Pub Date : 2021-10-10DOI: 10.33696/immunology.3.105
{"title":"Novel Combination Treatments for AML","authors":"","doi":"10.33696/immunology.3.105","DOIUrl":"https://doi.org/10.33696/immunology.3.105","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46340556","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}
Pub Date : 2021-09-12DOI: 10.33696/immunology.4.148
Ji Ma, Xianping Ma, Rang Wang, Fang Li, T. Hu, Huashan Yi
for Detection of the NS4
用于检测NS4
{"title":"Establishment of an Indirect Enzyme-linked Immunosorbent Assay for Detection of the NS4 Protein of Bluetongue Virus","authors":"Ji Ma, Xianping Ma, Rang Wang, Fang Li, T. Hu, Huashan Yi","doi":"10.33696/immunology.4.148","DOIUrl":"https://doi.org/10.33696/immunology.4.148","url":null,"abstract":"for Detection of the NS4","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46865439","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}
Pub Date : 2021-09-01DOI: 10.33696/immunology.3.100
W. L. Gluck, Wesley M. Smith, S. P. Callahan, Robert A. Brevetta, A. Stenbit, J. Martin, Anna V. Blenda, S. Arce, W. Edenfield
Observations early in the viral pandemic of 2020 noted the resemblance between severe coronavirus disease 2019 (COVID-19) infection and the hypercytokinemic state of secondary hemophagocytic lymphohistiocytosis (sHLH) [1]. Conti and colleagues [2] have outlined the binding of COVID-19 to the Toll-like receptor with subsequent cytokine driven fever and pneumonitis, while in Kenderian’s [3] murine model of CRS, ruxolitinib abrogated the development of cytokine excess. Cao [4] reported faster clinical recovery with JAK inhibition and Capochiani’s RESPIRE trial reported an 89% overall response rate (ORR) with ruxolitinib therapy [5]. Discordant findings regarding JAK inhibition have been reported on the superiority of baricitinib plus remdesivir over remdesivir alone in shortening recovery times in hospitalized patients [6] while the randomized RUXCOVID trial failed to impact severe complications of the disease by adding ruxolitinib to standard of care [7]. Other groups [8,9] have reported inflammatory cytokine profiles along with evidence that elevated IL-6 and TNFα are strong predictors of disease severity and survival. While cytokine excess could be an epiphenomenal surrogate for another process, therapeutic strategies have evolved around addressing the excessive cytokine levels complicating a significant fraction of COVID-19 patients.
{"title":"Efficacy of Therapeutic Plasma Exchange Alone or in Combination with Ruxolitinib for the Treatment of Penn Class 3 and 4 Cytokine Release Syndrome Complicating COVID-19","authors":"W. L. Gluck, Wesley M. Smith, S. P. Callahan, Robert A. Brevetta, A. Stenbit, J. Martin, Anna V. Blenda, S. Arce, W. Edenfield","doi":"10.33696/immunology.3.100","DOIUrl":"https://doi.org/10.33696/immunology.3.100","url":null,"abstract":"Observations early in the viral pandemic of 2020 noted the resemblance between severe coronavirus disease 2019 (COVID-19) infection and the hypercytokinemic state of secondary hemophagocytic lymphohistiocytosis (sHLH) [1]. Conti and colleagues [2] have outlined the binding of COVID-19 to the Toll-like receptor with subsequent cytokine driven fever and pneumonitis, while in Kenderian’s [3] murine model of CRS, ruxolitinib abrogated the development of cytokine excess. Cao [4] reported faster clinical recovery with JAK inhibition and Capochiani’s RESPIRE trial reported an 89% overall response rate (ORR) with ruxolitinib therapy [5]. Discordant findings regarding JAK inhibition have been reported on the superiority of baricitinib plus remdesivir over remdesivir alone in shortening recovery times in hospitalized patients [6] while the randomized RUXCOVID trial failed to impact severe complications of the disease by adding ruxolitinib to standard of care [7]. Other groups [8,9] have reported inflammatory cytokine profiles along with evidence that elevated IL-6 and TNFα are strong predictors of disease severity and survival. While cytokine excess could be an epiphenomenal surrogate for another process, therapeutic strategies have evolved around addressing the excessive cytokine levels complicating a significant fraction of COVID-19 patients.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46372997","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}
