Animal models are used for the study of a number of human

autoimmune diseases, including multiple sclerosis, diabetes,

rheumatoid
arthritis,
systemic
lupus
erythematosis
and
spondyloarthropathies. Induced, spontaneous and genetically
manipulated animal models can be described in terms of their
parallels to human disease and as valuable tools for the
development of potential therapies. Studies in animal models have
led to a number of important discoveries, which have increased our
understanding of the pathogenesis of autoimmune disease,
including the roles played by regulatory T cells and TH17 cells. In
addition, important therapeutic advances have emerged as a result
of studies of immune intervention in animal models of autoimmunity.
For example, tumour necrosis factor (TNF) blocking drugs, which are
widely used for the treatment of rheumatic diseases, were
developed following preclinical testing in animal models.
Animal models may be either spontaneously occurring or induced as
a result of genetic manipulation, immunization with a selfantigen or
triggered by pathogenassociated molecular patterns (PAMPs) in
genetically susceptible hosts.
No animal model completely mimics human disease.
Animal models can be used to delineate common mammalian
immunological mechanisms, test novel therapeutic concepts and

Immune complexes derive from complex interactions

between antibody, antigens, complement and various
receptors as a part of adaptive immunity. Antigens bound to
antibodies in immune complexes are normally cleared by
various cellular mechanisms physiologically capable of
eliminating even small quantities of foreign antigens from
circulation. Immune complexes can form when humans are
exposed to foreign substances like proteins (infections,
vaccines, drugs, etc.) or nonprotein materials (haptens)
which need a protein carrier to activate the cascade.
Autoimmune disorders develop when immune complexes
deposit pathologically in different organs, initiating
inflammatory cascades which lead to organ damage/disease.
Immune complex disease can manifest in a myriad of ways
when dysregulation in one or more of these components
occur. Even some recombinant protein therapeutic agents
used to treat autoimmunity may paradoxically form immune
complexes,
neutralizing
therapeutic
efficacy
and/or
manifesting as immune complex disease.

Latticed immune complexes are pathologically capable of depositing

systemically in any of a variety of tissue sites, creating downstream
cellular damage with many different clinical presentations, all of
which fall into the category of immune complex disease (the
prototype originally being referred to as serum sickness).
Several experimental animal models of immune complex disease
have emerged yielding useful information on the cellular and soluble
elements involved in its pathogenesis.
Immune complex disease in humans is seen primarily in the setting
of infection and/or in response to various therapeutic agents of
protein or nonprotein nature.
Adaptive immunity has also evolved to readily discriminate between
self and foreign antigens. Loss of ability to recognize selfantigens
results in Autoimmunity in which both cellular and soluble immune
responses against selfantigens pathologically occur.
Many different autoimmune disorders in humans feature immune
complex disease manifestations and generally derive from unknown
selfantigens complexed to selfantibodies. Even some recombinant
protein therapeutic agents used to treat autoimmunity may induce
formation of immune complexes, neutralizing therapeutic efficacy
and/or manifesting as immune complex disease.