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CD4+CD25+FOXP3+ regulatory T cells (Treg) are of critical importance for the maintenance of immune homeostasis, as numerous experimental mouse models for autoimmune diseases correlate the presence of functional Tregs with amelioration of disease severity [1], [2].

Targeting the interaction between ICAM-1 and LFA-1 as a treatment for (auto immunity has been the subject in a number of studies (reviewed in [17]), and was shown to have beneficial effects in animal models for autoimmune diseases [9], [10].

Experimental mouse models for autoimmune diseases obviously cannot entirely mimic human diseases.

This might suggest shared disease pathways in different models for autoimmune diseases controlled by the same genes within this interval.

Dissections of disease loci in models for autoimmune diseases have shown that one locus can contain more than one gene linked to disease [ 5, 6].

Owing to the general importance of peptide toxins for drug discovery, toxin analogs were characterized extensively in vitro and in vivo in mouse models for autoimmune diseases such as multiple sclerosis, delayed-type hypersensitivity, rheumatoid arthritis and for chronic-relapsing, as well as acute adoptive autoimmune encephalomyelitis [40,44].

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An acute transfer model for autoimmune diabetes was employed by introduction of fluorescently labeled splenocytes harboring diabetogenic TCR-transgenic CD8 T cells into recipients expressing both antigen and GFP in their beta cells.

Although EAN is a representative model for autoimmune diseases of peripheral neurons, experimental autoimmune encephalomyelitis is a representative model for autoimmune diseases of the CNS and is a model for human multiple sclerosis.

The Smyth line (SL) chicken is the only animal model for autoimmune vitiligo that spontaneously displays all clinical and biological manifestations of the human disorder [ 2, 3].

The NOD mouse is a valuable experimental model for autoimmune diabetes; it possesses I-Ag7 as the sole class II molecule [ 55].

CIA is a model for autoimmune arthritis characterized by autoantibody production and massive infiltration of effector cells to joints [ 29, 30].

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