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    Generation of splenic follicular structure and B cell movement in tumor necrosis factor-deficient mice.

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    44
    Author
    Cook, MC; Körner, H; Riminton, DS; Lemckert, FA; Hasbold, J; Amesbury, M; Hodgkin, PD; Cyster, JG; Sedgwick, JD; Basten, A
    Date
    1998-10-19
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Hodgkin, Philip
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Cook, M. C., Körner, H., Riminton, D. S., Lemckert, F. A., Hasbold, J., Amesbury, M., Hodgkin, P. D., Cyster, J. G., Sedgwick, J. D. & Basten, A. (1998). Generation of splenic follicular structure and B cell movement in tumor necrosis factor-deficient mice.. J Exp Med, 188 (8), pp.1503-1510. https://doi.org/10.1084/jem.188.8.1503.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259240
    DOI
    10.1084/jem.188.8.1503
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213402
    Abstract
    Secondary lymphoid tissue organogenesis requires tumor necrosis factor (TNF) and lymphotoxin alpha (LTalpha). The role of TNF in B cell positioning and formation of follicular structure was studied by comparing the location of newly produced naive recirculating and antigen-stimulated B cells in TNF-/- and TNF/LTalpha-/- mice. By creating radiation bone marrow chimeras from wild-type and TNF-/- mice, formation of normal splenic B cell follicles was shown to depend on TNF production by radiation-sensitive cells of hemopoietic origin. Reciprocal adoptive transfers of mature B cells between wild-type and knockout mice indicated that normal follicular tropism of recirculating naive B cells occurs independently of TNF derived from the recipient spleen. Moreover, soluble TNF receptor-IgG fusion protein administered in vivo failed to prevent B cell localization to the follicle or the germinal center reaction. Normal T zone tropism was observed when antigen-stimulated B cells were transferred into TNF-/- recipients, but not into TNF/LTalpha-/- recipients. This result appeared to account for the defect in isotype switching observed in intact TNF/LTalpha-/- mice because TNF/LTalpha-/- B cells, when stimulated in vitro, switched isotypes normally. Thus, TNF is necessary for creating the permissive environment for B cell movement and function, but is not itself responsible for these processes.

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