{"title":"An <i>in silico</i> approach for prediction of B cell and T cell epitope candidates against Chikungunya virus.","authors":"Amrit Venkatesan, Usha Chouhan, Sunil Kumar Suryawanshi, Jyoti Kant Choudhari","doi":"10.1080/25785826.2023.2202038","DOIUrl":"10.1080/25785826.2023.2202038","url":null,"abstract":"<p><p>Several outbreaks of Chikungunya virus (CHIKV) had been reported since 1952 when mankind had his first encounter against the virus in Tanzania. Although these reports designate the CHIKV to be rarely fatal, cases of outbreaks in the last decade accompanied by severe complications and death poses a challenge to the development of effective treatment methods. Several attempts to vaccine development against CHIKV still remains unsuccessful. In this study, we aimed at the prediction of B-cell and T cell epitopes against CHIKV by using immunoinformatics. This, in turn, can contribute to development of an epitope based vaccine against CHIKV. Both linear and discontinuous B-cell epitopes, as well as Cytotoxic T-lymphocyte epitopes, were predicted for the CHIKV Envelope (E1 and E2) glycoproteins and (NS2). The antigenic CTL epitopes with highest binding affinities with type-1 MHC were selected and the peptides were docked to them. Docking followed by molecular dynamics simulations were performed to assess the stability of the docked complexes.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":" ","pages":"163-174"},"PeriodicalIF":4.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9378647","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":"Involvement of the complement system in immune thrombocytopenia: review of the literature.","authors":"Risa Shindo, Ryohei Abe, Kenji Oku, Tomoki Tanaka, Yu Matsueda, Tatsuhiko Wada, Yoshiyuki Arinuma, Sumiaki Tanaka, Tatsuyoshi Ikenoue, Yoshitaka Miyakawa, Kunihiro Yamaoka","doi":"10.1080/25785826.2023.2213976","DOIUrl":"10.1080/25785826.2023.2213976","url":null,"abstract":"<p><p>Immune thrombocytopenia (ITP) is a thrombocytopenic condition induced by autoimmune mechanisms and includes secondary ITP with underlying diseases such as connective tissue diseases (CTD). In recent years, it has been elucidated that the subsets of the ITP are associated with complement abnormalities but much remains unclear. To perform a literature review and identify the characteristics of complement abnormalities in ITP. PUBMED was used to collect the literature published up to June 2022 related to ITP and complement abnormalities. Primary and secondary ITP (CTD-related) were examined. Out of the collected articles, 17 were extracted. Eight articles were related to primary ITP (pITP) and 9 to CTD-related ITP. Analysis of the literature revealed that the ITP severity was inversely correlated with serum C3, C4 levels in both ITP subgroups. In pITP, a wide range of complement abnormalities was reported, including abnormalities of initial proteins, complement regulatory proteins, or the end products. In CTD-related ITP, reported complement abnormalities were limited to the initial proteins. Activation of the early complement system, mainly through activation of C3 and its precursor protein C4, was reported for both ITPs. On the other hand, more extensive complement activation has been reported in pITP.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":" ","pages":"182-190"},"PeriodicalIF":4.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9524030","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}
Immunological MedicinePub Date : 2023-12-01Epub Date: 2023-04-19DOI: 10.1080/25785826.2023.2202050
Faegheh Ebrahimi Chaharom, Ali Asghar Ebrahimi, Faroogh Feghhi Koochebagh, Zohreh Babalou, Morteza Ghojazadeh, Leili Aghebati Maleki, Nader D Nader
