Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology最新文献

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Severe combined immunodeficiency: From its discovery to the perspective. 严重联合免疫缺陷:从发现到透视。
Hirokazu Kanegane, Kohsuke Imai, Tomohiro Morio
{"title":"Severe combined immunodeficiency: From its discovery to the perspective.","authors":"Hirokazu Kanegane,&nbsp;Kohsuke Imai,&nbsp;Tomohiro Morio","doi":"10.2177/jsci.40.145","DOIUrl":"https://doi.org/10.2177/jsci.40.145","url":null,"abstract":"<p><p>Severe combined immunodeficiency (SCID) is impaired in lymphocyte development and function. Affected children have extreme susceptibility to infections, which are fatal in the first year of life without treatment. The estimate of incidence is one in approximately 50,000 live birth. The first series of diseases were described in 1950s, and all patients died in infancy. The first transplant for SCID was carried out in 1968, and it has been described that SCID patients could be treated by hematopoietic stem cell transplantation (HSCT) since then. Adenosine deaminase and common gamma chain were identified to be causative genes for SCID in 1972 and 1993, respectively. SCID arises from a variety of genetic defects. The early intervention of healthy SCID infants without infections affords higher survival rate, and newborn screening (NBS) was suggested. T-cell receptor (TCR) exicision circles (TRECs) are circular DNA formed from the leftover fragment generated from the TCR rearrangement. TRECs can be measured from a small aliquot of DNA such as Guthrie card by quantitative PCR. SCID patients lack TRECs, and TRECs quantification is useful for NBS for SCID. NBS for SCID have been already carried out in most of the Unite States, and the early introduction is desired in Japan to save SCID children.</p>","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 3","pages":"145-154"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35204370","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}
引用次数: 3
Autoinflammatory diseases in dermatology: DITRA and CAMPS. 皮肤病学中的自身炎症性疾病:DITRA和CAMPS。
Kazumitsu Sugiura
{"title":"Autoinflammatory diseases in dermatology: DITRA and CAMPS.","authors":"Kazumitsu Sugiura","doi":"10.2177/jsci.40.169","DOIUrl":"https://doi.org/10.2177/jsci.40.169","url":null,"abstract":"<p><p>Deficiency of interleukin thirty-six receptor antagonist (DITRA) and CARD14 mediated psoriasis (CAMPS) are autoinflammatory diseases in dermatology. The causative genes of DITRA and CMAPS have been identified recently. In this paper, IL36RN and CARD14, the causative gene for DITRA and CAMPS, respectively were explained. In addition, clinical features and therapies for generalized pustular psoriasis not associated with psoriasis vulgaris (GPP without PsV), and pityriasis rubra pilaris type V (PRP type V) were described. GPP without PsV and PRP type V are representative diseases of DITRA and CAMPS, respectively.</p>","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 3","pages":"169-173"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.169","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35204373","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}
引用次数: 1
WS2-3 乾癬・蕁麻疹治療のエビデンスと経験から WS2-3银屑病和荨麻疹治疗的证据和经验
儒人 濱口
{"title":"WS2-3 乾癬・蕁麻疹治療のエビデンスと経験から","authors":"儒人 濱口","doi":"10.2177/JSCI.40.266A","DOIUrl":"https://doi.org/10.2177/JSCI.40.266A","url":null,"abstract":"","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/JSCI.40.266A","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68275104","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}
引用次数: 0
LS1-1 脊椎関節炎とIL-17:乾癬性関節炎を中心に LS1-1脊椎关节炎和IL-17:以干癣性关节炎为主
敦夫 谷口
{"title":"LS1-1 脊椎関節炎とIL-17:乾癬性関節炎を中心に","authors":"敦夫 谷口","doi":"10.2177/jsci.40.285b","DOIUrl":"https://doi.org/10.2177/jsci.40.285b","url":null,"abstract":"","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.285b","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68275834","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}
引用次数: 0
P1-32 シェーグレン症候群による亜急性感覚失調性ニューロパチーの1例 P1-32谢格伦综合征引起的亚急性觉失调神经官能症1例
岡野 隆一, 三枝 淳, 森信 暁雄, 明石 健吾, 白井 太一朗, 大木 洋子, 永本 匠, 藤川 良一, 高橋 宗史, 千藤 荘, 大西 輝
{"title":"P1-32 シェーグレン症候群による亜急性感覚失調性ニューロパチーの1例","authors":"岡野 隆一, 三枝 淳, 森信 暁雄, 明石 健吾, 白井 太一朗, 大木 洋子, 永本 匠, 藤川 良一, 高橋 宗史, 千藤 荘, 大西 輝","doi":"10.2177/jsci.40.305d","DOIUrl":"https://doi.org/10.2177/jsci.40.305d","url":null,"abstract":"","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.305d","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68276489","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}
引用次数: 0
Prospects for personalized combination immunotherapy for solid tumors based on adoptive cell therapies and immune checkpoint blockade therapies. 基于过继细胞疗法和免疫检查点阻断疗法的实体瘤个性化联合免疫疗法的前景。
Daiki Kato, Tomonori Yaguchi, Takashi Iwata, Kenji Morii, Takayuki Nakagawa, Ryohei Nishimura, Yutaka Kawakami