Pub Date : 2021-09-01DOI: 10.33696/immunology.3.104
Nicolas Vitale
{"title":"Body Mass Index and Covi d-19: Likely Causes for Obesity and Undernutrition Correlation with Disease Severity","authors":"Nicolas Vitale","doi":"10.33696/immunology.3.104","DOIUrl":"https://doi.org/10.33696/immunology.3.104","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44507618","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}
Pub Date : 2021-07-16DOI: 10.33696/immunology.3.102
K. Pusic, L. Won, R. P. Kraig, A. Pusic
Environmental enrichment produces beneficial effects in the brain at genetic, molecular, cellular and behavior levels, and has long been studied as a therapeutic intervention for a wide variety of neurological disorders. However, the complexity of applying a robust environmental enrichment paradigm makes clinical use difficult. Accordingly, there has been increased interest in developing environmental enrichment mimetics, also known as enviromimetics. Here we review the benefits of environmental enrichment for migraine treatment, and discuss the potential of using extracellular vesicles derived from interferon gamma-stimulated dendritic cells as an effective mimetic.
{"title":"Environmental Enrichment and Its Benefits for Migraine: Dendritic Cell Extracellular Vesicles as an Effective Mimetic","authors":"K. Pusic, L. Won, R. P. Kraig, A. Pusic","doi":"10.33696/immunology.3.102","DOIUrl":"https://doi.org/10.33696/immunology.3.102","url":null,"abstract":"Environmental enrichment produces beneficial effects in the brain at genetic, molecular, cellular and behavior levels, and has long been studied as a therapeutic intervention for a wide variety of neurological disorders. However, the complexity of applying a robust environmental enrichment paradigm makes clinical use difficult. Accordingly, there has been increased interest in developing environmental enrichment mimetics, also known as enviromimetics. Here we review the benefits of environmental enrichment for migraine treatment, and discuss the potential of using extracellular vesicles derived from interferon gamma-stimulated dendritic cells as an effective mimetic.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 1","pages":"215 - 225"},"PeriodicalIF":0.0,"publicationDate":"2021-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43949540","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}
Pub Date : 2021-06-30DOI: 10.33696/immunology.3.095
Sardar Sindhu, R. Ahmad, F. Al-Mulla
The coronavirus disease (COVID)-19 pandemic has profoundly devastated human health and wellbeing all over the world, along with colossal setback to global economy in terms of soaring new infections, hospitalizations, ICU admissions, work losses, closures of businesses and institutions, bankruptcies, and precautionary measures involving social distancing, hygiene, and travel restrictions across the globe. COVID-19 was declared by the World Health Organization (WHO) as a public health emergency of international concern in January 2020, and then as a pandemic in March 2020. There are over 154.64 million confirmed coronavirus infections and more than 3.23 million deaths reported to the WHO globally until date (as of 11:21 a.m. CEST, 6 May, 2021) [1]. The disease is caused by a zoonotic positive-sense single-stranded ssRNA virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is known to have four structural proteins: spike (S), envelope (E), membrane (M), and nucleocapsid (N), with close genetic similarity to bat coronaviruses. The global science initiative source called “Global Initiative on Sharing Avian Influenza Data” (GISAID) has reported seven SARS-CoV-2 clades as G, GH, GR, L, O, S, and V [2].
