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Inhibition of antiskin allograft immunity induced by infusions with photoinactivated effector T lymphocytes (PET cells).

Induction of tolerance for skin allotransplantation requires selective suppression of the host response to foreign histocompatibility antigens. This report describes a new approach which employs pre-treatment with 8-methoxypsoralen (8-MOP) and ultraviolet A light (UVA) to render the effector cells of graft rejection immunogenic for the syngeneic recipient. Eight days after BALB/c mice received CBA/j skin grafts, their splenocytes were treated with 100 ng/ml 8-MOP and 1 J/cm2 UVA prior to reinfusion into naive BALB/c recipients. Recipient mice were tested for tolerance to alloantigens in mixed leukocyte culture (MLC), cytotoxicity (CTL), delayed-type hypersensitivity assays (DTH), and challenge with a fresh CBA/j graft. Splenocytes from BALB/c recipients of photoinactivated splenocytes containing the effector cells of CBA/j alloantigen rejection proliferated poorly in MLC and generated lower cytotoxic T-cell responses to CBA/j alloantigens in comparison with sensitized and naive controls and suppressed the MLC and CTL response to alloantigen from sensitized and naive BALB/c mice. In vivo, the DTH response was specifically suppressed to the relevant alloantigen in comparison with controls. BALB/c mice treated in this fashion retained a CBA/j skin graft for up to 42 days post-transplantation without visual evidence of rejection. These results showed that reinfusion of photoinactivated effector cells resulted in an immunosuppressive host response which specifically inhibited in vitro and in vivo responses that correlate with allograft rejection and permitted prolonged retention of histoincompatible skin grafts.

Animals↗
PubMed1986

Effects of dietary nutrients on substrate and effector levels of lipogenic enzymes, and lipogenesis from tritiated water in rat liver.

When fasted rats were refed for 4 days with a carbohydrate and protein diet, a carbohydrate diet (without protein) or a protein diet (without carbohydrate), the effects of dietary nutrients on the fatty acid synthesis from injected tritiated water, the substrate and effector levels of lipogenic enzymes and the enzyme activities were compared in the livers. In the carbohydrate diet group, although acetyl-CoA carboxylase was much induced and citrate was much increased, the activity of acetyl-CoA carboxylase extracted with phosphatase inhibitor and activated with 0.5 mM citrate was low in comparison to the carbohydrate and protein diet group. The physiological activity of acetyl-CoA carboxylase seems to be low. In the protein diet group, the concentrations of glucose 6-phosphate, acetyl-CoA and malonyl-CoA were markedly higher than in the carbohydrate and protein group, whereas the concentrations of oxaloacetate and citrate were lower. The levels of hepatic cAMP and plasma glucagon were high. The activities of acetyl-CoA carboxylase and also fatty acid synthetase were low in the protein group. By feeding fat, the citrate level was not decreased as much as the lipogenic enzyme inductions. Comparing the substrate and effector levels with the Km and Ka values, the activities of acetyl-CoA carboxylase and fatty acid synthetase could be limited by the levels. The fatty acid synthesis from tritiated water corresponded more closely to the acetyl-CoA carboxylase activity (activated 0.5 mM citrate) than to other lipogenic enzyme activities. On the other hand, neither the activities of glucose-6-phosphate dehydrogenase and malic enzyme (even though markedly lowered by diet) nor the levels of their substrates appeared to limit fatty acid synthesis of any of the dietary groups. Thus, it is suggested that under the dietary nutrient manipulation, acetyl-CoA carboxylase activity would be the first candidate of the rate-limiting factor for fatty acid synthesis with the regulations of the enzyme quantity, the substrate and effector levels and the enzyme modification.

Acetyl Coenzyme A↗
PubMed1987

Formation of autoimmune effectors after transfer of virus-induced autoreactive precursors to syngeneic intact receptor animals.

We verified the assumption that autoimmune responses underlie immunosuppression developing in the course of virus infection. It has been shown by adoptive transfer that administration of Langat-virus-induced autoreactive lymphocytes (ARL) to the syngeneic recipient is followed by accumulation of autoreactive effectors (AE) eliciting a graft-verus-host reaction (GVHR) in the syngeneic system (AEgvhr). In addition, cytotoxic T-lymphocytes (AEc) appeared against the syngeneic macrophages. This effect was mediated by the H-2 restriction principle for ARL donors and their recipients. The infection triggered a T-suppressor-mediated reaction inhibiting the differentiation of precursors into mature autoreactive effectors. In the absence of T-cell suppressor effect (on consecutive syngeneic transfer) ARL will cause systemic pathologic changes in the recipients, namely, infiltrative and necrotic lesions in different organs and tissues. This mechanism is attributed to the activation of precursors in the body of intact recipient and to the formation of mature effectors owing to cytokines released by donor ARL.

