| Autor: |
Marie Hudson, Witold Mazur, Hani El-Gabalawy, Michael Procino, Murray Baron, Marvin J. Fritzler, Marianna M. Newkirk, Zhenhong Li, Simeon Mitchell, Vuokko L. Kinnula, Manuel G. Cosio |
| Rok vydání: |
2012 |
| Předmět: |
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| Zdroj: |
European Journal of Immunology. 42:1051-1061 |
| ISSN: |
0014-2980 |
| DOI: |
10.1002/eji.201141856 |
| Popis: |
The impact of cigarette smoke (CS), a risk factor for rheumatoid arthritis (RA), on sauto-antibody production was studied in humans and mice with and without chronic lung disease (LD). Rheumatoid factor (RF), anti-cyclic citrullinated peptides (CCPs), and anti-HSP70 autoantibodies were measured in several mouse strains and in cohorts of smokers and nonsmokers with and without autoimmune disease. Chronic smoking-induced RFs in AKR/J mice, which are most susceptible to LD. RFs were identified in human smokers, preferentially in those with LD. Anti-HSP70 auto-antibodies were identified in CS-exposed AKR/J mice but not in ambient air exposed AKR/J controls. Whereas inflammation could induce anti-HSP70 IgM, smoke exposure promoted the switch to anti-HSP70 IgG autoantibodies. Elevated anti-CCP autoantibodies were not detected in CS-exposed mice or smokers. AKR/J splenocytes stimulated in vitro by immune complexes (ICs) of HSP70/anti-HSP70 antibodies produced RFs. The CD91 scavenger pathway was required as anti-CD91 blocked the HSP70-IC-induced RF response. Blocking Toll-like receptors did not influence the HSP70-IC-induced RFs. These studies identify both anti-HSP70 and RFs as serological markers of smoke-related LD in humans and mice. Identification of these autoantibodies could suggest a common environmental insult, namely CS, in a number of different disease settings. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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