Japanese Journal of Clinical Immunology
Online ISSN : 1349-7413
Print ISSN : 0911-4300
ISSN-L : 0911-4300
Volume 35, Issue 5
Displaying 1-9 of 9 articles from this issue
Erratum
  • Hirofumi SHODA, Keishi FUJIO, Kazuhiko YAMAMOTO
    2012Volume 35Issue 5 Pages 387
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
    Erratum to: [Japanese Journal of Clinical Immunology 30(5): 398-403 (2007)]
    In the review article, “Rheumatoid arthritis and Interleukin-32”, the authors regret to have omitted to quote their previous review entitled Rheumatoid Arthritis and Interleukin-32 (Shoda H. et al., Cell. Mol. Life Sci. 64, 2671-2679, 2007). The content of the present article in Japanese Journal of Clinical Immunology (JJCI) is largely similar to the previous review. In addition, the authors regret to have reproduced in the present article, without permission, 3 figures of their review in Cell. Mol. Life. Sci. (Figures 1, 3 and 4 in JJCI). The authors suggest, when others are referring to their work, to quote the original article in Cell. Mol Life Sci.
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Feature Articles
Review Articles
  • Yoshiki TOKURA
    2012Volume 35Issue 5 Pages 388-392
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      Th17 cells have crucial functions in host defense, and dysregulated Th17 responses mediate a variety of autoimmune and inflammatory conditions. Th17 cells coexpress IL-22, and its receptor is expressed on epidermal keratinocytes. IL-17 and /or IL-22 induce the production of certain cytokines, chemokines and antimicrobial peptides by keratinocytes, and its cooperation with IL-22 has been documented. Recent findings have suggested that Th17 cells profoundly participate in the pathogenesis of certain skin disorders, in particular, psoriasis. The involvement of Th17 cells has also been shown in allergen-specific immune responses. The percentage of Th17 cells is increased in peripheral blood of patients with atopic dermatitis (AD) and associated with the severity of AD. Drug eruption is another disease where circulating Th17 cells are increased.
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  • Sachiko MIYAKE
    2012Volume 35Issue 5 Pages 393-398
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      Mucosal associated invariant T (MAIT) cells are restricted by a nonpolymorphic MHC-related molecule-1 (MR1), and express an invariant TCRα chain: Vα7.2-Jα33 in humans and Vα19-Jα33 in mice. MAIT cells are selected in the thymus, but, interestingly, MAIT cells require B cells as well as commensal flora for their peripheral expansion. Bourhis et al demonstrated that MAIT cells display antimicrobial capacity. Both human and mouse MAIT cells have been shown to be activated by Escherichia coli-infected antigen presenting cells in an MR1-dependent manner. MAIT cells show a protective role against Mycobacteriu abscessus or E. coli infections in mice. Human MAIT cells are capable of producing IFNγ and IL-17 and are found in Mycobacterium tuberculosis-infected lung tissues. Thus, MAIT cells play an antimicrobial function under these infectious conditions. MAIT cells play a protective role against autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS), whereas they play a pathogenic role in murine models of arthritis. In patients with autoimmune diseases, the frequency of MAIT cells in peripheral blood was significantly reduced. The frequency of MAIT cells reflected the disease activity in MS patients, suggesting the involvement of MAIT cells in the regulation of autoimmune diseases.
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  • Tomohisa SUJINO, Takanori KANAI
    2012Volume 35Issue 5 Pages 399-411
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      The hypothesis of helper T (T(h))1/T(h)2 cytokine balance was often invoked to explain the development of inflammatory diseases, including inflammatory bowel diseases (IBD). Recently, a newly identified class of regulatory T cells (Tregs), which suppress inflammation and helper T(Th)17 cells, which produce Th17 family cytokines has been recognized as an essential subpopulation in the development of almost all kinds of human and animal inflammatory diseases. T cell subsets can act as terminally differentiated lineages, but they have been increasingly noted to demonstrated plasticity, depending on their surrounding such as intestinal microbiota. Th17 cells and Th1 cells coordinate to play a critical role in the formation of inflammatory bowel diseases. We showed Th1 and Th17 cells are competitive in lymphopenic mice, and that their orchestration results in a merged clinical phenotype of the two types of murine colitis. We also showed that Th17 and Th17/Th1 cells become colitogenic alternative Th1 cells via Th17, Th17/Th1, and Th1-like cells, independently of classical Th1 cells. Treg cells suppress this pathway, resulting in accumulation of Th17 and Th17/Th1 cells. Here we review T cell development including their plasticity and recent advances in the study of such Treg cells and Th17 cells in the pathogenesis of IBD.