Animals↗
PubMed1985

Splenic immune effector and suppressor cells in mice bearing a growing plasmacytoma.

The occurrence of tumor immunity in mice bearing a growing plasmacytoma (PC) was studied by local adoptive transfer assay. Spleen cells from mice with a large PC but not with a nonpalpable or small PC retarded and often inhibited entirely the growth of homologous PC. They occasionally caused late regression of growing homologous and heterologous PC. The individual tumor-specific immune effector cells were found to be radiosensitive, non-adherent, Thy 1-positive T-cells. They were resistant to treatment of mice with high-dose cyclophosphamide (CTX). Their generation, however, was abrogated by low-dose CTX and irradiation at the early stage of their development. Spleen cells from PC-bearing mice treated with high-dose CTX were enhanced in their effector activity, suggesting the co-existence of CTX-sensitive suppressor cells. The suppressor cells could be demonstrated in spleens of mice bearing a heterologous PC and were found also to be radiosensitive, non-adherent, Thy 1-positive T-cells. Their generation was blocked by treatment of mice with CTX during the early stage of PC development. These findings provide evidence for the occurrence of immune effector T-cells in mice with a growing PC. This immunity appears to be down-regulated by CTX-sensitive suppressor cells.

Animals↗
PubMed1986

[Control by major histocompatibility complex genes of macrophage interaction with thymocytes during induction of T-effectors of graft vs host reaction. I. Genetic control on the cellular level].

H-2 complex control of interaction between macrophages and thymocytes during induction of T-cell effectors GVH was studied. Intensity of the local GVH reaction was evaluated by the index of the lymph nodes enlargement. Genes of the H-2 system control interaction of macrophages with thymocytes during the formation of T-cell effectors GVH. H-2K subregion genes identity of interacting cells was necessary and sufficient for the effective induction of T-effectors GVH. I and D region differences did not affect the formation of T-cells inducing GVH.

Animals↗
PubMed1986

The role of adherent accessory cells in the generation of effector suppressor T cells.

The role of accessory cell populations in the generation of effector suppressor (Ts3) cells was studied. By using an in vitro culture system, it was previously determined that the induction of NP-specific effector suppressor activity requires T cells, antigen, and an anti-idiotypic B cell population. We now demonstrate that the generation of Ts3 cells in this system also requires accessory cells. The accessory population appears to play a role in the processing and presentation of antigen. These antigen-presenting accessory cells are required early in the induction phase of Ts3 generation. These accessory cells can present NP coupled to immunogenic or non-immunogenic polypeptide carriers, including polymers of L-amino acids. However, NP coupled to polymers of poorly metabolized D-amino acids fail to induce suppressor T cell generation. Furthermore, the data demonstrate that an H-2 homology must exist between the Ts3 precursors and the antigen-presenting cell population if suppressor activity is to be generated. We also characterize the differential genetic restrictions that govern the induction of Ts3 cells that control suppression of either T cell or B cell responses. The data suggest that although I-J region encoded gene products control the induction and effector phases of suppressor cell activity as measured on T cell responses, the suppression of B cell responses appear to be controlled by I-A gene products. Possible cellular mechanisms that might explain these findings are discussed.

Amino Acids↗
PubMed1988

The elevated natural killer sensitivity of targets carrying surface-attached C3 fragments require the availability of the iC3b receptor (CR3) on the effectors.