{"title":"Increased Binding Affinity of Furin to D614G Mutant S-glycoprotein May Augment Infectivity of the Predominating SARS-CoV-2 Variant","authors":"Sardar Sindhu, R. Ahmad, F. Al-Mulla","doi":"10.33696/immunology.3.095","DOIUrl":"https://doi.org/10.33696/immunology.3.095","url":null,"abstract":"The coronavirus disease (COVID)-19 pandemic has profoundly devastated human health and wellbeing all over the world, along with colossal setback to global economy in terms of soaring new infections, hospitalizations, ICU admissions, work losses, closures of businesses and institutions, bankruptcies, and precautionary measures involving social distancing, hygiene, and travel restrictions across the globe. COVID-19 was declared by the World Health Organization (WHO) as a public health emergency of international concern in January 2020, and then as a pandemic in March 2020. There are over 154.64 million confirmed coronavirus infections and more than 3.23 million deaths reported to the WHO globally until date (as of 11:21 a.m. CEST, 6 May, 2021) [1]. The disease is caused by a zoonotic positive-sense single-stranded ssRNA virus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is known to have four structural proteins: spike (S), envelope (E), membrane (M), and nucleocapsid (N), with close genetic similarity to bat coronaviruses. The global science initiative source called “Global Initiative on Sharing Avian Influenza Data” (GISAID) has reported seven SARS-CoV-2 clades as G, GH, GR, L, O, S, and V [2].","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47435250","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}
Pub Date : 2021-06-30DOI: 10.33696/immunology.3.093
Seitz Tamara, Kelani Hasan, Wenisch Christoph, Laferl Hermann
The ongoing SARS-CoV-2 pandemic led to a high number of deaths worldwide as well as an overload of healthcare systems and an economic collapse. One of the reasons can be attributed to the lack of knowledge about the duration of infectivity at the beginning of the pandemic, resulting in hospital isolation of patients and absence periods of employees. In particular, the absence of healthcare workers placed an unprecedented strain on healthcare systems. Thereupon, at least one negative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) test from a respiratory specimen was required for ending isolation [1]. However, prolonged SARS-CoV-2 RNA shedding was reported for several weeks following infection [2-9]. The aim of this paper is to discuss the current state of knowledge about duration of SARS-CoV-2 infectivity and necessity of isolation.
{"title":"Duration of SARS-CoV-2 Infectivity","authors":"Seitz Tamara, Kelani Hasan, Wenisch Christoph, Laferl Hermann","doi":"10.33696/immunology.3.093","DOIUrl":"https://doi.org/10.33696/immunology.3.093","url":null,"abstract":"The ongoing SARS-CoV-2 pandemic led to a high number of deaths worldwide as well as an overload of healthcare systems and an economic collapse. One of the reasons can be attributed to the lack of knowledge about the duration of infectivity at the beginning of the pandemic, resulting in hospital isolation of patients and absence periods of employees. In particular, the absence of healthcare workers placed an unprecedented strain on healthcare systems. Thereupon, at least one negative real-time reverse transcriptase-polymerase chain reaction (RT-PCR) test from a respiratory specimen was required for ending isolation [1]. However, prolonged SARS-CoV-2 RNA shedding was reported for several weeks following infection [2-9]. The aim of this paper is to discuss the current state of knowledge about duration of SARS-CoV-2 infectivity and necessity of isolation.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43153880","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}
Pub Date : 2021-06-30DOI: 10.33696/immunology.3.097
S. Wilz
SARS-Cov-2 is the virus that causes the disease COVID-19. The disease has led to the worst worldwide health crisis in 100 years. While many patients remain asymptomatic, most patients develop a mild respiratory infection. Symptoms include cough, fever and chills, fatigue and body aches, headache and loss of the sense of taste or smell. However, a proportion of patients develop severe disease. Symptoms of severe disease include higher fever, hypoxia and respiratory distress, leading to hospitalization, and sometimes the need for mechanical ventilation and ultimately death [1].
