The carrier effect in the secondary response to hapten‐protein conjugates. V. Use of antilymphocyte serum to deplete animals of helper cells

Treatment of mice primed with bovine serum albumin, chicken γ‐globulin or keyhole limpet hemocyanin with rabbit anti‐mouse lymphocyte serum (ALS) depresses the secondary response, and particularly the adoptive secondary response, to these antigens. If, however, the transferred cells are boosted with NIP (4‐hydroxy‐5‐iodo‐3‐nitro‐phenacetyl‐) or DNP (2,4‐dinitrophenyl‐) conjugates of the protein with which they had been primed, their ability to make an anti‐protein response can be partially restored by adding cells primed against the hapten. Such hapten‐primed cells can be obtained, for example, by immunization with the hapten conjugated to another carrier. These helper cells can therefore be regarded as hapten‐specific. DNP‐specific helper cells can be obtained, as expected, from lethally‐irradiated thymocyte‐repopulated, FDNB (2,4‐dinitrofluorobenzene) skin‐painted donors. Hapten‐specific helper cells can be demonstrated in guinea pigs according to the same principle. As in mice, there is no correlation between helper activity and antibody‐forming‐cell‐precursor activity in terms of anti‐hapten antibody. ALS suppression spares the secondary response to high doses of conjugate, suggesting that this type of response is helper‐independent; it also indicates that the loss of carrier‐effect obtainable with high doses of conjugate cannot be attributed to the operation of hapten‐specific helper cells. These ALS experiments strengthen the evidence for the identification of helper cells in the adoptive secondary response to conjugates as thymus‐derived lymphocytes mediating cellular immunity. The case for this identity is summarized in the discussion.