Human serum-treated Raji and Daudi cells were shown to bind C3 fragments on their surface as a consequence of their capacity to activate C via the alternative pathway. C3 molecules were detectable on the cell surfaces up to 24 h after serum exposure. The C3 fragment-coated cells showed increased sensitivity to spontaneous lymphocyte-mediated cytotoxicity. The effector lymphocytes involved in the enhanced cytotoxicity were NK cells with low buoyant density, carrying both CR3 and FcR. Blocking of the FcR and CR3 with F(ab)2 fragments from Leu-11c or Leu-15 mAb, respectively, did not influence the lysis of targets that did not carry C3 fragments. In contrast, the accessibility of CR3 on the effector lymphocytes was essential for the C3 fragment-mediated enhancement of cytotoxicity. In addition to the Leu-15 antibody, N-acetyl-D-Glucosamine, a compound known to block iC3b binding to CR3, also abrogated the C3 fragment-imposed effect. Our previous experiments showed that the C3 fragments bind to acceptor sites on target cells. The present experiments show that the C3 fragments fixed onto the target bind to CR3 on effector cells. These data substantiate the hypothesis that the bivalent C3 fragments, which are fixed on the targets, promote their interaction with lytic lymphocytes by bridging the two cells.

Binding Sites↗
PubMed1986

Effector mechanism in antitumor activity of monoclonal antibodies produced against an ascitic mouse mammary tumor.

Therapeutic effects of monoclonal antibodies with different immunoglobulin classes, detecting the same antigenic determinant of tumor specific antigen expressed on ascitic mouse mammary tumor MM46, were examined. With i.v. administration of gamma 2a, gamma 2b, or gamma 1 antibody we were able to keep a significant proportion of mice tumor free against i.p. inoculation of 5 X 10(4) MM46 cells with doses as small as 0.5 micrograms, but with administration of mu, gamma 3, or alpha antibody we were not able to keep mice tumor free with doses up to 5 micrograms. With 200 micrograms of antibody, however, an antitumor effect was observed even with mu or gamma 3 antibody, although alpha antibody still showed no effect at all. The therapeutic effect of gamma 2a was further examined in mice challenged with an increasing dose of tumor cells, and a significant effect was demonstrated against 1 X 10(6) cells with 200 micrograms of antibody but not against 5 X 10(6) cells. To assess the effector cells in antitumor activity of antibody in vivo, a histological examination of the tumor cells treated with each class of antibody was carried out. The tumor treated by gamma 2a antibody revealed a remarkable cell infiltration consisting predominantly of mononuclear cells, whereas those treated by mu, gamma 3, or alpha antibody did not. The tumor cells treated by gamma 1 or gamma 2b antibody showed a moderate cellular reaction. Next, a Winn assay was carried out in athymic C3H/HeN-nu/nu mice using gamma 2a antibody. A significant antitumor effect was observed even in those mice, indicating that T-cells are not predominant effector cells. The role of macrophages was studied in mice treated with two macrophage toxic agents, carrageenan and silica particles. These agents were shown to reduce the antitumor effect of gamma 2a antibody in both Winn assays and therapeutic experiments. Thus, histological examination and the blocking effect of macrophage toxic agents suggested the participation of host macrophages as effector cells in antibody-mediated tumor cell suppression in vivo.

Animals↗
PubMed1986

Lymphokine-induced cytotoxicity: characterization of effectors, precursors, and regulatory ancillary cells.

In the present study, we have characterized the effectors, precursors, and regulatory ancillary cells involved in the in vitro generation of lymphokine-induced cytotoxicity. It was first shown that at least two lymphokines are needed for the generation of lymphokine-induced cytotoxicity. They are interleukin 2 and a novel lymphokine, the cytotoxic cell differentiation factor (CCDF). CCDF was produced primarily by the macrophages. The effectors of the lymphokine-induced cytotoxic cells thus generated selectively killed tumor targets of different etiological origins. The serological phenotype of lymphokine-induced cytotoxic cell effectors were found to be Thy 1+, Lyt 2-, and AGM1-; therefore, they were neither classic natural killer (NK) cells nor cytotoxic T-lymphocytes. Extensive characterization of the precursors by sequential column separation and antibody lysis and also by limiting dilution analysis showed that they were AGM1+ and Lyt 2-; thus they were NK-like cells. In addition to NK-like cells being identified as the precursors, two other cell compartments were identified as ancillary cells which regulate the lymphokine-induced cytotoxicity. They were the macrophages and T-cells. Macrophages were needed to produce CCDF and to activate the Lyt 1+ helper T-cells to produce interleukin 2. The Lyt 2+ T-cells play a negative role in the regulation of the lymphokine-induced cytotoxic cell response. The process of lymphokine-induced cytotoxicity thus involves a complex interaction between at least two lymphokines (interleukin 2 and CCDF) and three cell compartments, namely, NK-like cells, macrophages, and T-cells of Lyt 1+ and Lyt 2+ phenotypes.