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  • Takashi NISHIMURA
    2012Volume 35Issue 5 Pages 412-423
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      During past decades, cancer vaccine therapy has been focused on only the activation of CTL, but its therapeutic effect was not successful though long SD was induced. The failure of cancer vaccine is derived from (i) the existence of a strong tumor escape mechanisms and (ii) the ignorance of helper T cell activation. We have proposed that Th1-dominant immunity played a critical role for overcoming immunosuppressive tumor-escape mechanisms to induce tumor-specific CTL, which are essential for the complete cure of tumor and prevention of tumor recurrence. To apply these basic findings, we started a clinical trial of a novel cancer vaccine/cell therapy (Th1 cell therapy) using H/K-HELP of MAGE-A4 or Survivin cancer antigen. In phase I study, H/K-HELP consisted of both killer and helper epitopes and Th1 adjuvants (OK-432 and Montanide) were subcutaneously administered into cancer patients 4 times at 2 wks intervals. Both MAGE-A4-H/K-HELP and Survivin-H/K-HELP cancer vaccine induced cancer-specific Th1 and Tc1 immune responses and cancer-specific C-fixing antibodies (IgG1 and IgG3) in cancer patients. Moreover, Survivin-H/K-HELP vaccination induced a complete regression of chemo and radio-resistant lateral deep cervical node recurrence of triple-negative breast cancer. H/K-HELP vaccination with Th1 adjuvants or its combination with Th1 cells will become a promising cancer vaccine/cell therapy of human cancer.
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  • Shigeru SAITO, Tomoko SHIMA, Akitoshi NAKASHIMA
    2012Volume 35Issue 5 Pages 424-428
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      During pregnancy, semiallograftic fetus is allowed to grow without being rejected by the maternal immune system. Recent data show that paternal antigen specific- or male antigen HY specific-regulatory T cells (Treg) increase during pregnancy. Seminal plasma is necessary for the accumulation of Treg cells in uterine draining lymph modes just before implantation, and in uterus just after implantation. It has been reported that decreased number of Treg cells in peripheral blood or pregnant uterus in abortion or preeclampsia. In human and rodent pregnant uterus, NK cells are the major population (∼80%) of lymyhocytes, we have reported that CD25+ NK cells increase in mouse pregnant uterus, and these NK cells produce immunoregulatory cytokines such as IL-10 and TGF-β. They inhibit the expression of MHC class II antigen on dendritic cells and inhibit the cytotoxic T cell induction, suggesting that these NK cells have an ability for immunoregulation. Both Treg cells and regulatory NK cells play important roles for maintenance of pregnancy.
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Case Reports
  • Yuki NANKE, Tsuyoshi KOBASHIGAWA, Toru YAGO, Hisashi YAMANAKA, Shigeru ...
    2012Volume 35Issue 5 Pages 429-432
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      We described a patient with secondary Sjögren's syndrome suspected showing multiple cranial neuropathies at the different time. A 68-year old woman has been treated as rheumatoid arthritis since 1963. In 2001, she was also diagnosed with Sjögren's syndrome suspected. Afterward, abducent and trigeminal neuropathies and uveites occurred. This case is important to insight into the cranial neuropathy with Sjögren's syndrome.
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  • Takuma WADA, Yuji AKIYAMA, Kazuhiro YOKOTA, Kojiro SATO, Yu FUNAKUBO, ...
    2012Volume 35Issue 5 Pages 433-438
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      We report a case of rheumatoid arthritis (RA) complicated with interstitial pneumonia that deteriorated after the administration of abatacept. A 55-year-old man developed RA and interstitial pneumonia. Although interstitial pneumonia was improved by high-dose glucocorticoids, various disease-modifying antirheumatic drugs including infliximab were ineffective for his arthritis. Tacrolimus was effective but was discontinued due to refractory itching and diarrhea. After 2 months, he was registered on the Phase III trial of abatacept in Japan because of worsening of arthritis. From 2 days after the abatacept administration, frothy sputum frequently appeared, but sputum culture was negative. On 13 days after the administration, the interstitial shadow was deteriorated by chest CT as compared with that of 2 months before, and he was dropped out from the trial. On 27 days after the administration, the dose of prednisolone was increased from 2 to 10 mg/day for his arthritis. On 44 days after the administration, the interstitial pneumonia improved. Abatacpet might be the cause of the deterioration of the interstitial pneumonia, but other possibilities such as discontinuation of tacrolimus, flare-up of RA itself or viral infection should be considered. This is the first report of deteriorated interstitial pneumonia after the abatacept administration in the literature. Further cases are needed to identify the relation between abatacept and interstitial pneumonia, however this possibility should be always kept in mind when we use abatacept.
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  • Yuko KURIHARA, Kayo OKU, Atsushi SUZUKI, Yasuo OHSONE, Yutaka OKANO
    2012Volume 35Issue 5 Pages 439-445
    Published: 2012
    Released on J-STAGE: October 31, 2012
    JOURNAL FREE ACCESS
      We report a case of calcinomatous polyarthritis presenting rheumatoid arthritis-like polyarthritis as the initial symptom of gastric cancer. A 79-year-old male visited to our hospital with complaint of pain and swelling of multiple joints including bilateral hands, bilateral knees, elbows and small joints of fingers. He also complained of neck and back stiffness. Both of rheumatoid factor test and anti-cyclic citrullinated peptide antibody were negative. Non-steroidal anti-inflammatory drug did not relieve his arthritic pain. He showed anorexia, body weight loss and was anemic. Upper gastrointestinal endoscopic evaluation demonstrated a gastric cancer. The patient underwent subtotal gastrectomy. Within 1 week after the subtotal gastrectomy, both polyarthritis and stiffness started to improve. The polyarthritis in this case was diagnosed as calcinomatous plyarthritis for its features. Paraneoplastic rheumatism remains a rare event, but knowledge of it is essential for early diagnosis of underlying cancer.
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