Autoimmunity and Angiogenesis

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.