Animals↗
PubMed1986

[Control by genes of the major histocompatibility complex of macrophage-thymocyte interaction during induction of T-effectors of graft versus host reaction. II. Analysis at the level of humoral factor activity].

The data are presented on the genetic restriction of interaction between humoral factors and intact thymocytes during the formation of T-cell effectors GVH from thymus cells. The source of humoral factors was a cultural medium from combined cultivation of macrophages and syngeneic thymocytes during 18 h. The intensity of the local GVH reaction was evaluated by the index of the lymph nodes enlargement. Genes of the H-2 system control interaction of mediators with thymocytes during the formation of T-cell effectors. H-2 region genes identity of supernatant generative cells and intact thymocytes was necessary for the effective induction of T-effectors GVH. I and D region differences did not affect the formation of T-cells inducing GVH.

Animals↗
PubMed1988

Antibody dependent cell mediated cytotoxicity against anti-D sensitized human erythrocytes. Influence of various effector cells and enzyme treatment of the target cells.

Antibody dependent cell mediated cytotoxicity (ADCC) was measured against anti-D sensitized erythrocytes using various mononuclear cell populations from peripheral blood in a chromium release assay. Adherent effector cells gave stronger cytotoxicity than unseparated and non-adherent cells, and were less dependent on pretreatment of the target cells with papain. However, close correlations were found between the cytotoxicity obtained with the various effector cell populations, indicating that either of them might be used for the purpose of establishing in vitro methods to determine the clinical significance of erythrocyte antibodies. The optimal choice of effector cells is discussed.

Adult↗
PubMed1979

Cell-mediated immunity in interstitial nephritis. II. T lymphocyte effector mechanisms in nephritic guinea pigs: analysis of the renotropic migration and cytotoxic response.

The present studies investigate the effector role of lymphocytes in guinea pigs with an interstitial nephritis. Several observations were made relative to a number of functions expressed by these cells. The results of adoptive cell migration studies suggest that a subpopulation of T cells in nephritic animals traffic renotropically to either normal or damaged kidneys on transfer. Similar lymphocytes were also tested in vitro for direct effector function by utilizing target kidney cell monolayers in a cell-mediated cytotoxicity assay. The kinetics of the observed cytotoxic response were studied over the life span of nephritic animals. Optimal target-cell lysis occurred 12 to 17 days after sensitization, simultaneous with the onset of active histopathologic changes. The cytotoxicity was stoichiometrically titratable and relatively specific for fetal kidney tissue. In addition, cells from the spleen or lymph nodes of diseased animals effectively suppressed this cytotoxic response. These findings demonstrate that a diverse population of T lymphocytes are both capable of damaging the renal interstitium as well as modulating effector-cell functions on a regional basis with the immune system.

Animals↗
PubMed1988

Positive effectors of the binding of an active site-directed amino steroid to rabbit cytochrome P-450 3c.

The binding of the amino steroid, 22-amino-23,24-bisnor-5-cholen-3 beta-ol (22-ABC), to rabbit liver cytochrome P-450 3c was studied using purified P-450 3c and liver microsomes prepared from rifampicin-treated B/J rabbits. 22-ABC binds to purified cytochrome P-450 3c producing a type II spectral change reflecting the coordination of the amine with the heme iron of the protein. In the absence of allosteric effectors, the binding is characterized by a Ks of 5 microM. In the presence of alpha-naphthoflavone or progesterone, the Ks decreases to 0.8 microM, indicating that these two compounds serve as positive effectors of the binding of 22-ABC to cytochrome P-450 3c. The antibiotic rifampicin induces cytochrome P-450 3c in rabbit liver microsomes, and the benzo(a)pyrene hydroxylase, estradiol 2-hydroxylase, and progesterone 6 beta-hydroxylase activities of these microsomes are stimulated by alpha-naphthoflavone. Moreover, the progesterone 6 beta-hydroxylase activity catalyzed by these microsomes exhibits a dependence on substrate concentration that is consistent with activation of the enzyme by the substrate, progesterone. The magnitude of the type II spectral change elicited by 22-ABC for microsomes prepared from rifampicin-treated B/J rabbits is greater than that observed for microsomes from untreated rabbits. For microsomes from rifampicin-treated rabbits, the apparent binding constant for 22-ABC was decreased 5-fold in the presence of alpha-naphthoflavone. We propose that the effects of alpha-naphthoflavone and progesterone on the binding of 22-ABC to cytochrome P-450 3c mimic the effects of the two positive effectors on the metabolism of substrates by increasing the affinity of the enzyme for substrate.

