Pub Date : 2022-12-31DOI: 10.33696/immunology.4.154
{"title":"Is Omicron Variant of COVID-19 Threatening Health Like Other Variants?","authors":"","doi":"10.33696/immunology.4.154","DOIUrl":"https://doi.org/10.33696/immunology.4.154","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44318150","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 : 2022-12-31DOI: 10.33696/immunology.4.153
{"title":"Vγ2+ γδ T Cells and Their Regulatory Potential in Skin Allograft Survival","authors":"","doi":"10.33696/immunology.4.153","DOIUrl":"https://doi.org/10.33696/immunology.4.153","url":null,"abstract":"","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48686547","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 : 2022-12-09DOI: 10.33696/immunology.4.149
Katherine E. Kaugars, Angelo R. Retamal-Diaz, Anna Paula de Oliveira, P. González, W. Jacobs
Protective
保护
{"title":"Going above and Beyond: Using an Attenuated Herpes Viral Vaccine Vector to Elicit Protective Immune Responses Through Neutralizing and Non-neutralizing Functions of Antibodies","authors":"Katherine E. Kaugars, Angelo R. Retamal-Diaz, Anna Paula de Oliveira, P. González, W. Jacobs","doi":"10.33696/immunology.4.149","DOIUrl":"https://doi.org/10.33696/immunology.4.149","url":null,"abstract":"Protective","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41400616","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 : 2022-12-09DOI: 10.33696/immunology.4.147
L. Bramasole, S. Meiners
A
英语字母表的第1个字母
{"title":"Profiling Proteasome Activities in Peripheral Blood – A Novel Biomarker Approach","authors":"L. Bramasole, S. Meiners","doi":"10.33696/immunology.4.147","DOIUrl":"https://doi.org/10.33696/immunology.4.147","url":null,"abstract":"A","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43151779","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":"Sialyllactose Prevents Cartilage Damages via M0 Macrophage Maintenance in Yucatan Mini-Pig Osteoarthritis Model","authors":"Kyung-Tai Kim, Young-Kyu Kim, Mi-Jin Yang, Min-young Kim, Lila Kim, J. Hwang","doi":"10.33696/immunology.4.145","DOIUrl":"https://doi.org/10.33696/immunology.4.145","url":null,"abstract":". Sialyllactose Prevents Cartilage Damages via M0 Macrophage Maintenance in Yucatan Mini-Pig Osteoarthritis Model. J Cell Immunol. 2022;4(5):158-166.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45669971","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 : 2022-09-29DOI: 10.33696/immunology.4.141
Andrew Cinquina, Jia Feng, Hongyu Zhang, Yupo Ma
The introduction of chimeric antigen receptor (CAR) immunotherapy has been revolutionary in the treatment of hematological malignancies [1]. Remarkable success has been achieved in the clinical treatment of B-cell malignancies through the use of CD19 CARs [2-7]. However, translation of CAR therapy for T-cell malignancies has been more difficult for several reasons. As the CAR cells predominantly used are T cells, a CAR T cell manufactured to target malignant T cells using T-cell markers is at risk for fratricide. This would prevent the expansion of the CAR T cell population necessary for proper tumor eradication. Additionally, as both malignant and non-malignant express these T-cell markers, there is concern that a T-cell-directed CAR cell would lead to T-cell deficiency and subsequent opportunistic infections.