{"title":"Prospects for personalized combination immunotherapy for solid tumors based on adoptive cell therapies and immune checkpoint blockade therapies.","authors":"Daiki Kato,&nbsp;Tomonori Yaguchi,&nbsp;Takashi Iwata,&nbsp;Kenji Morii,&nbsp;Takayuki Nakagawa,&nbsp;Ryohei Nishimura,&nbsp;Yutaka Kawakami","doi":"10.2177/jsci.40.68","DOIUrl":"https://doi.org/10.2177/jsci.40.68","url":null,"abstract":"<p><p>  Immune checkpoint blockade (ICB) and adoptive cell therapies (ACT) with antigen-receptor gene-engineered T cells have been shown to be successful for a limited number of patients with solid tumors. Responders to ICB therapy typically have T cell-inflamed tumors. Thus, it is important to develop strategies that convert non-T cell-inflamed tumors to T cell-inflamed tumors. Although chimeric antigen receptor transduced T (CAR-T) cell therapy targeting hematological malignancies demonstrated durable clinical responses, the success of gene-engineered T cell therapies in solid tumors is hampered by a lack of unique antigens, antigen loss in cancer cells, and the immune-suppressive tumor microenvironment (TME) of solid tumors. However, gene-engineered T cells possess strong killing activity and cytokine production capacity, which can induce antigen spreading and modulate the TME of non-T cell-inflamed tumors seen in non-responders to ICB therapy. Immune responses against cancer are highly heterogeneous, not only between tumor types, but also within a patient or between different patients with the same type of cancer, indicating that personalized immunotherapy should be employed, based on the immune status of the individual patient. Here, we offer our perspective for personalized combination immunotherapy for solid tumors based on ACT and ICB therapies.</p>","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 1","pages":"68-77"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.68","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35024083","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}
引用次数: 21
Omenn Syndrome and DNA recombination defects. Omenn综合征和DNA重组缺陷。
Akihiro Yachie
{"title":"Omenn Syndrome and DNA recombination defects.","authors":"Akihiro Yachie","doi":"10.2177/jsci.40.179","DOIUrl":"https://doi.org/10.2177/jsci.40.179","url":null,"abstract":"<p><p>Mutations in the RAG1/RAG2 genes are associated with a broad spectrum of clinical phenotypes, ranging from severe combined immunodeficiency to various autoimmune diseases. The diversity of the clinical symptoms is determined not only by the residual RAG recombinase enzyme activity as determined by the mutations, but also by multiple environmental factors and, in rare cases, by second site mutations within the RAG1/RAG2 genes. The residual recombinase activity is responsible for the oligoclonal expansion of autoreactive T cells. Omenn syndrome is the result of intense Th2 type inflammation involving the skin and multiple other organs triggered by these T cells. In this review, the molecular pathology of diseases caused by RAG1/RAG2 mutations, in particular Omenn syndrome, will be discussed. Furthermore, abnormalities in other molecules involved in V(D)J recombination will be discussed in relation to Omenn-like syndrome.</p>","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 3","pages":"179-189"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.179","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35202679","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}
引用次数: 2
{"title":"","authors":"","doi":"10.2177/jsci.40.262b","DOIUrl":"https://doi.org/10.2177/jsci.40.262b","url":null,"abstract":"","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 4","pages":"262b"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.262b","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35284741","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}
引用次数: 0
WS3-1 IL-6と関節リウマチ WS3-1 IL-6与类风湿关节炎
祐子 金子
{"title":"WS3-1 IL-6と関節リウマチ","authors":"祐子 金子","doi":"10.2177/jsci.40.267a","DOIUrl":"https://doi.org/10.2177/jsci.40.267a","url":null,"abstract":"","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.267a","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68275190","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}
引用次数: 0
WS5-1 機能獲得型変異による慢性炎症・自己免疫疾患を呈する原発性免疫不全症 WS5-1功能获得型变异引起的慢性炎症、自身免疫性疾病的原发性免疫缺陷
耕輔 今井
{"title":"WS5-1 機能獲得型変異による慢性炎症・自己免疫疾患を呈する原発性免疫不全症","authors":"耕輔 今井","doi":"10.2177/jsci.40.270a","DOIUrl":"https://doi.org/10.2177/jsci.40.270a","url":null,"abstract":"","PeriodicalId":79359,"journal":{"name":"Nihon Rinsho Men'eki Gakkai kaishi = Japanese journal of clinical immunology","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2177/jsci.40.270a","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68275210","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}
引用次数: 0
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