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Increased expression of I-region-associated antigen (Ia) on B cells after cross-linking of surface immunoglobulin.
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1981
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Immunocytochemical TechniqueHumoral ResponseImmunologyI-region-associated AntigenAntigen ProcessingDermatologyImmune SystemImmunotherapyImmunochemistryEpitope BiologyCell SignalingAutoimmune DiseaseAllergyB Cell SiaB CellsAutoimmunityT Cell ImmunityHumoral ImmunitySurface ImmunoglobulinSurface IgCell BiologyAntibody BiologySurface IaImmunoglobulin EMedicineImmune Cell Activation
Surface Ig and Ia are key regulators of B‑cell activation. The study examined how cross‑linking surface Ig influences Ia expression on B cells using flow cytometry. Flow cytometry with anti‑Ia antibodies quantified Ia expression after Ig cross‑linking. Cross‑linking surface Ig with anti‑delta, anti‑mu, or anti‑kappa antibodies dramatically up‑regulated Ia expression on mature B cells, a T‑cell–independent, protein‑synthesis–dependent increase that occurs after 24 h in vitro or 2–3 fold in vivo. Additional data were collected via intravenous administration.
Both surface Ig (sIg) surface Ia (sIa) have been shown to have important roles in B lymphocyte activation. In order to investigate a possible relationship between these molecules, we studied the effects of cross-linking of sIg on the expression of sIa, as measured by fluorescence-activated cell sorter analysis of lymphoid cells stained with conventional anti-Ia anti-serum or with fluorescein-labeled anti-Ia antibodies. Exposure of cells for 24 hr in vitro to anti-delta, anti-mu, anti-kappa antibodies, or their F(ab')2 fragments induced a very dramatic increase in expression of sIa. Similarly, i.v. injection of anti-delta antibodies into adult mice induced a 2- to 3-fold increase in expression of B cell sIa on spleen, lymph node, and Peyer's patch lymphocytes. There was no increase under these conditions in expression of other B lymphocyte surface antigens, including H-2, 4B9, and 17C9. Furthermore, exposure of B lymphocytes to antibodies directed to B lymphocyte surface antigens other than sIg did not result in an increase in expression of sIa. The anti-Ig-induced increase in sIa expression appeared to be T independent, required cellular protein synthesis, and required more time to occur than did the cross-linking and removal of sIg. This increase in expression of sIa did not occur on B lymphocytes obtained from mice younger than 3 wk old. This increase in expression of sIa may reflect a proximal event in B lymphocyte activation that occurs after cross-linking of sIg by antigen and that may enhance subsequent cellular interactions involving B lymphocytes.