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KMID : 0357119930150010011
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Korean Journal of Immunology
1993 Volume.15 No. 1 p.11 ~ p.23
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Effect of Immune Complex on the Cytokine Production and Host Resistance of Mice Against Intracellular Bacteria
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Lee Hyun-Chul
Cho Saeng-Koo
Hwang Tai-Ju
Kang In-Chol
Oh Jong-Suk
Ahn Tae-Hew
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Abstract
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Immune complexes is related extensively to autoimmune diseases, hypersensitivity, and some acquired immunodeficiencies with a variety of unknown mechanisms. Thus, the present study was undertaken to investigate the effects of exogenously administered immune complexes, composed of ovalbumin(OVA0 and anti-OVA antibody, on host resistance to Listeria monocytogenes (LM) and Salmonella typhimurium (ST) infection at the cellular level.
A significantl inhibition of resistance to LM or ST was found when non-immune mice were injected with immune complexes preformed in vitro. When dehydroepiandrosterone (DHEA) was supplemented to immune complexd- or
glucocorticosfteroid(GCS)-treated mice, it showed some protective effect on murine LM infection.
To elucidate the possible mechanisms for immune suppression by immune complexes, he effects of pretreatment of mice with immune complexes on the production of IFN-γby activated splenocytes and TNF-αby macrophages were assessed. Immune complex inhibited in a dose dependent manner TNF-α production by macrophages when they were cultivated on immune complexcoated culture plate. The capacity of mouse splenocytes to produce IFN-γ, however, was not affected by this immune complex treatment.
Although LM infection caused a marked increase in MHC class II molecule(Ia antigen) expression, immune complex treatment resulted in inhibiting effect on Ia expression on the macrophages during LM infection in vivo as well as during cultivation in the presence of IFN-γ in vitro. In addition, DHEA supplement to immune complex treatment resulted in augmenting effect on Ia expression on macrophages in vivo but no effect in vitro.
These findings usggest that suppression of immune response to LM and ST by immune complex is associated with decreased capacities of macrophages to produce TNF-α, in addition to decrease of Ia molecule expression on the macrophages.
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KEYWORD
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Immune complex, Cytokine, Infection
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