{"title":"CAR Therapy for T-cell Malignancies","authors":"Andrew Cinquina, Jia Feng, Hongyu Zhang, Yupo Ma","doi":"10.33696/immunology.4.141","DOIUrl":"https://doi.org/10.33696/immunology.4.141","url":null,"abstract":"The introduction of chimeric antigen receptor (CAR) immunotherapy has been revolutionary in the treatment of hematological malignancies [1]. Remarkable success has been achieved in the clinical treatment of B-cell malignancies through the use of CD19 CARs [2-7]. However, translation of CAR therapy for T-cell malignancies has been more difficult for several reasons. As the CAR cells predominantly used are T cells, a CAR T cell manufactured to target malignant T cells using T-cell markers is at risk for fratricide. This would prevent the expansion of the CAR T cell population necessary for proper tumor eradication. Additionally, as both malignant and non-malignant express these T-cell markers, there is concern that a T-cell-directed CAR cell would lead to T-cell deficiency and subsequent opportunistic infections.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45439154","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 : 2022-09-28DOI: 10.33696/immunology.4.144
P. Gaudeaux, R. D. Moirangthem, Pauline Rault, H. Sadek, F. Carbone, Marieke, Lavaert, A. Joshi, T. Taghon, I. André, O. Nègre, T. Soheili
Manufacturing of Human T-lymphoid Progenitors from Two Different Hematopoietic Stem Cell Sources and Perspective for New Immunotherapies. Abstract The adaptive immune system depends on the efficient response of lymphocytes, protecting the organism from infection or malignant diseases. T-cell immunodeficiency, innate or acquired, put the patient at risk for developing opportunistic infections and cancers. We previously described a novel approach to overcome the major limitations of T-cell immunotherapy and hematopoietic stem cell transplant (HSCT) by transplanting human T-lymphoid progenitors (HTLP), with the aim to achieve shortened immune reconstitution and fully functional naïve T-cell repertoire in immunodeficient or immunocompromised patients. By complementing our DL4-based cell culture with TNFα we developed and scaled-up clinical strategies involving hematopoietic stem and progenitor cells (HSPC) differentiated into T-lymphoid progenitors. We discuss here recent advances made in the characterization of different cell sources used as starting materials for T-lymphoid progenitors manufacturing, as well as gene modification of these cells, highlighting new perspectives for the development of therapeutical strategies.
{"title":"Manufacturing of Human T-lymphoid Progenitors from Two Different Hematopoietic Stem Cell Sources and Perspective for New Immunotherapies","authors":"P. Gaudeaux, R. D. Moirangthem, Pauline Rault, H. Sadek, F. Carbone, Marieke, Lavaert, A. Joshi, T. Taghon, I. André, O. Nègre, T. Soheili","doi":"10.33696/immunology.4.144","DOIUrl":"https://doi.org/10.33696/immunology.4.144","url":null,"abstract":"Manufacturing of Human T-lymphoid Progenitors from Two Different Hematopoietic Stem Cell Sources and Perspective for New Immunotherapies. Abstract The adaptive immune system depends on the efficient response of lymphocytes, protecting the organism from infection or malignant diseases. T-cell immunodeficiency, innate or acquired, put the patient at risk for developing opportunistic infections and cancers. We previously described a novel approach to overcome the major limitations of T-cell immunotherapy and hematopoietic stem cell transplant (HSCT) by transplanting human T-lymphoid progenitors (HTLP), with the aim to achieve shortened immune reconstitution and fully functional naïve T-cell repertoire in immunodeficient or immunocompromised patients. By complementing our DL4-based cell culture with TNFα we developed and scaled-up clinical strategies involving hematopoietic stem and progenitor cells (HSPC) differentiated into T-lymphoid progenitors. We discuss here recent advances made in the characterization of different cell sources used as starting materials for T-lymphoid progenitors manufacturing, as well as gene modification of these cells, highlighting new perspectives for the development of therapeutical strategies.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46813582","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 : 2022-09-28DOI: 10.33696/immunology.4.143
Janneke Ruinemans-Koerts, Monique van Uum-Otters, Don van Baar, J. V. Neerven, Judit Wesseling
These false-positive outcomes can be a consequence of IgE binding to an epitope in the food protein used in these tests that may be inactivated after consumption due to food processing or digestion. Alternatively, the BAT protocol can be less sensitive to interference of inhibiting factors such as allergen specific IgG4 and IgA produced during tolerance development due to e.g. consumption of trace amounts of allergen. However, the influence of inhibiting factors can be detected when allergens are pre-incubated with serum, allowing IgG/IgA binding to allergens, before addition to basophils, as shown by the fact that a decrease in basophil sensitivity to Ara h2 predicted sustained unresponsiveness after peanut oral immunotherapy [4]. In our recent study on the indirect BAT for the diagnosis of peanut allergy we observed a few false-positive BAT outcomes [3]. We hypothesized that these false-positive BAT outcomes might among others be due to inhibiting factors, like IgG4 and IgA, produced during natural tolerance development which effect on basophil activation can’t be adequately detected in the regular BAT protocol. Therefore, we re-analysed with a modified indirect BAT protocol (called “BA(blocking antibodies)-BAT”) the serum samples (n=3) from our indirect BAT peanut study with a false-positive BAT Ara h2 or Ara h6 outcome.