{"title":"The Variable Immune Response to SARS-CoV-2 Infection and Potential Treatment with Combination IL-15 and IL-21","authors":"S. Wilz","doi":"10.33696/immunology.3.097","DOIUrl":"https://doi.org/10.33696/immunology.3.097","url":null,"abstract":"SARS-Cov-2 is the virus that causes the disease COVID-19. The disease has led to the worst worldwide health crisis in 100 years. While many patients remain asymptomatic, most patients develop a mild respiratory infection. Symptoms include cough, fever and chills, fatigue and body aches, headache and loss of the sense of taste or smell. However, a proportion of patients develop severe disease. Symptoms of severe disease include higher fever, hypoxia and respiratory distress, leading to hospitalization, and sometimes the need for mechanical ventilation and ultimately death [1].","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48842713","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}
Pub Date : 2021-06-30DOI: 10.33696/immunology.3.092
K. Fiedorowicz, M. Kurpisz
Recently, stem/progenitor cell therapies have been intensively pursued. An increasing body of evidence has shown the promising results with respect to transient recovery of cardiac function in a variety of animal models with the use of stem cells interventions. Unfortunately, it is still not possible to fully and functionally replace the irreversibly damaged heart tissue. Moreover, the optimal cell population for organ regeneration has not been yet identified. Prior to possible optimization strategy to find ideal cell candidates, we shall keep in mind that successful organ regeneration is a very complex process. Within such development, the administered cells require proper homing and a graft retention that would be next followed by the cell electromechanical coupling with recipient organ cardiomyocytes [1]. Recent advances in molecular imaging techniques opened many platforms that would allow tracking of transplanted cells and optimization of delivery protocols with their subsequent multimodal imaging [2].
{"title":"Promoter Reporter Systems for Imaging of Cells Transplanted into Post-infarcted Heart","authors":"K. Fiedorowicz, M. Kurpisz","doi":"10.33696/immunology.3.092","DOIUrl":"https://doi.org/10.33696/immunology.3.092","url":null,"abstract":"Recently, stem/progenitor cell therapies have been intensively pursued. An increasing body of evidence has shown the promising results with respect to transient recovery of cardiac function in a variety of animal models with the use of stem cells interventions. Unfortunately, it is still not possible to fully and functionally replace the irreversibly damaged heart tissue. Moreover, the optimal cell population for organ regeneration has not been yet identified. Prior to possible optimization strategy to find ideal cell candidates, we shall keep in mind that successful organ regeneration is a very complex process. Within such development, the administered cells require proper homing and a graft retention that would be next followed by the cell electromechanical coupling with recipient organ cardiomyocytes [1]. Recent advances in molecular imaging techniques opened many platforms that would allow tracking of transplanted cells and optimization of delivery protocols with their subsequent multimodal imaging [2].","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49397988","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}
Pub Date : 2021-01-01DOI: 10.33696/immunology.3.082
Joseph B Moore, Marcin Wysoczynski
Myocardial infarction (MI) due to coronary artery stenosis compromises vascular endothelial integrity and increases vascular permeability [1,2]. Concurrently, ensuing myocardial tissue death and necrosis results in the release of danger associated molecular patterns (DAMPs), cytokines, chemokines, bioactive lipids, as well as activation of the complement cascade [1-3]. Collectively, these events direct a pronounced and immediate immune response, which includes the recruitment of peripheral blood leukocytes to the site of injury [2,3]. These infiltrating neutrophils are primarily responsible for the clearance of necrotic tissue and cellular debris in ischemic regions via their release of a host of proteolytic enzymes/proteases. While this constitutes a necessary early step in the myocardial repair process at the site of injury, neutrophil-derived reactive oxygen species (ROS) and pro-inflammatory cytokines/chemokines can contribute to collateral damage of surviving myocardium and amplify tissue injury [3,4]. Nevertheless, neutrophils are imperative