|  Help  |  About  |  Contact Us

Publication : Cryptosporidium muris in adult mice: adoptive transfer of immunity and protective roles of CD4 versus CD8 cells.

First Author  McDonald V Year  1994
Journal  Infect Immun Volume  62
Issue  6 Pages  2289-94
PubMed ID  7910592 Mgi Jnum  J:18455
Mgi Id  MGI:66738 Doi  10.1128/iai.62.6.2289-2294.1994
Citation  McDonald V, et al. (1994) Cryptosporidium muris in adult mice: adoptive transfer of immunity and protective roles of CD4 versus CD8 cells. Infect Immun 62(6):2289-94
abstractText  The aim of this study was to investigate the role of the CD4 and CD8 T cells in immunity to cryptosporidia by using Cryptosporidium muris and a mouse model of infection. Two approaches were used, each involving the use of rat anti-T-cell surface marker monoclonal antibodies (MAbs). In the first, the adoptive transfer of immunity was studied by using the CB.17 SCID mouse (which lacks T and B cells) as the host; in the second, the effect on susceptibility of BALB/c mice to infection was examined following depletion of T cells or subsets of T cells. In adoptive immunity experiments, the conditions which differentiated between resistance associated with reconstitution of SCID mice with naive BALB/c lymphocytes and the transfer of immunity with primed lymphocytes from infected animals were determined. Primed spleen or mesenteric lymph node cells conferred better protection to recipients than naive cells when obtained from donors which had developed resistance to infection. Adoptive immunity was abrogated when Thy.1 cells or CD4 cells were depleted from primed cells, while depletion of CD8 cells could reduce the level of protection. In the study of C. muris in BALB/c mice, treatment with either anti-Thy.1 plus anti-Lyt.1 or anti-CD4 MAbs increased susceptibility to a primary infection as determined by the size and duration of oocyst production, but an anti-CD8 MAb produced an increase only in oocyst shedding. Thus, both CD4 and, to a lesser extent, CD8 cells appeared to be involved in resistance to primary and secondary C. muris infection.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

0 Bio Entities

0 Expression