Faculty Research 1990 - 1999

B7-1 and B7-2 have overlapping, critical roles in immunoglobulin class switching and germinal center formation.

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Animal, Antigens: im, Antigens-CD: bi, ph, Antigens-CD80: bi, ph, Antigens-Differentiation: bi, Antigens-T-Independent: im, Freund's-Adjuvant: im, Germinal-Center: de, im, me, Hemocyanin: im, Immunoglobulin-Class-Switching: de, im, Immunoglobulins-Fc: bi, Membrane-Glycoproteins: bi, ph, Mice, Mice-Inbred-BALB-C, Mice-Inbred-C57BL, Mice-Knockout, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

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Immunity 1997 Mar;6(3):303-13


PO1AI35225/AI/NIAID, 1P30AR42689/AR/NIAMS, T32HLO7627


Humoral immune responses were characterized in mouse strains lacking either or both B7 molecules. Mice deficient in both B7-1 and B7-2 failed to generate antigen-specific IgG1 and IgG2a responses and lacked germinal centers when immunized by a number of routes and even in the presence of complete Freund's adjuvant. These results demonstrate that B7-mediated signaling plays a critical role in germinal center formation and immunoglobulin class switching in vivo. Mice lacking only B7-1 or B7-2 mounted high-titer antigen-specific IgG responses when immunized in complete Freund's adjuvant, indicating that B7-1 and B7-2 can have overlapping, compensatory functions for IgG responses. When immunized intravenously without adjuvant, B7-2-deficient mice failed to switch antibody isotypes or form germinal centers, whereas B7-1-deficient mice gave antibody responses comparable with wild-type mice. Thus, B7-2 has an important role in initiating antibody responses in the absence of adjuvant, but the induction of B7-1 by adjuvant in B7-2-deficient mice can compensate for the absence of B7-2.