期刊
BLOOD
卷 102, 期 13, 页码 4567-4575出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2002-11-3409
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- NCI NIH HHS [P01-CA-66996, P01-CA-78378, K08-CA-87720] Funding Source: Medline
- NHLBI NIH HHS [P50-HL-54785] Funding Source: Medline
- NIAID NIH HHS [P01-AI-41584] Funding Source: Medline
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. (C) 2003 by The American Society of Hematology.
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