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Results for “Antigenic Modulation”

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PubMed1998

Identification and characterization of the RNA chaperone activity of hepatitis delta antigen peptides.

In this study, we identified an activity of the hepatitis delta antigen that both modulates the cis-cleaving activities of hepatitis delta virus (HDV) genomic RNA fragments and facilitates the trans-cleavage reactions between hammerhead ribozymes and the cognate substrates of various lengths in vitro. Hepatitis delta antigen peptides exert their effect by accelerating the unfolding and refolding of RNA molecules and by promoting strand annealing and strand dissociation. In addition, the stimulatory effect of hepatitis delta antigen peptide on hammerhead catalysis is observed whether the peptide is removed or not by phenol/chloroform extraction prior to the initiation of trans-cleavage reaction. Therefore, hepatitis delta antigen peptide acts as an RNA chaperone. The RNA chaperone domain of hepatitis delta antigen overlaps with the coiled-coil domain that is rich in lysine residues. The RNA binding domains of hepatitis delta antigen previously identified are not required for the RNA chaperone activity identified herein. The RNA chaperone activity of hepatitis delta antigen may be important for the regulation of HDV replication in vivo.

Amino Acid Sequence↗

PubMed1988

Mouse p53 blocks SV40 DNA replication in vitro and downregulates T antigen DNA helicase activity.

Immunopurified mouse p53 proteins were used to gain experimental access to the mechanisms underlying nonprimate p53 directed suppression of SV40 origin directed DNA replication in vivo. In replication competent HeLa cell extracts containing exogenous T antigen, mouse p53 blocks T antigen dependent DNA synthesis as in vivo. However, in transcription competent HeLa extracts, mouse p53 has no effect either on overall transcription or on the ability of immunopurified T antigen to downregulate SV40 early transcription. We show that although mouse p53 has no significant effect on T antigen encoded activities such as ATPase and DNA binding, helicase activity is somewhat reduced suggesting that the in vivo suppression by mouse p53 of SV40 replication may be due, at least in part, to direct modulation of T antigen function.

Adenosine Triphosphatases↗

PubMed1992

Monoclonal antibodies against human T cell adhesion molecules--modulation of immune function in nonhuman primates.

The cytotoxic T cell is thought to be a primary effector of allograft rejection. In vitro studies have demonstrated that the interaction between cytotoxic T cells and target cells involves cell surface adhesion molecules that result in conjugate formation, with subsequent antigen recognition, T cell activation, and target cell lysis. Experiments have also demonstrated the ability of monoclonal antibodies with specificity for two human T cell adhesion molecules, lymphocyte function associated (LFA) antigen-1 (LFA-1, CD11a, alpha-chain/CD18, beta-chain) and LFA-2 (CD2), to inhibit conjugate formation in vitro. Studies in a nonhuman primate model were undertaken to determine whether the in vivo administration of monoclonal antibodies with specificity for the alpha chain of LFA-1 (CD11a) or with specificity for CD2 could modulate in vivo T cell function. Cynomolgus monkeys (Macaca fascicularis) received 10 daily intravenous infusions of either anti-CD11a, anti-CD2 or both anti-CD11a and anti-CD2 monoclonal antibodies. Antibody administration was well tolerated and resulted in high levels of circulating murine monoclonal antibody in the peripheral circulation. Nearly all the animals generated antimurine antibodies that were specific for both idiotypic and nonidiotypic determinants of the infused mouse protein. Circulating lymphocytes and T cells were not depleted by treatment with anti-CD11a or anti-CD2 mAbs; in fact, treatment with the combination of anti-CD11a plus anti-CD2 or anti-CD11a alone led to increased numbers of circulating lymphocytes and T cells. Modulation of the LFA-1 molecule on circulating T cells occurred as a result of treatment with anti-CD11a (or the combination of anti-CD11a plus anti-CD2), whereas treatment with anti-CD2 (or anti-CD11a plus anti-CD2) did not result in modulation of the CD2 antigen despite detectable levels of circulating anti-CD2 mAb. In vivo T cell function was assessed by placement of skin allografts. As compared with treatment with saline or a control mAb, allograft survival was significantly prolonged in animals treated with anti-CD11a or combination treatment but not in animals receiving anti-CD2 alone. We conclude that the in vivo administration of anti-LFA-1 mAb may be useful for the blockade of effector T cell activity during allograft rejection, that saturation of antigen and antigen modulation may be important for efficacy of such antibody effects in vivo, and that monoclonal antibodies with specificity for functionally important T cell surface molecules may alter T cell function in vivo without lymphocyte depletion.

