In:
Arthritis & Rheumatology, Wiley, Vol. 32, No. 7 ( 1989-07), p. 914-918
Abstract:
The 76‐kd human interferon (IFN)–induced MX protein is the homolog to the murine protein, which is necessary and sufficient to provide adequate resistance to influenza virus infection in murine cells and in mice. Fifty‐one patients with systemic lupus erythematosus (SLE) were screened for the presence of the MX homolog in mononuclear cells and for IFN and anti‐IFN antibodies in serum. In 47 of 51 patients, significant levels of the MX homolog were found, while only 15 of 51 patients had measurable α‐IFN in their serum. The IFN activity found in these sera was characterized as a partially acid‐labile α‐IFN, by means of acid‐stability cross‐reactivity on heterologous cells, trypsin sensitivity, and neutralization by homologous or heterologous anti‐sera. Four of the patients had no detectable MX homolog in their leukocytes; 3 of these 4 possessed an anti–α‐IFN antibody that was able to neutralize both a natural α‐IFN preparation and the acid‐labile IFN in SLE sera. Also, acid‐labile α‐IFN–containing SLE sera induced the MX homolog in vitro in mononuclear cells from healthy donors. These observations suggest that endogenously produced α‐IFN is responsible for the observed induction of the MX homolog in SLE and that the IFN system is activated in more than 90% of SLE patients.
Type of Medium:
Online Resource
ISSN:
2326-5191
,
2326-5205
DOI:
10.1002/j.2326-5205.1989.tb00024.x
Language:
English
Publisher:
Wiley
Publication Date:
1989
detail.hit.zdb_id:
2754614-7
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