PMID- 10233715
OWN - NLM
STAT- MEDLINE
DCOM- 19990721
LR  - 20190513
IS  - 0019-2805 (Print)
IS  - 1365-2567 (Electronic)
IS  - 0019-2805 (Linking)
VI  - 96
IP  - 3
DP  - 1999 Mar
TI  - Mechanism of mercury-induced autoimmunity: both T helper 1- and T helper 2-type 
      responses are involved.
PG  - 348-57
AB  - Mercury can induce a systemic autoimmune disease in susceptible mouse strains. 
      H-2s mice are particularly susceptible to mercury-induced autoimmunity and other 
      mouse strains are more or less resistant. T helper 1/T helper 2 (Th1/Th2) 
      dichotomy has been proposed for resistance or susceptibility, respectively. In 
      the current study we show that mercury treatment induced a full autoimmune 
      response in both C57BL/6 (H-2b) wild-type and interleukin-4 (IL-4)-deficient 
      mice. Antibody production of all isotypes were induced, except that in 
      IL-4-deficient mice there was no immunoglobulin E (IgE) and very low levels of 
      immunoglobulin G1 (IgG1) antibody synthesis. Autoantibodies of different 
      specificities were produced. The granular pattern of all IgG subclasses deposits 
      were detected in the kidneys. In contrast to mercury-treated H-2s seconds mice, 
      we did not detect any anti-nucleolar autoantibodies in the sera of 
      mercury-treated wild-type or IL-4-deficient mice. To further explore the role of 
      Th1/Th2 cytokines in the mercury model, we performed anti-interferon-gamma 
      antibody treatment in IL-4-deficient mice together with mercury treatment and 
      found that the production of IgG2a and IgG3, but not IgG2b, antibodies was 
      downregulated. This indicated that besides Th2-type cytokines, Th1-type and other 
      cytokines were involved as well in mercury-induced autoimmune response. Thus, 
      C57BL/6 mice with H-2b genotype are highly susceptible to mercury-induced 
      autoimmunity, and the genetic susceptibility to mercury involves more than a 
      predisposition of a Th1-or Th2-type response.
FAU - Hu, H
AU  - Hu H
AD  - Department of Immunology, Arrhenius Laboratories for Natural Sciences, Stockholm 
      University, Stockholm, Sweden.
FAU - Moller, G
AU  - Moller G
FAU - Abedi-Valugerdi, M
AU  - Abedi-Valugerdi M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Immunology
JT  - Immunology
JID - 0374672
RN  - 0 (Antibodies, Antinuclear)
RN  - 0 (Autoantibodies)
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
RN  - 207137-56-2 (Interleukin-4)
RN  - 82115-62-6 (Interferon-gamma)
RN  - FXS1BY2PGL (Mercury)
SB  - IM
MH  - Animals
MH  - Antibodies, Antinuclear/biosynthesis
MH  - Autoantibodies/biosynthesis
MH  - Autoimmunity/*drug effects
MH  - Cytokines/*immunology
MH  - Down-Regulation/immunology
MH  - Fluorescent Antibody Technique, Direct
MH  - Immunoglobulin G/metabolism
MH  - Interferon-gamma/immunology
MH  - Interleukin-4/immunology
MH  - Kidney/immunology
MH  - Mercury/*immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Spleen/immunology
MH  - Th1 Cells/*immunology
MH  - Th2 Cells/*immunology
PMC - PMC2326774
EDAT- 1999/05/08 00:00
MHDA- 1999/05/08 00:01
PMCR- 2000/03/01
CRDT- 1999/05/08 00:00
PHST- 1999/05/08 00:00 [pubmed]
PHST- 1999/05/08 00:01 [medline]
PHST- 1999/05/08 00:00 [entrez]
PHST- 2000/03/01 00:00 [pmc-release]
AID - imm671 [pii]
AID - 10.1046/j.1365-2567.1999.00671.x [doi]
PST - ppublish
SO  - Immunology. 1999 Mar;96(3):348-57. doi: 10.1046/j.1365-2567.1999.00671.x.