, including SLE. However, current progress on the role and potential mechanism of Th2-associated immunity in SLE remains largely unknown. The work by Wang et al. have provided an in-depth association of Th2-associated immunity with SLE and the clinical application perspectives. We provide a more comprehensive and up-to-date commentary on Th2-associated immunity in regulating SLE to explore new therapeutic targets.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"23 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136034771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antimicrobial Prophylaxis in Lymphoma by Chemotherapy Regimen","authors":"Kamen W. Kossow, Joseph G. Bennett, Marc S Hoffmann","doi":"10.33696/immunology.5.175","DOIUrl":"https://doi.org/10.33696/immunology.5.175","url":null,"abstract":"Treatment of lymphomas involves a wide variety of chemotherapy, immunotherapy, and targeted-agents tailored to disease biology and patient characteristics. Each of these regimens carry their own risk of opportunistic infections in an immunocompromised population. In addition to the treatment associated immunosuppression, lymphoma itself is immunosuppressive. Lymphoma associated immunosuppression is secondary to increased production of abnormal lymphocytes resulting in decreased production of normally functioning lymphocytes. Additionally, lymphoma cells induce both humoral and cellular immunosuppression through effects on numerous cytokines, T-cells, myeloid-derived suppressor cells, and macrophages. Clinical trials, patient co-morbidities, and institutional preferences all play a role in determining the preferred antimicrobial prophylaxis. While there is a paucity of data on systematic reviews and guidelines for standardized chemotherapy regimens in lymphoma patients, the efficacy and recommendations for antimicrobial prophylaxis in specific chemotherapy regimens for lymphoma has not been fully reviewed. According to the National Comprehensive Cancer Network, lymphoma is generally regarded as an ‘intermediate risk’ cancer with regards to overall infection risk. This results in discordance between research data and clinical practice. This is reiterated in the SIGNIFICANT trial which reported that while guidelines previously advised against fluoroquinolone prophylaxis in lymphoma and solid cancers, a survey of 3,600 physicians revealed that 45% routinely used fluoroquinolone prophylaxis despite these recommendations. This review article analyzes numerous research studies with summarization of findings and antimicrobial prophylaxis recommendations based on specific lymphoma chemotherapy regimens. With regards to each specific chemotherapy regimen assessed, indications for antibacterial, anti-viral, anti-fungal, and Pneumocystis jiroveci pneumonia (PJP) prophylaxis were determined for each regimen. The degree of immunosuppression and the necessary prophylaxis varies across different regimens and lymphoma subgroups; and thus, an individualized approach is necessary to optimize the supportive care during lymphoma treatment.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"76 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136032641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}