Adaptive Differentiation of Murine Lymphocytes

Abstract

Abstract Responses to the synthetic terpolymer L-glutamic acid, L-lysine, L-phenylalanine (GLΦ) and hapten derivatives thereof are controlled by two complementing H-2-linked Ir genes in the mouse. F1 hybrids derived from two different nonresponder strains (one of which possesses the α and the other β Ir-GLΦ gene) are phenotypic responders to GLΦ and 2,4-dinitrophenyl (DNP)-GLΦ. Moreover, spleen cells from DNP-GLΦ-primed F1 mice can adoptively transfer secondary anti-DNP antibody responses to irradiated F1 recipients that have been challenged with DNP-GLΦ. When, however, GLΦ-primed F1 helper T cells are transferred together with the DNP-specific F1 B cells that had been primed in separate mice altogether by DNP coupled to an unrelated protein carrier, such mixtures failed to develop adequate adoptive secondary anti-DNP responses to DNP-GLΦ. This contrasted with the ability of the same GLΦ-primed F1 T cells to provide helper activity for DNP-primed B cells from responder recombinant B10.A (5R) mice. More important, the apparent defect of GLΦ-primed F1 T cells in providing help for DNP-primed F1 B cells (primed to a DNP-protein conjugate) could be readily overcome by using DNP-primed B cells from donor F1 mice primed with DNP-GLΦ. As discussed herein, these results suggest that interacting T and B lymphocytes pair off into partner cell sets, any pair of which interact optimally when a “best fit” reciprocal self-recognition occurs between them.