{"title":"Association of IL-17 serum levels with clinical findings and systemic lupus erythematosus disease activity index.","authors":"Faegheh Ebrahimi Chaharom, Ali Asghar Ebrahimi, Faroogh Feghhi Koochebagh, Zohreh Babalou, Morteza Ghojazadeh, Leili Aghebati Maleki, Nader D Nader","doi":"10.1080/25785826.2023.2202050","DOIUrl":"10.1080/25785826.2023.2202050","url":null,"abstract":"<p><p>The current study aims to investigate the relationship betweSen serum IL-17 (IL-17) levels and systemic lupus erythematosus disease activity index (SLE-DAEI) in systemic lupus erythematosus (SLE) patients. In this case-control study, 36 patients with SLE and 40 healthy individuals matched for age and sex were included as the control group. The study measured serum IL-17 in both groups. The correlation between serum IL-17 with disease activity (as per SLE-DAI) and organ involvement in SLE patients. The case group in this study consisted of 4 males and 32 females with a mean age of 35 (17-54) years old, and the control group included six males and 34 females with a mean age of 37 (25-53) years old (<i>p</i> = .35). Serum IL-17 was higher in the cases than in the controls (536 pg/mL vs. 110 pg/mL; <i>p</i> < .001). There was a positive correlation between the serum levels of IL-17 and disease activity index (<i>p</i> < .001, rho = 0.93) among cases. Additionally, the serum levels of IL-17 were higher in patients with renal (<i>p</i> = .003) or central nervous system involvement (<i>p</i> < .001) than in patients without such involvement. Serum Il-17 is associated with SLE, and its serum levels correlate positively with the disease activity and renal and nervous system involvement.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":" ","pages":"175-181"},"PeriodicalIF":4.4,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9737384","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":"JAK inhibitors ∼ overview∼.","authors":"Hideto Kameda","doi":"10.1080/25785826.2023.2183594","DOIUrl":"https://doi.org/10.1080/25785826.2023.2183594","url":null,"abstract":"<p><p>Among various tyrosine kinases, a family of Janus kinases (JAK) has been elucidated as key players in signal transduction from vital cytokine receptors, such as interleukins and interferons. Indeed, recent rapid progress in JAK inhibitors in addition to biological agents provided therapeutic options for various diseases, including immune-mediated inflammatory diseases and hematological disorders. Efforts have culminated in the approval of nine JAK inhibitors in Japan in the recent decade. The safety profiles of JAK inhibitors seem to largely depend on patient populations and drug dosing, rather than on JAK selectivity. Thus, the comparison of various disease indications is pivotal for the understanding and proper use of JAK inhibitors.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 3","pages":"108-111"},"PeriodicalIF":4.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9918819","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":"Exploring the role of Janus kinase (JAK) in atopic dermatitis: a review of molecular mechanisms and therapeutic strategies.","authors":"Toshiaki Kogame, Gyohei Egawa, Kenji Kabashima","doi":"10.1080/25785826.2023.2214324","DOIUrl":"https://doi.org/10.1080/25785826.2023.2214324","url":null,"abstract":"<p><p>Recent studies have demonstrated that Janus kinase (JAK) plays a crucial role in signal transduction by directly affecting various cytokine receptors involved in inflammatory diseases such as atopic dermatitis (AD). Large-scale clinical trials on AD utilizing JAK inhibitors and biologic reagents, such as dupilumab, which targets the IL-4Rα receptor subunit of the Th2 cytokines IL-4 and IL-13, have yielded highly favorable results in comparison to traditional therapies. This indicates that therapeutic strategies based on molecular biology are efficacious in clinical settings. However, in September 2021, the U.S. Food and Drug Administration (FDA) indicated that tofacitinib, a JAK inhibitor, may carry various risks, including severe heart disease. Similar concerns have been raised for other JAK inhibitors, and further safety evaluations are underway. Thus, human biology involving JAKs appeared more complicated than we expected. In this article, we provide an overview of the molecular mechanisms of AD and examine the molecular targeting drugs for AD from the perspective of JAK-related biology.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 3","pages":"112-120"},"PeriodicalIF":4.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9919927","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}
