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Lymphotoxin-alpha-deficient mice. Effects on secondary lymphoid organ development and humoral immune responsiveness.

Targeted mutagenesis in embryonic stem cells was used to generate mice deficient in lymphotoxin-alpha (LT-alpha). Mice lacking LT-alpha -/- (LT-alpha -/- mice) exhibit a phenotype dominated by defects in secondary lymphoid organ development. LT-alpha -/- mice lack lymph nodes and Peyer's patches, and possess spleens in which the usual architecture is disrupted. However, in a few of the mutants, abnormal lymph node-like structures were observed, mainly within the mesenteric fat. Abnormal clusters of lymphocytes were also found to accumulate in the periportal and perivascular regions of the liver and lung of LT-alpha -/- mice. Yet, lymphocytes from LT-alpha -/- mice appeared phenotypically normal, expressing the expected ratios of B and T cell surface markers as well as the lymphocyte homing marker, L-selectin. In addition, bone marrow cells from LT-alpha -/- mice were able to successfully reconstitute the lymphoid organs of severe combined immunodeficient mice. However, LT-alpha -/- mutant mice examined for humoral immune responsiveness were found to be impaired in their ability to respond to different Ag. These data illustrate the utility of this mouse model as a system for understanding lymphoid organ development and its effects on immune responsiveness.

Pubmed ID: 7636227


  • Banks TA
  • Rouse BT
  • Kerley MK
  • Blair PJ
  • Godfrey VL
  • Kuklin NA
  • Bouley DM
  • Thomas J
  • Kanangat S
  • Mucenski ML


Journal of immunology (Baltimore, Md. : 1950)

Publication Data

August 15, 1995

Associated Grants

  • Agency: NEI NIH HHS, Id: EY05093

Mesh Terms

  • Animals
  • Antibody Formation
  • Base Sequence
  • Female
  • Flow Cytometry
  • Immunoglobulins
  • Lymphoid Tissue
  • Lymphotoxin-alpha
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, SCID
  • Molecular Sequence Data