Animals↗
PubMed1988

Lymphokine-activated killer cells in rats: analysis of progenitor and effector cell phenotype and relationship to natural killer cells.

The progenitor and effector cell phenotype of lymphokine-activated killer (LAK) cells generated in F344 rats by recombinant human interleukin 2 (IL-2) (rIL-2) were analyzed. Highly purified populations of peripheral blood large granular lymphocytes (LGL) exhaustively depleted of T-cells were fully capable of generating high levels of LAK activity by 3 to 5 days in culture while purified populations of resting T-cells devoid of LGL could not generate LAK activity. This pure population of LGL expressed surface markers characteristic of rat natural killer (NK) cells [i.e., OX8+, asialomonoganglioside (asialo-GM1+), laminin+, OX19-, R1-3B3-, W3/25-, Ia-, surface immunoglobulin negative (SIg-)]. Further evidence that NK cells were the progenitors of cells with LAK activity was obtained by treatment of spleen or peripheral blood lymphocytes with anti-laminin or anti-asialo-GM1 antibodies plus complement or with the lysosomotropic agent L-leucine methyl ester. These treatments effectively depleted LGL/NK cell activity and the subsequent generation of rIL-2-induced LAK activity. Analysis of the LAK effector phenotype by cell sorting demonstrated that the majority of cells with LAK activity were OX8+, asialo-GM1+, laminin+, OX6+, OX19-, R1-3B3-, W3/25-, and SIg-. Furthermore, treatment of LAK cells with L-leucine methyl ester also significantly reduced their cytolytic activity. Thus, the LAK effector cells were also LGL and expressed surface marker characteristic of activated NK cells and not those of mature T- or B-cells. The proliferative response of rat spleen or blood lymphocytes to rIL-2 appeared to be primarily associated with LGL/NK cells since depletion of NK cells by anti-asialo-GM1 or anti-laminin antibody plus complement or by L-leucine methyl ester significantly (P less than 0.001) reduced the incorporation of [3H]thymidine into DNA. In contrast, depletion of T-cells (by anti-T-cell antibody plus complement) did not significantly affect rIL-2-induced proliferation. Similarly, T-cell-depleted, highly purified populations of LGL gave substantial proliferative responses to rIL-2. These studies clearly indicate that in the rat, the major cell population activated by rIL-2 is the LGL/NK cell and these cells appear to represent the major population of cells in blood or spleen which generate broad antitumor (LAK) cytotoxicity.

Animals↗
PubMed1988

In vivo effects of recombinant IL-2. I. Isolation of circulating Leu-19+ lymphokine-activated killer effector cells from cancer patients receiving recombinant IL-2.

This study was designed to isolate and phenotypically characterize lymphokine-activated killer (LAK) cells generated in vivo during administration of high dose rIL-2 to cancer patients. The development of circulating LAK effector cells in these patients was demonstrated by the ability of fresh PBL to exhibit lytic activity against the NK-resistant Daudi cell line and fresh tumor cells without prior in vitro culture with rIL-2. Kinetic studies demonstrated that circulating LAK effector cells are detectable 4 to 6 wk after the initiation of rIL-2 therapy. Cells isolated by FACS revealed that circulating LAK cells are Leu-19+, Leu-17+ but CD5-. We have previously reported that circulating Leu-19+ cells are heterogeneous with regard to the expression of CD16 and CD8. Since sorting of cells expressing Leu-19 and either low quantities of CD8 or CD16 resulted in cytolytic activity in both the positive and negative fractions, these latter two markers do not identify subpopulations of Leu-19+ cells with or without LAK cytolytic activity. Although all LAK cells generated in vivo were Leu-19+, we generated LAK cells from the Leu-19- subpopulation after in vitro culture with rIL-2, suggesting that at least some of in vitro generated LAK cells are derived from Leu-19- precursor cells. These LAK cells did not, however, express the Leu-19 surface marker. Based on the functional data reported in this paper, we conclude that circulating LAK effector cells are a phenotypically heterogeneous population that express surface Ag in association with NK cells and not T lymphocytes.

