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Hirano, N. et al.

Hirano, Butler, Von Bergwelt-Baildon, Maecker, Schultze, O'Connor, Schur, Kojima, Guinan, Nadler,

Autoantibodies frequently detected in patients with aplastic anemia.

Although accumulating evidence strongly suggests that aplastic anemia (AA) is a T cell-mediated autoimmune disease, no target antigens have yet been described for AA. In autoimmune diseases, target autoantigens frequently induce not only cellular T-cell responses but also humoral B-cell responses. We hypothesized that the presence of antigen-specific autoantibodies could be used as a "surrogate marker" for the identification of target T-cell autoantigens in AA patients. We screened a human fetal liver library for serologic reactivity against hematopoietic stem/progenitor cell antigens and isolated 32 genes. In 7 of 18 AA patients, an immunoglobulin G (IgG) antibody response was detected to one of the genes, kinectin, which is expressed in all hematopoietic cell lineages tested including CD34+ cells. No response to kinectin was detected in healthy volunteers, multiply transfused non-AA patients, or patients with other autoimmune diseases. Epitope mapping of IgG autoantibodies against kinectin revealed that the responses to several of the epitopes were shared by different AA patients. Moreover, CD8+ cytotoxic T cells raised against kinectin-derived peptides suppressed the colony formation of granulocyte macrophage colony-forming units (CFU-GMs) in an HLA class I-restricted fashion. These results suggest that kinectin may be a candidate autoantigen that is involved in the pathophysiology of AA.[1]

References

Autoantibodies frequently detected in patients with aplastic anemia. Hirano, N., Butler, M.O., Von Bergwelt-Baildon, M.S., Maecker, B., Schultze, J.L., O'Connor, K.C., Schur, P.H., Kojima, S., Guinan, E.C., Nadler, L.M. Blood (2003) [Pubmed]

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