This suggests that cytokine‐induced and Fas‐mediated apoptosis play roles in bone marrow failure because annihilation of CD34+ progenitor cells leads to hematopoietic stem cell deficiency. Frequently detected autoantibodies
A study of blood and bone marrow samples obtained from 18 aplastic anemia patients revealed more than 30 potential specific candidate autoantigens after the serologic screening of a fetal liver library with sera from 8 patients. The human fetal liver cDNA library (chosen because of its high enrichment of CD34+ cells), compared with peripheral blood or the bone marrow, significantly increased the likelihood of detection of possible stem cell autoantigens. ELISA and Western blot analysis revealed that an IgG antibody response to one of the candidate autoantigens, kinectin, was present in a significant number of patients (39%). In contrast, no antibody was detected in 35 healthy volunteers. Antibody was detected in both transfused and transfusion-naive patients, suggesting that antikinectin autoantibody development was not due to transfusion-related alloreactivity. Negative sera from patients with other autoimmune diseases (systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis) showed a specific association of antikinectin antibodies with aplastic anemia. These results support the hypothesis that immune response to kinectin may be involved in the pathophysiology of the disease. Kinectin is a large molecule (1,300 amino acid residues) expressed by CD34+ cells. Several kinectin-derived peptides can be processed and presented by HLA I and can induce antigen-specific CD8+ T-cell responses. Bone marrow microenvironment
A critical factor for healthy stem cell production is the bone marrow microenvironment.
Hydrops foetalis or hydrops fetalis is a condition in the fetus characterized by an accumulation of fluid, or edema, in at least two fetal compartments. By comparison, hydrops allantois or hydrops amnion is an accumulation of excessive fluid in the allantoic or amniotic space, respectively. Signs and symptoms
Locations can include the subcutaneous tissue on the scalp, the pleura (pleural effusion), the pericardium (pericardial effusion) and the abdomen (ascites). Edema is usually seen in the fetal subcutaneous tissue, sometimes leading to spontaneous abortion. It is a prenatal form of heart failure, in which the heart is unable to satisfy demand (in most cases abnormally high) for blood flow. Causes
Hydrops fetalis usually stems from fetal anemia, when the heart needs to pump a much greater volume of blood to deliver the same amount of oxygen. This anemia can have either an immune or non-immune cause. Non-immune hydrops can also be unrelated to anemia, for example if a fetal tumor or congenital cystic adenomatoid malformation increases the demand for blood flow. The increased demand for cardiac output leads to heart failure, and corresponding edema. Immune pathophysiology
Erythroblastosis fetalis, also known as Rh disease, is the only immune cause of hydrops fetalis. Rh disease is a hemolytic disease of newborns. Pregnant mothers do not always have the same blood type as their child. During birth or throughout the pregnancy, the mother may be exposed to the infants blood.