Neonatal infection with a milk-borne virus is independent of beta7 integrin- and L-selectin-expressing lymphocytes.

JENNIFER CZARNESKI; PAULA BERGUER; PEDRO BEKINSCHTEIN; DAVID C. KIM; PAUL HAKIMPOUR; NORBERT WAGNER; IRENE NEPOMNASCHY; ISABEL PIAZZON; SUSAN R. ROSS

EUROPEAN JOURNAL OF IMMUNOLOGY

Año: 2002 vol. 32 p. 945 - 956

0014-2980

Mouse mammary tumor virus (MMTV) is acquired by neonates through milk and first infects lymphocytes in Peyer's patches. We show here that newborn mice lacking beta7 integrin or L-selectin were infected with MMTV at wild-type levels in both their lymphoid and mammary tissues. Superantigen-mediated activation and cognate T cell deletion were also unimpaired in both types of null mice. A large proportion of neonatal Peyer's patch lymphocytes in wild-type mice were beta7 and beta1 integrin low and both populations increased in response to MMTV infection. These results suggest that adhesion molecules other than beta7 integrin or L-selectin play a role in lymphocyte homing in the gut, peripheral lymph nodes and mammary gland in response to MMTV infection.