Part of the book: Tuberculosis
Anti-lipid antibodies are present in some infectious and autoimmune diseases, such as Systemic Lupus Erythematosus (SLE). Particularly, anti-non-bilayer phospholipid arrangement (NPA) antibodies have been detected in patients with SLE, and these antibodies trigger a disease similar to human lupus in mice. NPA are lipid associations different from the lipid bilayer of cellular membranes and, since they are transient, they are not immunogenic. However, if NPA are stabilized by drugs, they induce an immune response with the production of anti-NPA antibodies, which bind to NPA on cell membranes and generate cell lysis. As a result, intracellular antigens are exposed and trigger an immune response that generates more auto-antibodies. In this chapter, we describe the formation and stabilization of NPA, the induction of B cell responses to generate anti-NPA antibodies, and the characteristics that the disease caused by these antibodies in mice shares with human lupus.
Part of the book: Systemic Lupus Erythematosus
Chagas disease, or American trypanosomiasis, is a zoonosis caused by the hemoflagellate parasite Trypanosoma cruzi. It is mainly transmitted by the bite of blood-sucking insects. It is endemic in Latin America and emerging in the rest of the world, affecting approximately six million people. The drugs Benznidazole and Nifurtimox currently used for its treatment are not totally effective in the chronic phase of the disease. In addition, they are toxic, and there are many resistant Trigonoscuta cruzi strains. Therefore, developing new drugs for the treatment of Chagas disease is necessary. This chapter describes the development of drugs that inhibit α-hydroxy acid dehydrogenase isoenzyme II, a key enzyme in parasite energy metabolism. These drugs have shown more significant trypanocidal activity than the currently used drugs, and they have also prevented the development of chronic Chagas disease in infected mice.
Part of the book: Current Topics in Zoonoses