Open AccessTheileria annulata induces abberrant T cell activation in vitro and in vivo
Author(s) -
CAMPBELL J. D. M.,
HOWIE S. E. M.,
ODLING K. A.,
GLASS E. J.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb05533.x
Subject(s) - biology , germinal center , immunology , immune system , lymph node , antigen , cytotoxic t cell , interleukin 21 , antigen presenting cell , theileria parva , t cell , cd8 , in vitro , cd40 , b cell , parasite hosting , antibody , biochemistry , world wide web , computer science
SUMMARY The protozoan parasite of cattle, Theileria annulata , causes a severe lymphoproliferative disease, developing initially in the draining lymph node, which is often fatal in naive animals. Infection of macrophages with T. annulata leads to an augmentation of their antigen‐presenting capability in vitro and infected cells can induce proliferation of autologous resting T cells from naive animals. This inappropriate activation of T cells may play an important role in the failure of the host to mount an effective immune response in vivo. To investigate this hypothesis we characterized further the response of T cells from naive cattle to infected cells in vitro , and also examined the development of the immune response in lymph nodes draining the sites of T. annulata infection. Both CD4 + and CD8 + T cells from naive peripheral blood mononuclear cells (PBMC) were induced to proliferate and express the activation markers IL‐2R and MHC class II when cultured with infected cells. This effect was seen in both ‘naive’ and ‘memory’ T cells, and was dependent upon contact with infected cells. In vitro , infected cells are therefore capable of activating T cells irrespective of their antigen specificity or memory status. In draining lymph nodes, although large numbers of IL‐2R + cells developed following infection, these activated cells were only associated with areas of parasite‐induced proliferating cells, and subsequently disappeared from the node. Cells expressing IL‐2R were not present in recognized sites for T cell development. Germinal centres were severely affected, losing T cell‐dependent zones followed by a total destruction of morphology. T cell function is therefore severely disrupted within draining nodes. This study has shown that parasitized cells supply sufficient signals in vitro to activate T cells irrespective of specificity. T cells also are not stimulated in a conventional manner in vivo , and this may play an important role in preventing an effective immune response from being generated.