|  Help  |  About  |  Contact Us

Publication : Salmonella abortusovis infection in susceptible BALB/cby mice: importance of Lyt-2+ and L3T4+ T cells in acquired immunity and granuloma formation.

First Author  Guilloteau L Year  1993
Journal  Microb Pathog Volume  14
Issue  1 Pages  45-55
PubMed ID  8321117 Mgi Jnum  J:12893
Mgi Id  MGI:61109 Doi  10.1006/mpat.1993.1005
Citation  Guilloteau L, et al. (1993) Salmonella abortusovis infection in susceptible BALB/cby mice: importance of Lyt-2+ and L3T4+ T cells in acquired immunity and granuloma formation. Microb Pathog 14(1):45-55
abstractText  The role of T cells in granulomatous responses and in acquired immunity against Salmonella abortusovis (SAO) infection was studied in a murine model. Mice were subcutaneously (s.c.) vaccinated with a live attenuated strain of SAO. One month after vaccination, the transfer of primed spleen cells (1 x 10(8) cells per mouse) to syngeneic recipient mice conferred a significant protection of 3 log10, measured by spleen colonization on day 6 after s.c. challenge. In vitro treatment of spleen cells, before the transfer, with anti-Lyt-2 monoclonal antibody (IgG2b isotype MAb) and complement significantly impaired the protective activity. Treatment with anti-L3T4 MAb also diminished transferred protection, but to a lesser degree. Depletion of both L3T4+ and Lyt-2+ T cells completely abrogated protection. MAb treatment of spleen cells in vitro did not seem to have any effect on antibody response in recipient mice. Six days after the challenge protected recipient mice showed organized granulomas in the liver containing Mac-1+ macrophages and L3T4+ T cells. In non-protected mice at 6 days post-challenge, large infiltrates of T lymphocytes and macrophages were observed, but as numerous lesions with necrosis of hepatocytes; no granuloma were seen. In our experimental conditions, Lyt-2+ and L3T4+ T cells appeared to play, alone and in synergy, a role in vaccine-induced immunity against SAO and hepatic granulomas may contribute to the control of the infection.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression