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Immunosuppression and cytokine production in mice infested with Ixodes ricinus ticks: a possible role of laminin and interleukin‐10 on the in vitro responsiveness of lymphocytes to mitogens
Author(s) -
GANAPAMO F.,
RUTTI B.,
BROSSARD M.
Publication year - 1996
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1996.450512.x
Subject(s) - biology , concanavalin a , immunology , antigen , lipopolysaccharide , cytokine , lymph node , microbiology and biotechnology , in vitro , biochemistry
T cells from BALB/c mice infested 9 days before with Ixodes ricinus nymphs had a suppressed response to in vitro concanavalin A (Con A) stimulation compared to cells from uninfested mice. When laminin (the main component of the extracellular matrix) was used as a coating agent, the Con A response of naive mice was characterized by a decrease in cell proliferation, whereas there was no significant effect on the mitogen response of cells from infested mice. In contrast, an increased response to lipopolysaccharide (LPS) was observed when assaying lymph node cells of infested mice, probably reflecting an increase in B‐lymphocyte number or activity. LPS cell stimulation was not modified by laminin. Supernatants of lymph node cells, taken 9 days after the first infestation of mice, stimulated with Con A in vitro , contained interleukin‐10 (IL‐10) but no significant levels of IL‐5 as tested by enzyme‐linked immunosorbent assay. At this stage of the infestation all T cells reactive with tick antigens generated in lymph nodes that drain the tick fixation site, were CD4 + cells, as determined by CD4 + depletion. With cells taken 9 days after the third infestation an increase of IL‐5 and IL‐10 was observed. The IL‐10 levels were higher than the IL‐5. According to these observations, we conclude that the reduction of T‐cell proliferation in response to Con A observed in lymph node cells from infested mice, may be due to the combined effect of laminin interaction with T lymphocytes during migration and IL‐10 production by these lymphocytes.