Animals↗

PubMed2003

Use of anti-CD3/CD28 mAb coupled magnetic beads permitting subsequent phenotypic analysis of activated human T cells by indirect immunofluorescence.

Functional analysis of T lymphocytes requires in vitro stimulation of these cells under experimental conditions that mimic as closely as possible physiological in vivo stimulation and that involve antigen/T cell receptor (TCR)-mediated activation. Because of the low frequency of antigen-specific T cells in human clinical samples, stimulation with a combination of anti-CD3 and anti-CD28 monoclonal antibodies (mAbs) is a preferred method. Interaction of these mAbs with their ligand results in modulation of the mAb-ligand complex from the cell surface. However, as a result of incomplete modulation, CD3/CD28 mAb complexes often remain at the cell surface, thereby precluding subsequent indirect immunofluorescence and flow cytometry analysis using mouse immunoglobulin (Ig)-specific antibodies. This is of importance in situations in which no specific fluorochrome-conjugated mAbs are available, such as in screening procedures of Ig-containing hybridoma culture supernatants. We propose here the use of CD3/CD28 mAbs, linked to magnetic beads allowing standardization of the activation conditions, optimal activation of T cells and complete modulation of antigen-antibody complexes from the cell surface.

ADP-ribosyl Cyclase↗

PubMedDate not supplied

Psychosocial modulation of antibody to Epstein-Barr viral capsid antigen and human herpesvirus type-6 in HIV-1-infected and at-risk gay men.

We investigated the effects of two behavioral interventions--aerobic exercise and cognitive behavioral stress management (CBSM)--on Epstein-Barr virus viral capsid antigen (EBV-VCA) and human herpesvirus type-6 (HHV-6) antibody modulation in 65 asymptomatic gay men measured at several time points in the 5 weeks preceding and following notification of their human immunodeficiency virus-type 1 (HIV-1) serostatus. After accounting for potential immunomodulatory confounds, we found that HIV-1 seropositive men had higher EBV-VCA antibody titers than those diagnosed as seronegative at every time point during the study; however, no significant differences were found with respect to HHV-6. Among HIV-1 seropositive and seronegative subjects, respectively, those randomized to either behavioral intervention had significant decreases in both EBV-VCA and HHV-6 antibody titers over the course of the intervention as compared with assessment-only controls (of HIV-1 seropositive and seronegative status) whose antibody titers did not significantly change and which remained consistently higher than either serostatus-matched intervention group over subsequent time points, independent of total immunoglobulin G levels and degree of polyclonal B cell activation. In attempting to explain serostatus differences in EBV and HHV-6 values, it was found that HIV-1 seropositive men had significantly lower CD4 cells, CD4:CD8 ratio, and blastogenic response to phytohemagglutinin (PHA), as well as significantly higher CD8 cells at baseline. No significant differences were found between the HIV-1 seropositive and seronegative men with respect to anxiety and depression at baseline. Since the greatest changes in EBV and HHV-6 occurred between baseline and week 10, we correlated changes in immune (CD4, CD8, CD4:CD8 ratio, PHA stimulation) and distress-related markers (state depression and anxiety) with EBV and HHV-6 change scores over this time period. No significant correlations were found between any of these immune- or distress-related variable and the antibody change scores suggesting that the mechanisms by which EBV and HHV-6 antibodies are being modulated by these interventions possibly involve other, yet to be determined, immune, neuroendocrine, and/or psychologic variables.

Acquired Immunodeficiency Syndrome↗

PubMed2002

Antigen presentation by Peyer's patch cells can induce both Th1- and Th2-type responses depending on antigen dosage, but a different cytokine response pattern from that of spleen cells.

