By Frank J. Dixon
From the studies of past Volumes "Provides unrivalled price in either educational and monetary phrases and will be bought by means of demanding pressed librarians as an immense precedence to be jealously defended." -JOURNAL OF clinical MICROBIOLOGY "Advances in Immunology needs to locate itself one of the such a lot energetic volumes within the libraries of our universities and institutions." -SCIENCE "A provocative and scholarly evaluate of research." -JOURNAL OF the yank clinical organization "Deserves an everlasting position in biomedical libraries as an relief in examine and in teaching." -JOURNAL OF IMMUNOLOGIC equipment
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Extra resources for Advances in Immunology, Vol. 55
1991b) studied primary bone STEM CELL FACTOR 51 marrow cells from mice separated by immunomagnetic bead selection for B220+ and B220- populations. As expected, recombinant IL-7 supported the proliferation of B cells only from the B220+ population. SCF alone supported the proliferation of small myeloid colonies from the B220- populations. However, when both factors were combined, there was a substantial increase in the size of colonies produced from either population, and all of the progeny were B220+.
Developing B lymphocytes express the VLA-4 integrin that interacts with what appears to be a VCAM-1 ligand on stromal cells. In addition, hyaluronate present on stromal cells has been implicated in mediating stromal cell-B lymphocyte interactions. Rolink et al. (1991)examined the role of SCF/SCF receptor interactions between pre-B cell lines and stromal cells by utilizing the ACK-2 neutralizing antibody to the SCF receptor. Addition of the ACK-2 antibody to the stromal cell cultures inhibited the growth of these pre-B cell lines, which require both contact with stromal cells and the costimulatory activity of IL-7 for continuous proliferation.
The observation that SZISCF mutant mice exhibit abnormal hematopoietic responses to acute injury, such as irradiation, indicates that another major role of SCF may be to contribute to hematopoiesis during states of hematopoietic stress (Russell, 1979). In accord with this hypothesis, Hunt et aZ. (1992) have reported evidence that SCF contributes to the rebound thrombocytosis that follows 5-fluorouracil treatment in mice. Since the isolation of cDNA for SCF and the generation of recombinant forms of this growth factor, a large number of studies have evaluated the effects of SCF in various in uitro assays of hematopoiesis or 46 STEPHEN J.
Advances in Immunology, Vol. 55 by Frank J. Dixon