for proper infarct healing as their depletion prior to MI leads to a dysregulated immune response, excessive scarring, and impaired ventricular function [5]. Within days of an MI, neutrophils undergo cell death and disappear from infarcted tissue [3,4]. Recruitment of neutrophils is followed by two waves of monocyte infiltration. First, early recruitment of Ly6CHigh monocytes expressing pro-inflammatory cytokines, and second, infiltration of Ly6CLow monocytes with pro-resolving and pro-reparative function [3,6,7]. Ly6CHigh monocyte migration is driven by the presence of tissue CCL2 chemokine gradients and their interaction with their cognate receptor, CCR2 [8]—a group of monocytes that are principally sourced from bone marrow and spleen. Subsequently, these monocytes differentiate into Ly6CLowCCR2High macrophages, known as monocyte-derived macrophages [9,10]. These are distinct from Ly6CLowCCR2Low macrophages deposited in the myocardial tissue during embryonic development [11-13]. Both macrophage populations (Ly6CLowCCR2High and Ly6CLowCCR2Low) contribute to myocardial repair by clearance of dead tissue via efferocytosis and production of pro-reparative and pro-resolving mediators. Macrophagederived cytokines play an essential role in the proliferation and activation of cardiac fibroblasts (fibroblast-myofibroblast conversion) that deposit collagen at the site of injury. This process of scar formation fulfills the immediate need to preserve the structural integrity
{"title":"Immunomodulatory Effects of Cell Therapy after Myocardial Infarction.","authors":"Joseph B Moore, Marcin Wysoczynski","doi":"10.33696/immunology.3.082","DOIUrl":"https://doi.org/10.33696/immunology.3.082","url":null,"abstract":"Myocardial infarction (MI) due to coronary artery stenosis compromises vascular endothelial integrity and increases vascular permeability [1,2]. Concurrently, ensuing myocardial tissue death and necrosis results in the release of danger associated molecular patterns (DAMPs), cytokines, chemokines, bioactive lipids, as well as activation of the complement cascade [1-3]. Collectively, these events direct a pronounced and immediate immune response, which includes the recruitment of peripheral blood leukocytes to the site of injury [2,3]. These infiltrating neutrophils are primarily responsible for the clearance of necrotic tissue and cellular debris in ischemic regions via their release of a host of proteolytic enzymes/proteases. While this constitutes a necessary early step in the myocardial repair process at the site of injury, neutrophil-derived reactive oxygen species (ROS) and pro-inflammatory cytokines/chemokines can contribute to collateral damage of surviving myocardium and amplify tissue injury [3,4]. Nevertheless, neutrophils are imperative for proper infarct healing as their depletion prior to MI leads to a dysregulated immune response, excessive scarring, and impaired ventricular function [5]. Within days of an MI, neutrophils undergo cell death and disappear from infarcted tissue [3,4]. Recruitment of neutrophils is followed by two waves of monocyte infiltration. First, early recruitment of Ly6CHigh monocytes expressing pro-inflammatory cytokines, and second, infiltration of Ly6CLow monocytes with pro-resolving and pro-reparative function [3,6,7]. Ly6CHigh monocyte migration is driven by the presence of tissue CCL2 chemokine gradients and their interaction with their cognate receptor, CCR2 [8]—a group of monocytes that are principally sourced from bone marrow and spleen. Subsequently, these monocytes differentiate into Ly6CLowCCR2High macrophages, known as monocyte-derived macrophages [9,10]. These are distinct from Ly6CLowCCR2Low macrophages deposited in the myocardial tissue during embryonic development [11-13]. Both macrophage populations (Ly6CLowCCR2High and Ly6CLowCCR2Low) contribute to myocardial repair by clearance of dead tissue via efferocytosis and production of pro-reparative and pro-resolving mediators. Macrophagederived cytokines play an essential role in the proliferation and activation of cardiac fibroblasts (fibroblast-myofibroblast conversion) that deposit collagen at the site of injury. This process of scar formation fulfills the immediate need to preserve the structural integrity","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"3 2","pages":"85-90"},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8098722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38889821","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}
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