Immunological MedicinePub Date : 2023-09-01Epub Date: 2023-04-10DOI: 10.1080/25785826.2023.2195522
Hiroshi Nakase
{"title":"Understanding the efficacy of individual Janus kinase inhibitors in the treatment of ulcerative colitis for future positioning in inflammatory bowel disease treatment.","authors":"Hiroshi Nakase","doi":"10.1080/25785826.2023.2195522","DOIUrl":"10.1080/25785826.2023.2195522","url":null,"abstract":"<p><p>Recent studies have gradually elucidated the pathogenesis of inflammatory bowel disease; thus, the Janus kinase (JAK)-signal transducers and activators of transcription pathway are strongly involved in the pathophysiology of inflammatory bowel disease. Generally, Janus kinase inhibitors are being used for the treatment of rheumatoid arthritis and other immunological diseases, with the therapeutic promising effects. Currently, in Japan, three Janus kinase inhibitors, namely tofacitinib, filgotinib, and upadacitinib, are available for the treatment of patients with active ulcerative colitis. Therefore, evaluating the efficacy and safety of each JAK inhibitor is essential for determining the role of JAK inhibitors in future therapeutic strategies for inflammatory bowel disease (IBD).</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 3","pages":"121-130"},"PeriodicalIF":4.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9891338","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}
Immunological MedicinePub Date : 2023-09-01Epub Date: 2022-10-28DOI: 10.1080/25785826.2022.2139317
Keita Kirito
{"title":"Recent progress of JAK inhibitors for hematological disorders.","authors":"Keita Kirito","doi":"10.1080/25785826.2022.2139317","DOIUrl":"10.1080/25785826.2022.2139317","url":null,"abstract":"Abstract JAK inhibitors are important therapeutic options for hematological disorders, especially myeloproliferative neoplasms. Ruxolitinib, the first JAK inhibitor approved for clinical use, improves splenomegaly and ameliorates constitutional symptoms in both myelofibrosis and polycythemia vera patients. Ruxolitinib is also useful for controlling hematocrit levels in polycythemia vera patients who were inadequately controlled by conventional therapies. Furthermore, pretransplantation use of ruxolitinib may improve the outcome of allo-hematopoietic stem cell transplantation in myelofibrosis. In contrast to these clinical merits, evidence of the disease-modifying action of ruxolitinib, i.e., reduction of malignant clones or improvement of bone marrow pathological findings, is limited, and many myelofibrosis patients discontinued ruxolitinib due to adverse events or disease progression. To overcome these limitations of ruxolitinib, several new types of JAK inhibitors have been developed. Among them, fedratinib was proven to provide clinical merits even in patients who were resistant or intolerant to ruxolitinib. Pacritinib and momelotinib have shown merits for myelofibrosis patients with thrombocytopenia or anemia, respectively. In addition to treatment for myeloproliferative neoplasms, recent studies have demonstrated that JAK inhibitors are novel and attractive therapeutic options for corticosteroid-refractory acute as well as chronic graft versus host disease.","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 3","pages":"131-142"},"PeriodicalIF":4.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9953916","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}
Immunological MedicinePub Date : 2023-09-01Epub Date: 2023-02-06DOI: 10.1080/25785826.2023.2172808
Kunihiro Yamaoka, Kenji Oku
