F1 hybrid mice (BALB/c x DBA/1) are resistant to collagen-induced arthritis with beta-glucan as an adjuvant.


:Collagen-induced arthritis (CIA) is an experimental model of rheumatoid arthritis (RA) used for studying the clinical, immunological and genetic factors of the disease. Many studies of genetic susceptibility to CIA have been performed, usually with two strains of mice, DBA/1 and B10.RIII, since they are highly susceptible to CIA. Furthermore, F1 hybrid mice of susceptible and resistant strains reportedly develop arthritis. Recently, we reported that particles of beta-glucan, OX-CA, prepared from Candida albicans by NaClO-oxidation, acted as an adjuvant for CIA. Although, there have been many studies about the relationship between antigen and the major histocompatibility complex (MHC) in F1 hybrid mice, little is known argument about susceptibility to adjuvants. Therefore, we checked the susceptibility of F1 hybrids to CIA using OX-CA as an adjuvant. BALB/c and DBA/1 were mated to generate F1 hybrids which were then immunized with type II collagen (CII) plus Freund's complete adjuvant (FCA) or OX-CA. The results showed that F1 hybrids injected with CII plus FCA developed severe arthritis at an incidence ratio 80%, versus only 20% in mice injected with CII plus OX-CA. Furthermore, levels of anti-CII antibody, especially of the IgG2a subclass, in sera from mice treated with CII plus OX-CA were significantly low. Susceptibility to CIA might depend on not only MHC but also the adjuvant used for immunoactivation.


Biol Pharm Bull


Hida S,Nagi-Miura N,Adachi Y,Ohno N




Has Abstract


2006-06-01 00:00:00














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    journal_title:Biological & pharmaceutical bulletin

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    journal_title:Biological & pharmaceutical bulletin

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    journal_title:Biological & pharmaceutical bulletin

    pub_type: 杂志文章


    authors: Li XQ,Gao QT,Chen XH,Bi KS

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    journal_title:Biological & pharmaceutical bulletin

    pub_type: 杂志文章


    authors: Takenaga M,Ohta Y,Tokura Y,Hamaguchi A,Shudo K,Okano H,Igarashi R

    更新日期:2009-02-01 00:00:00