Reproductive Immunology and Biology
Online ISSN : 1881-7211
Print ISSN : 1881-607X
ISSN-L : 1881-607X
25 巻, 2 号
選択された号の論文の2件中1~2を表示しています
  • 礒島 晋三
    2010 年 25 巻 2 号 p. 93-122
    発行日: 2010年
    公開日: 2011/06/16
    ジャーナル フリー
    Following is a summary of the 25 years history of JAPAN SOCIETY for IMMUNOLOGY of REPRODUCTION (JSIR). The 1st conference of reproductive immunology was held in 1981, Takarazuka (Hyogo) and around 60 scientists from interest groups on reproductive immunology of medicine, biology, immunology and agrobiology participated in this meeting and discussed mainly gamete immunology with their papers.
    Since that time, the same conference was held annually for 5 years until the establishment of two different “Japan Society for basic Immunology of Reproduction” and “Japan Sciety for medical Immunology of Reproduction” in 1986. In the 1st 5 years since 1981, the study of sperm immobilizing antibodies in women with unexplained sterility was the main focus. The incidences of antibody positive sterile women and clinical tests on how to detect antibodies exactly were the focuses of the study. The immunology of feto-maternal interface also gradually attracted scientists and the number of researchers increased.
    In 1986, two Japan Societies for Immunology of Reproduction were established, the basic and the medical. The annual meetings of both societies were held separately until the 5th annual meetings in 1990. However both basic and medical societies for immunology of reproduction were combined in 1991 and the new JAPAN SOCIETY for IMMUNOLOGY of REPRODUCTION was established, for achieving more effective developement of these research projects in the future. Considering the past 5 annual meetings organized by each society, the first joint meeting organized by the new established society was titled the “6th meeting of Japan Society for Immunology of Reproduction” to acknowledge the previous meetings. The 25th anniversary meeting of the society was held in Osaka, in 2010 as a satellite meeting of the international symposium of the International Congress of Immunology which was held in Kobe, in 2010.
    JSIR collaborated twice with the International Congress of Reproductive Immunology (ISIR). The 2nd International Congress of ISIR was held in Kyoto, in 1983 (Chairman of Organizing Commitee, Shinzo Isojima) and also the 9th International Congress of ISIR was held in Hakone, in 2004 (Chaima of Organizing Commitee, Tsunehisa Makino).
    Before the establishment of the JSIR, the “International Symposium on Immunology of Spermatozoa and Fertilization” was held in 1967, in Varna (Bulgaria), and 150 scientists from 20 countries attended. In this meeting, the “International Coodination Committee for Immunology of Reproduction (ICCIR)” was established, and the 1st international symposium of ICCIR was held in 1968, in WHO (Geneva) and then the symposia were held triennialy by the ICCIR until 2009 in Varna. Besides these international symposia, the “International Society for Immunology of Reproduction (ISIR)” was established in 1976 and the registration of this society to the French Government was accepted in the next year. At that time the constitution of the society and the 1st president (K.Bratanov) were decided on. The 1st International Congress of the ISIR started in 1980, in Paris and the 2nd International Congress was held in Japan (Kyoto), in 1983 and thereafter triennialy in different countries. The 16h International Congress was held in Australia, in 2010.
  • Tomomoto Ishikawa, Moira K. O'Bryan, Masato Fujisawa, Patricia L. Morr ...
    2010 年 25 巻 2 号 p. 123-135
    発行日: 2010年
    公開日: 2011/06/16
    ジャーナル フリー
    In testicular epithelial Sertoli cells (SC), IL-1β regulates estradiol and lactate production, transferrin secretion, and IL-6 expression; while each subsequently influences developing germ cells and spermatogenesis, little is known about the signalling mechanisms involved. In other specialized cell types, IL-1β potently induces reactive oxygen species (ROS) and/or cyclooxygenase-2 (COX-2). We review that IL-1β stimulates COX activity, mediating the expression of interleukins and steroidogenic acute regulatory (StAR)-related lipid transfer (START domain) proteins. IL-1β does not generate ROS but does rapidly phosphorylate cJun-NH2-terminal kinase (JNK), but not p44/42 or p38 mitogen-activated protein kinases. In atime- and dose-dependent manners, IL-1β significantly increases the levels of COX-2 mRNA and protein with concomitant increases in IL-1α, IL-6, and IL-1β mRNAs. Cyclohexamide (CHX) blocks increases in COX-2 protein. The intracellular StART domain levels are significantly altered consistent with posttranscriptional and posttranslational regulation. IL-1β rapidly decreases the levels of precursor and mature sterol regulatory element-binding protein-1 (SREBP-1), changes not affected by CHX, and suggesting coordinate regulation of StAR expression and cholesterol metabolism. Together these data demonstrate that COX-2 activity regulates SC cytokines and START domain lipid sensors. Also, IL-1β induces the production of prostaglandins (PG) PGE2 and PGF2α. IIL-1β-regulated PGE2 and PGF2α production, and cytokine expression require initial activation of cyclooxygenase-2 (COX-2) and JNK, as shown using specific enzyme inhibition. Sertoli cell PG receptor expression was determined; four known EP subtypes, and the FP and IP receptors were detected using RNA and protein analyses. IL-1β regulates both the EP2 mRNA and protein levels, the data being consistent with a regulatory feedback loop. Consistent with EP2-cAMP signaling, protein kinase A (PKA) inhibition blocks both IL-1β- and PGE2-induced cytokines. Together the data indicate an autocrine-amplifying loop involving an IL-1β-regulated Sertoli function mediated by COX-2-induced PGE2 and PGF2α production. PGE2 activates EP2 and/or EP4 receptor(s), and the PKA-cAMP pathway; PGF2α activates FP-PKC signalling. Further identification of the molecular mechanisms subserving these mediators may offer new insights into the physiological events as well as pro-inflammatory mediated pathogenesis in the testis.
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