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T‐Cell Effector Function and Unresponsiveness in the Murine Lymphocytic Choriomeningitis Virus Infection
Author(s) -
THOMSEN A. R.,
MARKER O.
Publication year - 1986
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.1365-3083.1986.tb02079.x
Subject(s) - lymphocytic choriomeningitis , adoptive cell transfer , cytotoxic t cell , virus , biology , priming (agriculture) , immunology , virology , t cell , cd8 , immune system , in vitro , biochemistry , botany , germination
An increase in the virus dose from 10 2 LD 50 (low dose) to 10 4 LD 50 (high dose) of lymphocytic choriomeningitis virus (LCMV) results in markedly delayed virus clearance, in spite of a potent cytotoxic T‐cell (T c ) response. However, virus‐specific delayed‐type hypersensitivity (DTH) reactivity is markedly depressed in high‐dose mice, suggesting an association between DTH and virus clearance. When virus‐primed memory cells are transferred, DTH reactivity as well as virus‐clearing capacity is restored in high‐dose mice, indicating that the virus is not present in a changed or concealed form. The role of T‐cells mediating DTH (T D cells) in virus clearance was also studied by adoptive transfer to naive recipients. Here the high‐dose primed cells did mediate virus clearance, although no DTH reaction was detectable 24–72 h after transfer. However, when footpad swelling was measured 96 h or more after transfer a DTH response emerged, indicating that T D priming had taken place in high‐dose animals. Pre‐irradiation of high‐dose primed cells markedly inhibited the antiviral activity as well as DTH, suggesting that upon transfer to naive recipients T D precursors from high‐dose mice would proliferate into effector cells capable of mediating both functions. Treatment with anti‐Lyt 2+C’ abrogated the capacity to induce virus‐specific DTH, thus confirming that the cells involved are not helper T (T H ) cells. We conclude that the DTH unresponsiveness in high‐dose mice reflects a defective differentiation of T D precursor into effector cells which is reversible upon transfer to a less antigen loaded environment. Furthermore, it is suggested that T D function is crucial to the process of virus clearance.