Abstract
Autoimmune disorders affecting circulating, formed elements of the blood were recognized more than half a century ago, and have been considered as the earliest historical stream of autoimmunity.1 However, the recognition of autoimmune myelopathies with, as targets, stem cells and/or committed progenitors has come much later and is still fraught with difficulties, owing to the sophisticated indirect technology involved, to the intricate humoral and cellular regulation of hemopoiesis, and to the problems posed by sensitizations due to blood transfusions. This is especially true when stem cell suppression is mediated by lymphocytes, since there are at least two subpopulations of T lymphocytes influencing the growth of peripheral blood-derived BFU-E, and most probably other progenitors the first with a stimulatory and the second with an inhibitory activity.2 Accordingly, there would appear to be some overlap between “immune” and “non-immune” mechanisms. In addition, a reduced stem cell compartment may become unduly sensitive, to so-called down regulatory mechanisms, or to stimulated suppressor lymphocytes, as after a viral infection. Humoral suppression of hemopoiesis, which is mediated by antibodies clearly characterized as immunoglobulins, is certainly easier to identify.
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© 1984 Plenum Press, New York
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Marmont, A.M. (1984). The Autoimmune Myelopathies. In: Fudenberg, H.H., Whitten, H.D., Ambrogi, F. (eds) Immunomodulation. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9358-4_31
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DOI: https://doi.org/10.1007/978-1-4615-9358-4_31
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