       Document 0522
 DOCN  M9620522
 TI    T cell-dependent loss of proliferative responsiveness to
       colony-stimulating factor-1 by a murine epidermal-derived dendritic cell
       line, XS52.
 DT    9602
 AU    Kitajima T; Ariizumi K; Bergstresser PR; Takashima A; Department of
       Dermatology, University of Texas Southwestern; Medical Center, Dallas
       75235, USA.
 SO    J Immunol. 1995 Dec 1;155(11):5190-7. Unique Identifier : AIDSLINE
       MED/96072792
 AB    We have reported previously that XS52 cells, a long-term dendritic cell
       (DC) line established from mouse epidermis, proliferate maximally in
       response to CSF-1, and that XS52 cells expanded in this manner induce
       brisk proliferation of HDK-1 T cells (KLH-specific Th1 clone) and 5S8 T
       cells (DNBS-specific Th0 clone) in the presence of Ag. Our purpose was
       to determine whether CSF-1-dependent mitotic potential of XS52 cells
       might be affected upon Ag-dependent interaction with these T cell
       clones. Both surface CSF-1R expression and mitotic responsiveness to
       CSF-1 became undetectable within 24 h after incubation with each T cell
       clone in the presence of relevant Ag. By contrast, incubation with T
       cells alone or Ag alone had minimal effect, indicating a requirement for
       both T cells and Ag. Exposure of fresh XS52 cells to the supernatant
       collected from complete XS52/HDK-1/KLH or XS52/5S8/DNBS coculture was
       sufficient to abrogate both CSF-1R expression and CSF-1 responsiveness.
       Importantly, both were restored by mAb against IFN-gamma, and both were
       diminished by rIFN-gamma in the absence of T cells or Ag. Thus,
       IFN-gamma, which was detected in relatively large amounts in the above
       supernatants, serves as a major mediator. rIFN-gamma reduced the number
       of CSF-1 binding sites on XS52 cell surface, without affecting CSF-1R
       mRNA expression. Thus, it appears that IFN-gamma down-regulates CSF-1R
       by a post-transcriptional mechanism. We interpret these results to
       document a novel, bi-directional signaling event in which Ag-dependent
       DC-T cell interaction promotes the growth of T cells, but inhibits the
       growth of DC.
 DE    Animal  Antigens/PHARMACOLOGY  Cell Division  Cell Line  Dendritic
       Cells/*IMMUNOLOGY  Down-Regulation (Physiology)  Hemocyanin/PHARMACOLOGY
       Interferon Type II/PHARMACOLOGY  Macrophage Colony-Stimulating
       Factor/*IMMUNOLOGY  Mice  Mice, Inbred BALB C  Receptors,
       Colony-Stimulating Factor/BIOSYNTHESIS  RNA, Messenger/ANALYSIS  Signal
       Transduction  Skin/CYTOLOGY  Support, Non-U.S. Gov't  Support, U.S.
       Gov't, P.H.S.  Th1 Cells/*IMMUNOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

