| pubmed-article:2285120 | pubmed:abstractText | An immune-mediated etiology for aplastic anemia was first supported by the observation that some patients recovered their marrow function after immunosuppressive or cytoreductive therapy. Subsequently, investigators tried to define this immune process by studying the effects of patient lymphocytes on the growth of hematopoietic colonies in vitro. Many investigators were able to demonstrate inhibition of in vitro hematopoiesis by mononuclear cells from aplastic anemia patients. In many cases, however, it appeared that allosensitization via blood transfusions was responsible for the inhibitory activity. In general, it has been difficult to determine if any abnormal lymphocyte activity observed in these patients is causal as opposed to consequential. Although these initial studies provided very little conclusive information regarding the pathogenesis of aplastic anemia, they did lead to a more complete understanding of the potential immune modulation of hematopoietic regulation. Taken together with the major technological advances achieved over the past decade, this new knowledge has made it possible to functionally dissect the hematopoietic system. By identifying the interactive cell populations in this system and determining what factors they produce and what activities these factors have, it should be possible to precisely define defects than can result in marrow failure. | lld:pubmed |