这些假阳性结果可能是这些测试中使用的食物蛋白中的IgE与表位结合的结果，该表位可能在食用后由于食物加工或消化而失活。另外，由于摄入了微量的过敏原，BAT方案可能对诸如在耐受性发展过程中产生的过敏原特异性IgG4和IgA等抑制因子的干扰不太敏感。然而，当将过敏原与血清预先孵育，允许IgG/IgA与过敏原结合，然后再加入嗜碱性粒细胞时，可以检测到抑制因子的影响，如嗜碱性粒细胞对Ara h2敏感性的降低预测花生口服免疫治疗[4]后持续无反应性。在我们最近对间接BAT诊断花生过敏的研究中，我们观察到一些BAT假阳性结果bbb。我们假设这些假阳性BAT结果可能是由于在自然耐受性发育过程中产生的抑制因子，如IgG4和IgA，这些抑制因子对嗜碱性粒细胞激活的影响在常规BAT协议中无法充分检测到。因此，我们使用改进的间接BAT方案(称为“BA(阻断抗体)-BAT”)重新分析了间接BAT花生研究中含有假阳性BAT Ara h2或Ara h6结果的血清样本(n=3)。
{"title":"Improvement of the Specificity of the Indirect BAT for the Diagnosis of Peanut Allergy; the BA(Blocking Antibodies)-BAT","authors":"Janneke Ruinemans-Koerts, Monique van Uum-Otters, Don van Baar, J. V. Neerven, Judit Wesseling","doi":"10.33696/immunology.4.143","DOIUrl":"https://doi.org/10.33696/immunology.4.143","url":null,"abstract":"These false-positive outcomes can be a consequence of IgE binding to an epitope in the food protein used in these tests that may be inactivated after consumption due to food processing or digestion. Alternatively, the BAT protocol can be less sensitive to interference of inhibiting factors such as allergen specific IgG4 and IgA produced during tolerance development due to e.g. consumption of trace amounts of allergen. However, the influence of inhibiting factors can be detected when allergens are pre-incubated with serum, allowing IgG/IgA binding to allergens, before addition to basophils, as shown by the fact that a decrease in basophil sensitivity to Ara h2 predicted sustained unresponsiveness after peanut oral immunotherapy [4]. In our recent study on the indirect BAT for the diagnosis of peanut allergy we observed a few false-positive BAT outcomes [3]. We hypothesized that these false-positive BAT outcomes might among others be due to inhibiting factors, like IgG4 and IgA, produced during natural tolerance development which effect on basophil activation can’t be adequately detected in the regular BAT protocol. Therefore, we re-analysed with a modified indirect BAT protocol (called “BA(blocking antibodies)-BAT”) the serum samples (n=3) from our indirect BAT peanut study with a false-positive BAT Ara h2 or Ara h6 outcome.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44749271","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 : 2022-09-28DOI: 10.33696/immunology.4.140
Jens C. Kleiner, Christian F. Krebs
For a long time Th1 cells were considered the key players in the induction of inflammation and progression of disease in autoimmune diseases. With the discovery of IL-17-producing CD4 + T cells (Th17) being abundant at inflammation sites, this soon changed. Investigating this new T helper subset, it became clear that in comparison to Th1 and Th2 cells, Th17 cells have an increased tendency to change their phenotype and therefore become either more pathogenic or immunoregulatory. This makes them an attractive target for therapeutic interventions. As plasticity of Th17 cells differs between different autoimmune diseases, understanding its drivers is complex. This review focusses on the role of plasticity within Th17 cells in induction, aggravation and resolution of disease and points out IL-23 as a potential key player in controlling Th17 fate. Finally, current treatments targeting IL-23 and Th17 plasticity are highlighted and an outlook on future therapeutics is given.