{"title":"JAK inhibitors in rheumatology.","authors":"Kunihiro Yamaoka, Kenji Oku","doi":"10.1080/25785826.2023.2172808","DOIUrl":"10.1080/25785826.2023.2172808","url":null,"abstract":"<p><p>Janus kinase inhibitors (JAKis) are a group of drugs with a different mechanism of action from biologics and are most rapidly uptaken in the rheumatology field. JAK is a protein kinase activated in the cytoplasm by multiple cytokines and hormones involved in inflammatory pathology. The expression of JAK has been observed in various diseases, indicating the utility of JAK inhibitors in a wide variety of immune-mediated inflammatory diseases. Clinical trials are underway for a number of different rheumatic diseases based on the therapeutic efficacy of JAKis, which is comparable to that of biologics. This article will review the current status of JAKis for rheumatic diseases in terms of efficacy and safety and extend to future clinical applications for rare diseases.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 3","pages":"143-152"},"PeriodicalIF":4.4,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9890831","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":"Hypocomplementemic urticarial vasculitis case with hemophagocytic lymphohistiocytosis following SARS-CoV-2 mRNA vaccination.","authors":"Narumichi Iwamura, Katsumi Eguchi, Tomohiro Koga, Kanako Tsutsumi, Takeshi Araki, Toshiyuki Aramaki, Ayuko Takatani, Kaoru Terada, Yukitaka Ueki","doi":"10.1080/25785826.2023.2193286","DOIUrl":"https://doi.org/10.1080/25785826.2023.2193286","url":null,"abstract":"<p><p>A 61-year-old man with no previous record of autoimmune disease developed fever, polyarthralgia, purpura, and urticaria-like rash 2 weeks after the first dose of the Moderna mRNA-1273 vaccine, and symptoms deteriorated following the second dose. He presented reduced erythrocyte and platelet counts, hyperferritinemia, high sIL-2R levels, and severe hypocomplementemia. We diagnosed hypocomplementemic urticarial vasculitis (HUVS), and his symptoms as well as laboratory findings improved following treatment with mPSL 1000 mg/day for 3 days and PSL 40 mg/day. Twelve weeks following treatment initiation, the patient relapsed with fever, sore throat, pancytopenia, and hyperferritinemia when the PSL dose was reduced to 12.5 mg/day. Bone marrow biopsy and MRI presented fatty marrow and hemophagocytosis. The patient's blood cells started recovering using ATG + CsA + EPAG therapy for hemophagocytic lymphohistiocytosis (HLH). This is the first case report of HUVS and HLH following SARS-CoV-2 mRNA vaccination. It is presumed that SARS-CoV-2 mRNA vaccine can induce the excessive production of certain types of cytokines, such as TNF-α, IL-1, IL-4, IL-5, IL-6, and IL-17 as a consequence of IL-6 Amplification (IL-6 Amp). SARS-CoV-2 mRNA-vaccines can cause disruption of immune homeostasis in healthy individuals. An extremely rare disease of HUVS complicated by HLH can be developed as a consequence.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 2","pages":"97-107"},"PeriodicalIF":4.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9479297","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":"The association between PD-1 gene polymorphisms and susceptibility to multiple sclerosis.","authors":"Nasrin Hassani, Arash Salmaninejad, Saeed Aslani, Eskandar Kamali-Sarvestani, Mahmood Vessal","doi":"10.1080/25785826.2022.2137967","DOIUrl":"https://doi.org/10.1080/25785826.2022.2137967","url":null,"abstract":"<p><p>Programmed cell death 1 (PD-1) is an immune checkpoint and has been reported to be associated with several autoimmune diseases. We aimed to investigate the association between human PD-1 gene (<i>PDCD1</i>) polymorphisms and multiple sclerosis (MS). This case-control study was conducted on 229 MS patients and 246 healthy controls. Genotyping of rs36084323 (PD-1.1 G/A), rs11568821 (PD-1.3 G/A) and rs2227981 (PD-1.5 C/T) polymorphisms was performed by PCR-RFLP technique. The frequency difference of PD-1.1 genotypes and alleles (-536 G/A) between patients and healthy controls was not significant. Regarding PD-1.3, the AA + AG genotype was found to be relatively higher in the control group. Concerning PD-1.5 (+7785 C/T), the frequency of T allele carriers (TT + CT) was relatively higher in MS patients, which was marginally insignificant (<i>p</i> = .07). PD-1 gene polymorphisms may be associated with MS; however, accurate conclusions require further studies with a larger number of samples.</p>","PeriodicalId":37286,"journal":{"name":"Immunological Medicine","volume":"46 2","pages":"69-76"},"PeriodicalIF":4.4,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9481911","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}