Immunodeficiency and radiation sensitivity

Many immunodeficient states have been associated with increased radiation sensitivity. Ataxia telangiectasia (AT) is associated with an increased sensitivity of T cells to the cytotoxic effect of ionizing radiation, with defective cell-mediated immunity, and with nervous system disorders. The gene responsible for this disorder (the Atm gene) has recently been identified as being important in the regulation of cell division. Lymphocytes from patients with AT do not exhibit normal cell cycle arrest and do not rapidly accumulate p53 following irradiation. Patients with AT have a high incidence of T cell leukemias with aberrant chromosomal rearrangements involving T cell receptor (TCR) genes.

Certain types of severe combined immune deficiency (SCID) are characterized by an inability of lymphocytes to rearrange TCR and Ig genes due to a functional loss of a recombinase. There is an increased sensitivity of these lymphocytes to the killing effects of radiation. Two protein subunits, called Ku proteins (originally identified as a nuclear antigen in certain autoimmune diseases) mediate the rearrangement of Ig and TCR genes by binding to a 350 kDa protein (catalytic subunit) which functions as a DNA-protein kinase. This DNA-protein kinase activity is absent in SCID mice and in some forms of human SCID. The radiation sensitivity of SCID cells is corrected by transfecting the DNA-protein kinase catalytic subunit, thus implicating this pathway in both Ig/TCR rearrangement and radiation sensitivity. Additional immunodeficient states such as Wegener's syndrome in humans, and the syndrome of 'wasted' mice are associated with radiation sensitivity. Studies of these abnormalities are likely to uncover more interactions between normal immune function and radioresistant^.

See also: Bone marrow and hematopoiesis; Hematopoietic stem cell transplantation; Immunosuppression; Lymphoma; Rheumatoid arthritis, human.

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