{"title":"Persistence, Pathogenicity and Plasticity: The Role of IL-23 in Th17 Fate","authors":"Jens C. Kleiner, Christian F. Krebs","doi":"10.33696/immunology.4.140","DOIUrl":"https://doi.org/10.33696/immunology.4.140","url":null,"abstract":"For a long time Th1 cells were considered the key players in the induction of inflammation and progression of disease in autoimmune diseases. With the discovery of IL-17-producing CD4 + T cells (Th17) being abundant at inflammation sites, this soon changed. Investigating this new T helper subset, it became clear that in comparison to Th1 and Th2 cells, Th17 cells have an increased tendency to change their phenotype and therefore become either more pathogenic or immunoregulatory. This makes them an attractive target for therapeutic interventions. As plasticity of Th17 cells differs between different autoimmune diseases, understanding its drivers is complex. This review focusses on the role of plasticity within Th17 cells in induction, aggravation and resolution of disease and points out IL-23 as a potential key player in controlling Th17 fate. Finally, current treatments targeting IL-23 and Th17 plasticity are highlighted and an outlook on future therapeutics is given.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43863292","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 : 2022-09-12DOI: 10.33696/immunology.4.139
A. Mackay
Microbial resistance to antibiotics has become a major area of research having caused over a million human deaths in 2019. At present, lower respiratory infection is the most burdensome disease. Antimicrobial Photodynamic Therapy (PDT) is regularly reported not to cause resistance in any pathogen, and to eradicate both microbes that are susceptible to antibiotics and those that are resistant. However, evidence now suggests that resistance to photosensitiser drugs at low concentrations is possible, and that tolerance to the reactive oxygen species (ROS) created during subsequent light exposure will occur eventually. Additionally, an increased optical fluence and the addition of medication have been necessary to destroy antibiotic resistant strains of Staphylococcus Aureus . Research has mostly focussed on bacteria, though the importance of fungi is highlighted here given the ubiquity of clinical manifestations like mycosis and urinary tract infection. Proposed next steps are the definition of terminology and methodology for experiments on microbial resistance/tolerance to PDT, varying the photosensitiser used for repeat PDT while controlling oxygen and salt levels, and alternative treatments including the interception of neuroimmunological signalling. Similar to the ESKAPE ranking of antibiotic resistant pathogens, a list summarising the degree of microbial resistance to PDT may have a place.
{"title":"Microbial Resistance to Photodynamic Therapy","authors":"A. Mackay","doi":"10.33696/immunology.4.139","DOIUrl":"https://doi.org/10.33696/immunology.4.139","url":null,"abstract":"Microbial resistance to antibiotics has become a major area of research having caused over a million human deaths in 2019. At present, lower respiratory infection is the most burdensome disease. Antimicrobial Photodynamic Therapy (PDT) is regularly reported not to cause resistance in any pathogen, and to eradicate both microbes that are susceptible to antibiotics and those that are resistant. However, evidence now suggests that resistance to photosensitiser drugs at low concentrations is possible, and that tolerance to the reactive oxygen species (ROS) created during subsequent light exposure will occur eventually. Additionally, an increased optical fluence and the addition of medication have been necessary to destroy antibiotic resistant strains of Staphylococcus Aureus . Research has mostly focussed on bacteria, though the importance of fungi is highlighted here given the ubiquity of clinical manifestations like mycosis and urinary tract infection. Proposed next steps are the definition of terminology and methodology for experiments on microbial resistance/tolerance to PDT, varying the photosensitiser used for repeat PDT while controlling oxygen and salt levels, and alternative treatments including the interception of neuroimmunological signalling. Similar to the ESKAPE ranking of antibiotic resistant pathogens, a list summarising the degree of microbial resistance to PDT may have a place.","PeriodicalId":73644,"journal":{"name":"Journal of cellular immunology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2022-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42938350","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}
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