Tomasi, Thomas B.

Summary Intact Fcα fragments from five human IgA myeloma proteins were produced by two different methods, high temperature trypsinolysis and IgA protease digestion. Three of the Fcα fragments activated the classical pathway as determined by the titers of the individual complement components. Two other fragments did not fix complement by either pathway.

Abstract Quantitative differences in the magnitude of antigen-induced proliferative responses of sensitized lymph node cells between low (C3H/Anf or C3H/Cr) and high (C3H/Hej or CBA/j) responder H-2k mice have been observed 1 to 2 weeks after in vivo sensitization with antigen (OVA, PPD, and GAT). We have shown that antigen presentation is less effective in the sensitized lymph node cell populations from low responder mice compared with those from high responder mice, suggesting that the number and/or functional status of antigen-presenting cells in the regional lymph nodes may be a key factor in determining the magnitude of antigen-induced proliferative responses. These data are consistent with the hypothesis that cell traffic after sensitization plays an important role in determining the immune responsiveness of lymph nodes.

Abstract Previous studies have shown that mice treated from birth with heterologous anti-µ antiserum are severely immuno-suppressed with respect to numbers of splenic plaque-forming cells (PFC) to sheep red blood cells (SRBC) in all immunoglobulin classes. In this study we have investigated, using in vitro techniques, the cellular site of the deficit created by anti-µ. The primary PFC response of spleen cells originating from anti-µ-treated mice was completely suppressed in vitro. The response was restored by the addition to the cultures of B cells but not T cells. T cells were derived from normal spleens which had been depleted of B lymphocytes and adherent cells by filtration through cotton wool columns, or by educated thymus cells obtained from the spleens of lethally irradiated mice injected with syngeneic thymocytes and SRBC. Restoration of the PFC response of spleen cells from anti-µ-treated mice by normal B cells suggested that a cellular deficiency rather than an activity process by inhibitory cells was the cause of the imunosuppression. Also, co-culturing spleen cells from normal and suppressed mice did not reveal the presence of inhibitory cells. Spleen cells from x-irradiated mice, injected with bone marrow from anti-µ-suppressed mice, gave rise to PFC cells when cultured with SRBC and normal T cells, suggesting that stem cells giving rise to B cells were not affected by anti-µ treatment. Similarly, educated thymus cells derived from suppressed mice could provide helper function when reconstituted in vitro with normal B cells. Exposure of normal bone marrow and spleen cells to anti-µ serum prior to passage through syngeneic x-irradiated recipients demonstrated that spleen cells were much more sensitive than were bone marrow cells to suppression by anti-µ antibodies. It is concluded that the target of anti-µ antibody is a µ-chain bearing B cell precursor to the IgM-, IgG-, and IgA-producing cell.