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

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Cook, MC; Körner, H; Riminton, DS; Lemckert, FA; Hasbold, J; Amesbury, M; Hodgkin, PD; Cyster, JG; Sedgwick, JD; Basten, ADate
1998-10-19Source Title
Journal of Experimental MedicinePublisher
Rockefeller University PressUniversity of Melbourne Author/s
Hodgkin, PhilipAffiliation
Medical Biology (W.E.H.I.)Metadata
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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 AccessOpen Access at PMC
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2213402Abstract
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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