Antigen presentation by hapten-specific B lymphocytes. I. Role of surface immunoglobulin receptors.

TLDR

The study discusses how these findings inform physiologic, histocompatibility‑restricted T‑B collaboration mechanisms. The study examines whether hapten‑specific murine splenic B lymphocytes can present hapten‑proteins to carrier‑specific T cell hybridomas. The authors isolated TNP‑specific BALB/cB splenic B cells from immune mice using elution from TNP‑gelatin‑coated dishes. TNP‑specific B cells presented TNP‑modified GL phi at 0.1 µg/ml, whereas unmodified GL phi required 1000‑fold higher concentrations, and this presentation was blocked by anti‑Ig or TNP proteins, yet binding of TNP proteins did not affect presentation of unrelated proteins or alloreactive stimulation, indicating that surface Ig receptors focus antigen onto specific B cells and enable highly efficient linked antigen presentation to T cells.

Abstract

The present study examines the ability of hapten-specific murine splenic B lymphocytes to present hapten-proteins to carrier-specific T cell hybridomas. BALB/cB cells specific for 2,4,6-trinitrophenyl (TNP) were isolated from spleens of immune mice by elution from TNP-gelatin-coated dishes. Such cells presented the TNP-modified terpolymer, GL phi, at concentrations as low as 0.1 microgram/ml, to a GL phi-specific, I-Ed-restricted, interleukin 2-producing T cell hybridoma. In contrast, the same B lymphocytes required 1,000-fold higher concentrations of unmodified GL phi to stimulate the same T cell hybridoma. The presentation of low concentrations of TNP-GL phi by TNP-specific B lymphocytes was significantly or completely blocked by anti-Ig antibody or TNP-proteins, indicating that surface Ig receptors were critically involved in this phenomenon. Finally, binding of TNP-proteins did not alter the ability of the B cells to present unrelated, unhaptenated proteins or to stimulate alloreactive T cells. These results suggest that surface Ig receptors serve to focus antigens onto specific B lymphocytes and that such cells are highly efficient at presenting linked antigenic determinants to T cells. The implications of these findings for the mechanisms of physiologic, histocompatibility-restricted T-B collaboration are discussed.