autoimmune encephalomyelitis

J Nutr. 2003 Aug;133(8):2635-8.  Links 

  
Iron-deficient mice fail to develop autoimmune encephalomyelitis.

Grant SM, Wiesinger JA, Beard JL, Cantorna MT.

Department of Nutrition, The Pennsylvania State University, 126 South
Henderson, University Park, PA 16802, USA.

Determinations of the effects of iron status on the immune system are
complicated by the fact that microorganisms and immune cells both utilize iron.
To determine the role of iron in immune function, we utilized a model
[experimental autoimmune encephalomyelitis (EAE)] in which a strong
antigen-specific CD4+ T-cell response develops in the absence of infection. EAE
is an autoimmune disease frequently used as a model for the human disease
multiple sclerosis (MS). EAE was induced in B10.PL mice fed low iron (1 mg/kg),
normal iron (10 mg/kg) or high iron (160 mg/kg) diets that were replete in all
other nutrients. Liver iron measurements verified iron status, i.e., low iron
mice had 1.9 micro mol/g tissue, normal iron mice, 3.27 micro mol/g tissue and
high iron mice, 5.35 micro mol/g tissue. EAE symptoms were most severe in
normal iron mice, and EAE did not develop in low iron mice. The incidence of
EAE was 71% in normal iron mice, 62% in iron-overloaded mice and 0% in
iron-deficient mice. Two of seven mice in the normal iron group developed
severe EAE and were euthanized. None of the iron-overloaded mice developed
severe EAE. Other measures of EAE severity were similar in the normal and
iron-overloaded mice. The data suggest that iron deficiency provides protection
from the development of EAE and that iron excess with its potential
contribution to free radical formation was not an important factor. The
mechanism of EAE inhibition in iron-deficient mice likely involves the delivery
and metabolism of iron for optimal CD4+ T-cell development.

PMID: 12888650 [PubMed - in process] 

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