The Th1 and Th2 preference induced by cells from the Peyer's patch (PP) and spleen (SPL) with various doses of an antigen was examined. The same splenic T cell receptor-transgenic CD4+ T cells were first incubated with PP or SPL cells in the presence of various doses of an antigen, and the cytokine response was observed after secondary stimulation. A Th2-type pattern was only obtained for primary stimulation at 10 microM of the antigen with PP cells, whereas a Th1 pattern was induced at both higher and lower concentrations. SPL cells in the presence of 0.1 to 1 microM of the antigen induced the secretion of Th2-type cytokines. Ten and 100 microM of the antigen plus SPL cells did not induce the release of a large quantity of cytokines. PP cells induced a different cytokine pattern at the antigen concentration that induced a similar level of T cell proliferation with SPL cells. Our findings suggest that the antigen-dose dependent development of Th1/Th2 cells is differentially modulated by the antigen-presentation function of cells in PP and SPL.

Animals↗

PubMed1989

Collaboration of Th1 and Th2 T cell clones in specific antibody responses: regulation of the IgM response to phosphorylcholine.

Carrier (KLH)-specific type 1 T cell clones (Th1), which are defined by secretion of IL-2 and IFN-gamma but not IL-4, and type 2 (Th2) clones, which secrete IL-4, but not IL-2 or IFN-gamma, have been isolated and analyzed for their ability to collaborate in providing help for B cells to secrete phosphorylcholine-specific IgM antibodies. The resulting antibody responses exhibited a characteristic pattern suggesting two distinct regulatory interactions among the Th1, Th2, and B cells. At low doses of antigen, Th1 cells enhanced the helper function of the Th2 cells, an effect due primarily to IL-2. At high doses of antigen, Th1 cells or IFN-gamma inhibited Th2-dependent antibody responses. The inhibitory effect of Th1 or IFN-gamma affected primarily the hapten-carrier-linked portion of the response. The overall effect was a modulation of the antigen dose-response curve for antibody production, eliminating the sharp increases in dose response mediated by isolated T cell clones. The data suggest that collaborative interactions of Th1 and Th2 cells in antibody production may have important physiological consequences.

Animals↗

PubMed1999

Cationic lipid DC-Chol induces an improved and balanced immunity able to overcome the unresponsiveness to the hepatitis B vaccine.

Th1 and Th2 immune responses against antigens can be modulated by the use of adjuvants. Since antibody isotypes (IgG1 and IgG2a) and cytokines induced may reflect the Th differentiation taking place during the immune response, the humoral and cellular immune responses induced in mice against hepatitis B virus surface antigen (HBsAg) were examined when the antigen was either adsorbed to aluminum hydroxyde or administered with a new adjuvant the cationic lipid 3beta-[N-(N',N'-dimethylaminoethane)carbamoyl]cholesterol (DC-Chol). The use of DC-Chol increased antibody responses in responding BALB/c mice, induced more consistent IgG1 and IgG2a antibody responses in OF1 mice and overcame the nonresponse to HBsAg in B10.M mice. Furthermore, DC-Chol was able to induce cellular immune responses to HBsAg. The DC-Chol induced a balanced Th1/Th2 response, which enabled mice to overcome the inherited unresponsiveness to HBsAg encountered with aluminum-adjuvanted vaccine. Thus, the DC-Chol provides a signal to switch on both Th1 and Th2 responses, which may have important implications for vaccination against hepatitis B virus, as well as for enhancing weak immunogenicity of other recombinant purified antigens in a nonresponder population.

Adjuvants, Immunologic↗

PubMed1994

Target-cell sensitivity to natural killer-cell lysis is determined by the expression of a novel antigen in conjunction with major histocompatibility complex class-I molecules.

Recently, a panel of monoclonal antibodies (MoAbs) was developed that identified a novel tumour-cell antigen conserved across species (mouse, rat and man). Fluorescence-activated cell sorter (FACS) analysis demonstrated that this antigen was expressed at highest levels on human tumour cell lines sensitive to natural killer (NK)-cell lysis. These MoAbs inhibited NK cell lysis of K562 target cells (by up to 90%), as well as a variety of other NK-sensitive target cells. Biochemical analyses revealed that the MoAbs reacted with a polypeptide of 42 kDaltons, distinct from other known cell surface antigens. Now the expression of this antigen has been analysed further with a panel of 24 tumour cell lines to determine its role in NK cell function. The expression of target cell major histocompatibility complex (MHC) molecules in conjunction with sensitivity to NK cell lysis was examined also. For each of the 24 cell lines it was found that the level of expression of the novel target cell antigen determined the sensitivity of the cell line to NK cell lysis. However, the level of MHC antigen expression could modulate target cell sensitivity to NK cell lysis, in that high levels of MHC class-I molecule expression resulted in a target cell that was insensitive to NK cell lysis regardless of the level of expression of the novel antigen. Thus, for most transformed cell lines, sensitivity to NK cell lysis appeared to be determined by the expression and levels of the novel antigen in association with MHC class-I molecules.

