Cytokines in induction of ANoA and hypergammaglobulinemia in mercury-induced autoimmunity: a lesson from Fc!RIII deficient mice

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Martinsson, KlaraLinköpings universitet,Institutionen för klinisk och experimentell medicin,Hälsouniversitetet (author)

Cytokines in induction of ANoA and hypergammaglobulinemia in mercury-induced autoimmunity : a lesson from Fc!RIII deficient mice

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LIBRIS-ID:oai:DiVA.org:liu-19159
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-19159URI

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Language:English
Summary in:English

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Subject category:ovr swepub-publicationtype

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Xenobiotic agents such as metals, drugs, toxic oils and pristane can induce autoimmune diseases. Heavy metal induction of autoimmunity has been observed for mercury (Hg), silver and gold in mice. Mercury-induced autoimmunity (HgIA) in mice is characterised by lymphoproliferation, hypergammaglobulinemia, antinucleolar autoantibodies (ANoA) and immune complex deposits in the renal glomerular mesangium and systemically in vessel walls. HgIA is T-cell dependent, IFNγ is necessary for all manifestations of HgIA, and the activating Fc!RIII enhance development of ANoA. This study focused firstly on exploring the cytokine profile in the genetically susceptible DBA/1 (H-2q) wild type (wt) and DBA/1 FcγRIII-/- mice treated with 15 mg/l Hg, and secondly on the hypothesis that IFN-! producing NK cells are vital for induction of ANoA in the HgIA model. DBA/1 wt mice showed a significantly more marked Th1 profile compared to DBA/1 FcγRIII-/- mice following Hg treatment, whereas the total Th2 and Th17 profile increased in both DBA/1 wt and DBA/1 FcγRIII-/- mice. However, during Hg treatment IL-21 mRNA expression was significantly reduced in DBA/1 FcγRIII-/- mice compared with DBA/1 wt mice. However, we were unable to show that the increased Th1 profile in the DBA/1 wt mice was due to IFN-γsecretion from NK cells. Our findings suggest that the delayed ANoA induction in DBA/1 FcγRIII-/- mice is due to the attenuated Th1 profile. In addition the reduced expression of IL-21 in DBA/1 FcγRIII-/- mice might be responsible for the lack of serum IgG1 response in these mice.

Subject headings and genre

Fc!RIII
NK-cells
autoimmunity
cytokines
mercury
MEDICINE
MEDICIN

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Cederbrant, KarinLinköpings universitet,Molekylär och immunologisk patologi,Hälsouniversitetet(Swepub:liu)karce90 (author)
Hultman, PerLinköpings universitet,Molekylär och immunologisk patologi,Hälsouniversitetet(Swepub:liu)perhu66 (author)
Linköpings universitetInstitutionen för klinisk och experimentell medicin (creator_code:org_t)

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