The journal of the Japanese Society of Lymphoreticular Tissue research
Online ISSN : 1883-681X
Print ISSN : 1342-9248
ISSN-L : 1342-9248
Current issue
Showing 1-5 articles out of 5 articles from the selected issue
  • Hiroshi Nishiura
    2000 Volume 40 Issue 4 Pages 169-174
    Published: January 31, 2001
    Released: October 30, 2009
    JOURNALS FREE ACCESS
    A monocyte specific chemotactic factor, S19 ribosomal protein homodimer, was originally isolated from rheumatoid arthritis-synovial tissue. The homodimer but not the monomer shared an immunologic epitope with the complement-derived leukocyte chemotactic factor, C5a. The monocyte chemotactic effect of the S19 protein homodimer was inhibited by an anti-C5a receptor monoclonal antibody or by a synthetic C5a receptor antagonist. The S19 protein homodimer competitively inhibited the binding of radiolabeled C5a to polymorphonuclear leukocytes. Furthermore, the S19 protein homodimer inhibited the chemotactic response of polymorphonuclear leukocytes to C5a in vitro and in vivo. These data indicate that the S19 protein homodimer possess a three-dimensional structure similar to C5a in terms of the receptor ligand, although homology between their primary structures is only 4%. The S19 protein homodimer with these opposite effects in the leukocyte chemotaxis, agonistic to monocytes and antagonistic to polymorphonuclear leukocytes, seems to be a factor to induce the monocyte/macrophage predominant infiltration in chronic inflammation.
    Download PDF (881K)
  • Tomoki Ito, Shirou Fukuhara
    2000 Volume 40 Issue 4 Pages 175-184
    Published: January 31, 2001
    Released: October 30, 2009
    JOURNALS FREE ACCESS
    Download PDF (1640K)
  • [in Japanese], [in Japanese], [in Japanese], [in Japanese]
    2000 Volume 40 Issue 4 Pages 185-194
    Published: January 31, 2001
    Released: October 30, 2009
    JOURNALS FREE ACCESS
    Download PDF (5824K)
  • Chikako Kaizu
    2000 Volume 40 Issue 4 Pages 195-204
    Published: January 31, 2001
    Released: October 30, 2009
    JOURNALS FREE ACCESS
    Kupffer cells were selectively eliminated in the macrophage colony stimulating factor (M-CSF)-deficient osteopetrotic (op/op) mice by intravenous administration of liposome-entrapped dichloromethylene diphosphonate. Repopulation of Kupffer cells was observed in the Kupffer cell-depleted littermate mouse (op/+) liver by 14 days after treatment. In contrast, repopulation of Kupffer cells was not observed in the Kupffer cell-depleted op/op mice through the observation period of 56 days. Daily administration of M-CSF induced remarkable repopulation of Kupffer cells and proliferation of macrophage precursor cells, whereas GM-CSF and IL-3 were less effective. These findings indicated that M-CSF plays a major role in Kupffer cell development.
    Download PDF (3364K)
  • Hideki MAKISHIMA, Kiyoshi KITANO
    2000 Volume 40 Issue 4 Pages 205-210
    Published: January 31, 2001
    Released: October 30, 2009
    JOURNALS FREE ACCESS
    A 68-year-old female was hospitalized because of general fatigue and edema. Physical examination revealed anemia and splenomegaly, and laboratory tests showed severe hypoproteinemia and pancytopenia. She was splenectomized and diagnosed as histiocytic sarcoma showing diffuse infiltration of large histiocytic cells (LCA-, CD45RO-, CD20-, CD15-, CD30-, CD35-, CD68+ FDC+, fascin+). While any test including gastrointestinal endoscopy and bone marrow cytology did not detect infiltration of the sarcoma cells, hypoproteinemia and pancytopenia continued after splenectomy. An alpha anti-trypsin test revealed protein-losing gastroenteropathy. Despite of CHOP therapy-resistance, treatment with etoposide and prednisolone improved hypoproteinemia and pancytopenia.
    Download PDF (1747K)
feedback
Top