Abstract:
CONTEXT:Serum IgA suppresses immune responses when exposed to antigens recognized by the antibody; however, the underlying mechanism remains unclear. OBJECTIVE:We herein clarified the relationships between changes in antigen distribution and antigen-dependent B cell activation in the presence or absence of IgA against the antigen in mice. MATERIALS AND METHODS:DBA/1J and HR-1 mice were intravenously injected with ovalbumin (OVA) and anti-OVA monoclonal IgA OA-4. The distribution of the antigen and B cell responses were measured. RESULTS:B cell activation by injected OVA, namely, increases in anti-OVA IgG production and the populations of B220(+)GL7(+) and B220(+)CD69(high) splenocytes, was diminished by the co-injection of OA-4. Co-injected OA-4 increased OVA in the serum as well as in the bile and gut. This was coincident with its decrease in the urine due to the inhibition of OVA monomer secretion through the formation of immune complexes. The apparent similarities in the association between fluorescein isothiocyanate (FITC)-OVA and splenic B cells in the presence and absence of OA-4 in vivo appeared to be attributed to compensation between the two effects of OA-4; an increase in serum OVA in vivo and inhibition of the association between OVA and B cells, as suggested by in vitro experiments. DISCUSSION:Based on these results, the stimulation of B cells by OVA may be directly reduced, at least partly, by the neutralization of OVA by OA-4. CONCLUSION:IgA may be an effective drug for the treatment of immune disorders due to its ability to blunt antigen-specific B cell activation.
journal_name
Immunopharmacol Immunotoxicoljournal_title
Immunopharmacology and immunotoxicologyauthors
Yamaki K,Yoshino Sdoi
10.3109/08923973.2016.1142559subject
Has Abstractpub_date
2016-01-01 00:00:00pages
131-44issue
2eissn
0892-3973issn
1532-2513journal_volume
38pub_type
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