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THE ROLE OF ADHERENT CELLS IN THE SECONDARY CELL‐MEDIATED RESPONSE IN VITRO TO A NATURAL POXVIRUS PATHOGEN
Author(s) -
Pang T,
Blanden RV
Publication year - 1976
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1976.57
Subject(s) - ectromelia virus , ectromelia , spleen , in vitro , biology , antigen , immune system , virus , cell , precursor cell , antigen presenting cell , b 1 cell , immunology , virology , microbiology and biotechnology , t cell , biochemistry , vaccinia , gene , recombinant dna
Summary The role of adherent cells in an in vitro secondary response to ectromelia virus infection was investigated. Spleen cells from ectromelia‐primed mice (“responder” cells) depleted of adherent cells by either carbonyl iron treatment, adherence to plastic or passage through cotton wool columns had a markedly decreased capacity to produce a secondary response, as indicated by decreased T cell‐mediated cytotoxicity against virus‐infected target cells, when cultured with virus‐infected “stimulator” cells. The secondary response was restored by the addition of peritoneal cells from cither normal or ectromelia‐immune mice. Small numbers of peritoneal cells completely reconstituted the response within a certain dose range but larger numbers produced a marked inhibition of the response. Spleen cells were less effective in restoring the response. The peritoneal cells were not merely acting as additional, infected “stimulator” or antigen‐presenting cells, since they could be added as late as 3 days after culture. Reconstituting activity was not affected by pretreatment with anti‐ θ serum and complement and cell separation studies showed that the activity was associated mainly with Ig‐negative cells and that the active cell probably bears Ia antigens on its surface. These results indicate that the adherent cells involved are probably macrophages and that they act non‐specifically to produce optimum conditions for the specific response of T cells.