Adolescent↗

PubMed1985

Selective killing of smooth muscle cells in culture by the ricin A-chain conjugated with monoclonal antibodies to a cell surface antigen via a dextran bridge.

Monoclonal antibodies to a surface antigen of the modulated smooth muscle cells originally isolated from the rat aorta media were conjugated with ricin A-chain via an oxidized dextran bridge. The interaction of cultured cells with the conjugates obtained and with control substances was monitored following incorporation of 14C-leucine radioactivity. It was found that 14C-leucine incorporation was suppressed by 80-90% at a conjugate concentration of 10(-6)-10(-7) M. Antigen-negative cells (line IAR; rat hepatocytes) were insensitive to the conjugate at any concentration used. Control use of purified ricin A-chain, native or oxidized dextran, specific and nonspecific IgG did not affect normal 14C-leucine incorporation. The data obtained may be useful for designing targeted drug transport systems and for selective screening of modulated smooth cells in vascular pathology models in vivo.

Animals↗

PubMed1983

A unique antigen expressed on myeloid cells and acute leukemia blast cells defined by a monoclonal antibody.

A murine hybridoma-derived monoclonal antibody, PM-81, was obtained from a fusion of cells of the NS-1 myeloma cell line with cells from a mouse immunized with the HL-60 promyelocytic leukemia cell line. This cytotoxic IgM monoclonal antibody was specific for myeloid cells. Employing indirect immunofluorescence and flow cytometry, we determined that this antibody reacts strongly with normal human granulocytes, eosinophils, and monocytes but not lymphocytes (including phytohemagglutinin-activated lymphocytes), null cells, red blood cells, or platelets. Moreover, the PM-81 antibody reacts with leukemia cells from 19 of 22 patients with acute myelocytic leukemia of all FAB subclasses, three of three patients with common acute lymphocytic leukemia, four of four patients with chronic myelocytic leukemia (CML) in myeloid blast crisis (terminal transferase (TdT)-negative) but did not react with cells from two patients with CML in lymphoid blast crisis (TdT-positive) or five patients with chronic lymphocytic leukemia. The myeloid cell lines HL-60, K562, KG-1, and U937 were all reactive with PM-81. The lymphoid lines CCRF-CEM and Daudi did not express PM-81 but HSB-2 was positive. The PM-81 antigen was absent on myeloid and erythroid progenitor cells as determined by their insusceptibility to complement-dependent lysis. In addition, only PM-81-unreactive cells were capable of colony formation. Furthermore, the PM-81 antibody does not appear to induce modulation of the antigen to which it binds. Thus, this monoclonal antibody appears to fulfill several criteria for clinical utility in the diagnosis and treatment of both acute myelocytic and acute lymphocytic leukemia.

Animals↗

PubMed1986

Surface antigen expression by bovine alveolar macrophages: functional correlation and influence of interferons in vivo and in vitro.

Alveolar macrophages (AM) procured by bronchoalveolar lavage of healthy calves were tested for the expression of two antigens defined by monoclonal antibodies. One of these, H34A, detects a MHC type II (Ia)-antigen; the other, B18A, a heterodimer of unknown function. No single AM-activity could be ascribed solely to the subpopulations defined by the presence or absence of these two surface antigens. The expression of both antigens could be modulated by in vitro treatment of the AM with recombinant E. coli-derived bovine interferon-gamma (rBoIFN-gamma), but not by interferon-alpha 1 (rBoIFN-alpha 1). Enhanced Ia-expression was detectable within 3 h of exposure to rBoIFN-gamma and reached a maximum by 24-48 h. