PRESENCE OF ACTIVATED ANTIGEN-BINDING B-CELLS DURING IMMUNIZATION ENHANCES RELATIVE LEVELS OF IFN-GAMMA IN T-CELL RESPONSES

Citation
C. Pasare et al., PRESENCE OF ACTIVATED ANTIGEN-BINDING B-CELLS DURING IMMUNIZATION ENHANCES RELATIVE LEVELS OF IFN-GAMMA IN T-CELL RESPONSES, The Journal of immunology, 160(2), 1998, pp. 778-787
Citations number
49
Categorie Soggetti
Immunology
Journal title
ISSN journal
00221767
Volume
160
Issue
2
Year of publication
1998
Pages
778 - 787
Database
ISI
SICI code
0022-1767(1998)160:2<778:POAABD>2.0.ZU;2-F
Abstract
To examine the influence of Ag presentation by B cells on immune respo nses, we have used mice transgenic for an Ig heavy chain from a monocl onal anti-azobenzenearsonate (Ars) Ab to deliver Ag to B cells during immunization, A large proportion of transgene-expressing B cells in th ese mice binds Ars, while transgenic serum Ig shows poor Ars binding. Transgenic B cells present Ars proteins better than their nonhaptenate d counterparts. This is associated with an increase in the proliferati ve responses of transgenic T cells to Ars protein immunization, Althou gh B cell numbers in the transgenic mice are lower, many B cells in th em show an activated phenotype, as identified by altered surface level s of peanut agglutinin reactivity, CD23, CD24, CD44, CD62L, and CD86. Even against nonhaptenated immunogens, transgenic responses show signi ficant enhancement in the relative proportions of the Th1 cytokine IFN -gamma over the Th2 cytokines IL-4 and IL-10. Haptenated immunogens fu rther enhance the predilection of transgenic mice to produce relativel y more IFN-gamma. Consistent with this, there is an increase in IgG2a/ IgG1 ratios in serum Abs in response to haptenated immunogens in trans genic mice, Adoptive transfer of primed hapten-specific secondary B ce lls into nontransgenic mice also induces an increase in relative level s of IFN-gamma in response to haptenated immunogens, Thus, presentatio n of immunogen in vivo by activated Ag-binding B cells contributes to enhanced immunogenicity and a Th1 cytokine bias.