Biological, phenotypical, molecular and functional analyses. (A) Hematobiological evolution of the patient with treatment courses. A-CD20, rituximab; SplX, splenectomy; VP16, etoposide; *, pneumopathy, #, pericarditis associated to arthritis; ☆, colic B-cell proliferation; ★, Evans syndrome aggravation with spleen enlargement crisis and circulating B-cell proliferation; ✜, acute myeloproliferation with pulmonary infiltration leading to death. (B) Cell sorting and sequencing of circulating leukocytes populations and primary derived fibroblasts. Fibro., fibroblasts; Mono., monocytes; Neutro, neutrophils. (C) In vitro apoptosis assays on superantigen stimulated T cells from the patient; results are compared with controls. ACAD, activated cells autonomous death using cytokines withdrawal; AICD, activation-induced cell death by T-cell receptor restimulation; Apo1.3, direct Fas stimulation with an agonist antibody. (D) Western blot of patient’s (P1) Bim expression on activated T cells. GAPDH, glyceraldehyde-3-phosphate dehydrogenase.