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Immunoregulation in experimental murine Trypanosoma congolense infection: anti‐IL‐10 antibodies reverse trypanosome‐mediated suppression of lymphocyte proliferation in vitro and moderately prolong the lifespan of genetically susceptible BALB/c mice
Author(s) -
Jude E. Uzonna,
Radhey S. Kaushik,
John Gordon,
H. Tabel
Publication year - 1998
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1046/j.1365-3024.1998.00156.x
Subject(s) - biology , splenocyte , isotype , immunology , antibody , spleen , trypanosoma , cytokine , monoclonal antibody , concanavalin a , in vivo , balb/c , immune system , virology , in vitro , biochemistry , microbiology and biotechnology
We infected highly susceptible BALB/c and relatively resistant C57BL/6 mice with cloned Trypanosoma congolense and followed the effects of these infections on the circulating parasite numbers, mouse mortality and cytokine expression. C57BL/6 mice controlled their parasitaemia and survived for up to 163 ± 12 days, while BALB/c mice could not control their parasitaemia and succumbed to the infection within 8.4 ± 0.5 days. Susceptible BALB/c mice had dramatically higher plasma levels of IL‐10 than the resistant C57BL/6 mice from day 7 forward. This was preceded by an earlier and higher level induction of splenic IL‐10 messenger RNA (mRNA) expression in the infected BALB/c mice. There was a strong negative correlation between the splenocyte proliferative responses to Concanavalin‐A (Con‐A) and their production of IL‐10 in these infected BALB/c mice. Co‐treatment of the Con‐A‐stimulated spleen cell cultures with monoclonal anti‐IL‐10 antibodies, but not isotype‐matched control antibodies, could completely reverse this suppression of the splenocyte proliferative response. Finally, in three experiments, anti‐IL‐10 antibody treatment in vivo reduced the peak circulating parasitaemia of infected BALB/c mice by 43% and increased their median survival periods by 38% relative to isotype‐matched control antibody‐treated mice .