Major histocompatibility complex-restricted self-recognition in responses to trinitrophenyl-Ficoll. A novel cell interaction pathway requiring self-recognition of accessory cell H-2 determinants by both T cells and B cells.
Open Access
- 1 February 1983
- journal article
- research article
- Published by Rockefeller University Press in The Journal of Experimental Medicine
- Vol. 157 (2), 486-501
- https://doi.org/10.1084/jem.157.2.486
Abstract
In vitro primary antibody responses to limiting concentrations of trinitrophenyl (TNP)-Ficoll were shown to be T cell dependent, requiring the cooperation of T helper (TH) cells, B cells, and accessory cells. Under these conditions, TH cells derived from long-term radiation bone marrow chimeras were major histocompatibility complex (MHC) restricted in their ability to cooperate with accessory cells expressing host-type MHC determinants. The requirement for MHC-restricted self-recognition by TNP-Ficoll-reactive B cells was assessed under these T-dependent conditions. In the presence of competent TH cells, chimeric B cells were found to be MHC restricted, cooperating only with accessory cells that expressed host-type MHC products. In contrast, the soluble products of certain monoclonal T cell lines were able to directly activate B cells in response to TNP-Ficoll, bypassing any requirement for MHC-restricted self-recognition. These findings demonstrate the existence of a novel cell interaction pathway in which B cells as well as TH cells are each required to recognize self-MHC determinants on accessory cells, but are not required to recognize each other. They further demonstrate that the requirement for self-recognition by B cells may be bypassed in certain T-dependent activation pathways.This publication has 24 references indexed in Scilit:
- Role of the major histocompatibility complex in T cell activation of B cell subpopulations. lyb-5(+) and lyb-5(-) B cell subpopulations differ in their requirement for major histocompatibility complex-restricted T cell recognitionThe Journal of Experimental Medicine, 1981
- A Single Major Pathway of T‐Lymphocyte Interactions in Antigen‐Specific Immune SuppressionScandinavian Journal of Immunology, 1981
- Concanavalin A-inducible, interleukin-2-producing T cell hybridoma.The Journal of Experimental Medicine, 1980
- Role of T lymphocytes in the response to TNP-AECM-Ficoll.The Journal of Immunology, 1980
- Role of accessory cells in B cell activation. I. Macrophage presentation of TNP-Ficoll: evidence for macrophage-B cell interaction.The Journal of Immunology, 1980
- Cellular and genetic control of antibody responses. V. Helper T-cell recognition of H-2 determinants on accessory cells but not B cells.The Journal of Experimental Medicine, 1979
- The role of H-2 linked genes in helper T-cell function. II. Isolation on antigen-pulsed macrophages of two separate populations of F1 helper T cells each specific for antigen and one set of parental H-2 products.The Journal of Experimental Medicine, 1978
- The role of macrophages in the generation of T-helper cells. II. The genetic control of the macrophage-T-cell interaction for helper cell induction with soluble antigens.The Journal of Experimental Medicine, 1975
- FUNCTION OF MACROPHAGES IN ANTIGEN RECOGNITION BY GUINEA PIG T LYMPHOCYTESThe Journal of Experimental Medicine, 1973
- CELL INTERACTIONS BETWEEN HISTOINCOMPATIBLE T AND B LYMPHOCYTESThe Journal of Experimental Medicine, 1973