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The Role of CD4 + T Cells in Cell‐Mediated Immunity to LCM V: Studies in MHC Class I and Class II Deficient Mice
Author(s) -
CHRISTENSEN J. P.,
MARKER O.,
THOMSEN A. R.
Publication year - 1994
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1994.tb03477.x
Subject(s) - lymphocytic choriomeningitis , t cell , cd8 , biology , virus , mhc class ii , mhc class i , immunity , cytotoxic t cell , major histocompatibility complex , immunology , immune system , inflammation , virology , acquired immune system , in vitro , biochemistry
Parameters of the virus‐specific T‐cell response were analysed in order to dissect the contribution of CD4 + and CDS + T cells to cell‐mediated immunity to lymphocytic choriomeningitis virus. In MHC class II deficient mice, initial T‐cell responsiveness was not impaired, but virus clearance was delayed, and virus‐specific T d activity declined more rapidly. Furthermore, class I restricted T c memory appeared to be impaired in these mice. To directly evaluate the role of CD4 + cells in virus clearance and T‐cell mediated inflammation, MHC class I deficient mice were also studied. No virus‐specific delayed‐type hypersensitivity reaction was detected following infection of the footpad, and only a few mice died from intracerebral challenge. However analysis of markers of T‐cell activation as well as direct evaluation of CSF infiammation unveiled a low degree of T‐cell activation and a chronic cellular exudate. This low‐grade response was associated with some degree of virus control as organ titres were lower in these animals than in matched T‐cell deficient nu/nu mice or class I deficient mice treated with anti‐CD4 monoclonal antibody. This confirms that CD4 + cells are not needed to induce a virus‐specific CD8 + T‐cell response, but our findings strongly suggest that CD4 + T cells are critical for maintaining full antiviral immunity. Furthermore, CD4 + T cells per se have a low potential for mediating virus‐specific infiammation that is associated with a low degree of virus control.