Adaptation du cours EVIVO au secteur du travail : concilier maladie chronique et vie professionnelle [EVIVO program adapted for the labor sector : a help for managing chronic condition and professional life]

EVIVO is a well-established chronic disease self-management program, having been successfully implemented during the last decade in Switzerland. The program has shown positive results in facilitation of self-management competences for patients living with chronic diseases and their relatives. EVIVO was designed to run for 6 weeks with weekly sessions of 2 and a half hour each. We tested the effectiveness of a shortened version of EVIVO, running it over five half days in order to make it more focused for patients who are challenged by managing their chronic illness within the context of their professional life. Participants in the five-session version showed comparable self-efficacy levels compared with those who had attended the standard six-week six-session courses. Overall, the five-session version was well accepted, considered very useful, met the participants' needs and changed their perception of their own expectations towards self-management of their illness

Production of IgG autoantibody requires expression of activation-induced deaminase in early-developing B cells in a mouse model of SLE

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of pathogenic IgG antinuclear antibodies. Pathogenic IgG autoantibody production requires B-cell activation, leading to the production of activation-induced deaminase (AID) and class switching of IgM genes to IgG. To understand how and when B cells are activated to produce these IgG autoantibodies, we studied cells from 564Igi, a mouse model of SLE. 564Igi mice develop a disease profile closely resembling that found in human SLE patients, including the presence of IgG antinucleic acid Abs. We have generated 564Igi mice that conditionally express an activation-induced cytidine deaminase transgene (Aicda^tg ), either in all B cells or only in mature B cells. Here, we show that class-switched pathogenic IgG autoantibodies were produced only in 564Igi mice in which AID was functional in early-developing B cells, resulting in loss of tolerance. Furthermore, we show that the absence of AID in early-developing B cells also results in increased production of self-reactive IgM, indicating that AID, through somatic hypermutation, contributes to tolerance. Our results suggest that the pathophysiology of clinical SLE might also be dependent on AID expression in early-developing B cells

Production of IgG autoantibody requires expression of activation-induced deaminase in early-developing B cells in a mouse model of SLE

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of pathogenic IgG antinuclear antibodies. Pathogenic IgG autoantibody production requires B-cell activation, leading to the production of activation-induced deaminase (AID) and class switching of IgM genes to IgG. To understand how and when B cells are activated to produce these IgG autoantibodies, we studied cells from 564Igi, a mouse model of SLE. 564Igi mice develop a disease profile closely resembling that found in human SLE patients, including the presence of IgG antinucleic acid Abs. We have generated 564Igi mice that conditionally express an activation-induced cytidine deaminase transgene (Aicdatg ), either in all B cells or only in mature B cells. Here, we show that class-switched pathogenic IgG autoantibodies were produced only in 564Igi mice in which AID was functional in early-developing B cells, resulting in loss of tolerance. Furthermore, we show that the absence of AID in early-developing B cells also results in increased production of self-reactive IgM, indicating that AID, through somatic hypermutation, contributes to tolerance. Our results suggest that the pathophysiology of clinical SLE might also be dependent on AID expression in early-developing B cells