HYPER-IMMUNOGLOBULIN G2 PRODUCTION BY B-CELLS FROM PATIENTS WITH LOCALIZED JUVENILE PERIODONTITIS AND ITS REGULATION BY MONOCYTES

Citation
Jb. Zhang et al., HYPER-IMMUNOGLOBULIN G2 PRODUCTION BY B-CELLS FROM PATIENTS WITH LOCALIZED JUVENILE PERIODONTITIS AND ITS REGULATION BY MONOCYTES, Infection and immunity, 64(6), 1996, pp. 2004-2009
Citations number
28
Categorie Soggetti
Immunology,"Infectious Diseases
Journal title
ISSN journal
00199567
Volume
64
Issue
6
Year of publication
1996
Pages
2004 - 2009
Database
ISI
SICI code
0019-9567(1996)64:6<2004:HGPBBF>2.0.ZU;2-Q
Abstract
Localized juvenile periodontitis (LJP) runs in families, and a predisp osition to develop disease appears to be inherited in an autosomal dom inant fashion. Patients with LJP have elevated levels of serum immunog lobulin G2 (IgG2), and this is most striking in black LJP patients. We hypothesized that the markedly elevated serum IgG2 levels related to LJP status and race may be attributable to a fundamental difference in the response of black LJP leukocytes. To test this possibility, leuko cytes from black LJP patients, black non-periodontitis (NP) controls, and white NP controls were cultured with a nonspecific mitogen (pokewe ed mitogen) which stimulates immunoglobulin production. The levels of IgG2 produced were measured using an enzyme-linked immunosorbent assay . The results revealed that the serum IgG2 level differences among bla ck LJP patients and white and black NP subjects were reproducible in p eripheral blood leukocytes in vitro. Analysis revealed that B cells fr om the LJP patients appeared to be predisposed to produce high levels of IgG2. Further analysis supported the concept that the high IgG2 res ponses of B cells from black LJP patients were regulated by monocytes. Replacing the monocytes in cultures from white NP subjects with LJP m onocytes from black patients resulted in production of IgG2 at levels that were comparable with those produced by the LJP B cells from black patients. In short, B cells from black LJP patients produce elevated levels of IgG2 in vitro, and at least part of this elevation appears t o be attributable to regulation via the LJP monocytes.