Aberrant development of thymocytes in mice lacking laminin-2.
AuthorMagner, WJ; Chang, AC; Owens, J; Hong, MJ; Brooks, A; Coligan, JE
University of Melbourne Author/sBrooks, Andrew
AffiliationMicrobiology and Immunology
Document TypeJournal Article
CitationsMagner, W. J., Chang, A. C., Owens, J., Hong, M. J., Brooks, A. & Coligan, J. E. (2000). Aberrant development of thymocytes in mice lacking laminin-2.. Dev Immunol, 7 (2-4), pp.179-193. https://doi.org/10.1155/2000/90943.
Access StatusOpen Access
Open Access at PMChttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2276047
In previous in vitro studies, we proposed a role for the extracellular matrix component, laminin-2, and its integrin receptor, VLA-6, in thymocyte development. The characterization of two dystrophic mouse strains with different defects in laminin-2 allowed us to examine this proposal in vivo. Mice deficient in laminin-2, dy/dy, show a significant reduction in thymus size and number of thymocytes compared to normal littermates. These mice also exhibited apparent alterations of thymic architecture. Examination of the CD4/CD8 populations in dy/dy thymi showed large relative increases in the DN (CD4- CD8-) and SP (CD4+ CD8-, CD4- CD8+) populations and a significant decrease in the DP (CD4+ CD8+) population. Further examination of the DN population for CD44 and CD25 expression showed a remarkable decrease in the more mature pre-T cell populations. Analysis of apoptosis in situ, and by flow cytometry, in dy/dy thymi revealed a significant increase in apoptotic DN thymocytes in the capsule and subcapsular regions. Interestingly, thymocyte development appeared to proceed normally in dystrophic mice expressing a mutant form of laminin-2, dy2J, as well as, in fetal and neonatal dy/dy mice. We propose that laminin-2 plays an active role in thymocyte development by delivering cell survival and differentiation signals at specific stages of development in young adult mice.
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