Lupus is a debilitating, inflammatory autoimmune disease most common in women ages 15-45, or during their reproductive years, in a ratio of 9 women to 1 man. This is a condition where the immune system reacts excessively causing inflammation in different organs and resulting in a broad range of clinical manifestations with periods of remission and flares. Patients affected by lupus have a reduced quality of life and productivity, while the care and treatment of lupus represent a social and economic burden for patients and the health care system. Currently, there is no treatment that cures lupus, in fact, treatments are limited to controlling pain and inflammation to reduce disease activity.
Lupus is a multifactorial disease where genetic susceptibility combined with environmental factors trigger the autoimmune response. The principal characteristic of the disease is the high levels of antibodies against self-nucleic acid structures produced by B cells, which make the basis of the disease. However, B cells have other functions, such as producing inflammatory and anti-inflammatory mediators, called cytokines, and can also help to activate other immune cells. Recent therapies targeting B cells showed positive results, emphasizing the importance of B cells in the pathogenesis of lupus. Therefore, it is important to further investigate the different functions of B cells and their regulation to develop more specific therapies to treat lupus.
It is known that in Europe 1 in 750 women suffer from lupus. These numbers represent a heavy economic and social burden since lupus affects women in their more productive years. Lupus affects every part of a patient´s life, work, school, finances, family, relationships, and mental and emotional well-being. Thus, finding novel and more specific treatments that help to reduce disease progression will reduce the negative impact of lupus in society.
Genetic factors have been associated with lupus development. Among them, a genetic variant of the B cell scaffold protein with Ankyrin repeats 1 (BANK1) has been identified as a genetic risk for developing lupus. BANK1 actively participates in the activation of B cells and in the production of autoantibodies in a lupus model. However, it is not known whether BANK1 regulates the production of either other antibodies or cytokines. Our general objective was to investigate the role of BANK1 signaling in the antibody production and antibody-independent functions of B cells in a mouse model of Lupus.
