The angiogenesis phenomenon is one of the most important parameters
in developing the inflammatory reactions. Angiogenesis is a biological event
mediated by several cell types and mediators, such as various types of macrophages,
endothelial cells, fibroblasts growth factors, cytokines and chemokines
that is essential not only in physiological processes, such as reproduction, embryonic
development, and tissue repair, but also in numerous pathological conditions
including autoimmune disorders and other inflammatory diseases. Autoimmune
diseases are the consequence of an immune response against self-antigens, due to
genetic or environmental factors which are categorized to organ- and/or nonorgan-
specific and are characterized by expanding the chronic inflammatory reactions.
In rheumatoid arthritis that is characterized by joints chronic inflammation,
angiogenesis process play an important role in the maintenance and progression of
this disease, and/or in multiple sclerosis which is an inflammatory demyelinating
disorder of the central nervous system with vascular features, angiogenesis can
represent a notable role in expanding the lesions contributing to disease
progression. The suppression of angiogenesis by blocking the function of
angiogenic mediators, or by the use of angiostatic compounds could be useful in
inhibiting the inflammatory reactions. An anti-inflammatory targeting in
autoimmune diseases including the inhibition of angiogenic mediator’s production,
such as D-penicillamine, gold salts, sulfasalazine, methotrexat can decrease the
production of angiogenic mediators in inflammatory cells. In this chapter, we will
review the correlation between the angiogenesis phenomenon and immunopathology
of autoimmune disease with particular focus on efficacy of antiangiogenesis
drugs for inhibiting the disease progression.
Keywords: Rheumatoid arthritis, diabetic retinopathy, IBD, TH1, TH2, TH17, Tregs.
