GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Rockefeller University Press  (2)
Material
Publisher
  • Rockefeller University Press  (2)
Language
Years
Subjects(RVK)
  • 1
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 183, No. 6 ( 1996-06-01), p. 2657-2662
    Abstract: Mice mutant for granulocyte macrophage colony-stimulating factor (GM-CSF) or the common receptor component (beta c) for GM-CSF, interleukin (IL)-3, and IL-5 exhibit a lung disorder similar to human pulmonary alveolar proteinosis, a rare disease with congenital, infantile, and adult forms. Bone marrow transplantation and hematopoietic reconstitution of beta c mutant mice with wild-type bone marrow reversed the established disease state in the lungs, defining this disease as hematopoietic in nature. It is likely that the disease involves alveolar macrophages, as donor myeloid cell engraftment into the lungs of mutant recipient mice correlated with reverting both the disease and an abnormal macrophage morphology seen in the lungs of affected animals. Recombination Activating Gene-2 mutant donor bone marrow, which lacks the potential to develop lymphocytes, reversed the pathology in the lungs to the same extent as whole bone marrow. These data establish that certain lung disorders, if of cell-autonomous hematopoietic origin, can be manipulated by bone marrow transplantation.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    RVK:
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1996
    detail.hit.zdb_id: 1477240-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Rockefeller University Press ; 1995
    In:  The Journal of experimental medicine Vol. 181, No. 4 ( 1995-04-01), p. 1519-1526
    In: The Journal of experimental medicine, Rockefeller University Press, Vol. 181, No. 4 ( 1995-04-01), p. 1519-1526
    Abstract: Interleukin (IL)-7 is a potent stimulus for immature T and B cells and, to a lesser extent, mature T cells. We have inactivated the IL-7 gene in the mouse germline by using gene-targeting techniques to further understand the biology of IL-7. Mutant mice were highly lymphopenic in the peripheral blood and lymphoid organs. Bone marrow B lymphopoiesis was blocked at the transition from pro-B to pre-B cells. Thymic cellularity was reduced 20-fold, but retained normal distribution of CD4 and CD8. Splenic T cellularity was reduced 10-fold. Splenic B cells, also reduced in number, showed an abnormal population of immature B cells in adult animals. The remaining splenic populations of lymphocytes showed normal responsiveness to mitogenic stimuli. These data show that proper T and B cell development is dependent on IL-7. The IL-7-deficient mice are the first example of single cytokine-deficient mice that exhibit severe lymphoid abnormalities.
    Type of Medium: Online Resource
    ISSN: 0022-1007 , 1540-9538
    RVK:
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 1995
    detail.hit.zdb_id: 1477240-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...