Antigens, Neoplasm↗
PubMed1988

Generation of non-MHC restricted killing in cultures stimulated with B cells from chronic lymphocytic leukaemia patients: phenotypic characterization of the precursor and effector cells.

Freshly isolated B cells from chronic lymphocytic leukaemia patients (B-CLL) have been previously shown to induce a strong proliferative response and high levels of NK-like activity in lymphocytes from healthy donors. The present paper deals with the origin, mitotic state, target spectrum and cell surface phenotype of the NK-like effectors generated after stimulation with B-CLL. Experiments using large granular lymphocytes (LGL) and T cells as responders demonstrated that most of the precursors of the newly generated NK-like effectors express the CD3 antigen. The induction of NK-like activity paralleled cell activation, as judged by blast transformation, thymidine uptake and appearance of cell surface activation markers. The newly generated NK-like effectors displayed a T cell phenotype and a broader target repertoire than native NK cells.

Antigens, Surface↗
PubMed1988

Effectors of Escherichia coli aspartate transcarbamoylase differentially perturb aspartate binding rather than the T-R transition.

New systematic methods developed for equilibrium isotope exchange kinetics have been used to analyze the effects of activator ATP and inhibitor CTP with Escherichia coli aspartate transcarbamoylase. This indepth approach requires (a) variation of [modifier] with fixed subsaturating levels of substrates, and (b) variation of at least three combinations of reactant-product pairs in constant ratio at equilibrium: [A,B,P,Q], [A,P], and [B,Q] with the co-substrates held constant, in the presence and absence of added modifier. Both ATP and CTP had much stronger effects on the [14C]Asp in equilibrium C-Asp exchange rate than on [32P]C-P in equilibrium Pi. The bisubstrate analog N-phosphonacetyl-L-aspartate activated, then inhibited, Asp in equilibrium C-Asp more strongly than C-P in equilibrium Pi. N-Phosphonacetyl-L-aspartate gave complete (100%) inhibition, whereas CTP inhibition of either exchange was only partial. Substrate saturation curves in the presence and absence of effectors indicate that ATP and CTP perturb the observed values of Rmax and S0.5 in different fashions without appreciably changing the observed Hill number. Computer simulations indicate that the primary site of ATP and CTP action is the association rate for Asp, not the allosteric T-R transition. This finding is substantiated by previous studies in which modified aspartate transcarbamoylase had lost cooperative Asp binding without loss of sensitivity to effectors, or in which sensitivity to one effector could be deleted selectively. The present results, with newly devised computer simulation and analysis methods, illustrate the usefulness of equilibrium isotope exchange kinetic probes for providing unique insights to enzyme regulatory mechanisms, to define exactly which steps are altered in a given kinetic mechanism.

Adenosine Triphosphate↗
PubMed1977

Antibody-dependent cellular cytotoxicity effector cells lack Ia antigens.

Surface immunoglobulin (sIg)-positive and sIg-negative subpopulations of macrophage-depleted murine splenic lymphocytes were obtained by Sephadex anti-Fab immunoabsorbent fractionation. These lymphocyte subpopulations were analyzed for the presence of Thy 1 and Ia alloantigens and also for Fc receptors by fluorescence microscopy. Concurrently, these lymphocyte subpopulations were studied for effector cell activity in antibody-dependent cellular cytotoxicity (ADCC). Effector cells mediating ADCC were contained in the sIg-negative lymphocyte subpopulation and sIg-positive lymphocytes did not mediate cytotoxicity. The majority of sIg-positive lymphocytes were found to bear Ia antigens and Fc receptors, and these cell surface structures were associated in that treatment of these cells with anti-Ia sera inhibited binding of complexed immunoglobulin to Fc receptors. In contrast, most sIg-negative, Thy 1-negative lymphocytes lacked Ia Antigens, and the Fc receptors detected on such cells were not blocked by anti-Ia sera. In addition, a small subpopulation of sIg-negative, Ia antigen-positive, Fc receptor-positive lymphocytes was found. Elimination of this subpopulation of Ia antigen-positive cells from sIg-negative lymphocytes, by treatment with anti-Ia serum and complement, did not diminish ADCC effector cell activity in the resultant cell population when compared with untreated sIg-negative lymphocytes. Thus, in murine spleen, nonphagocytic mononuclear cells that lack both sIg and Ia antigens were shown to mediate ADCC.

Animals↗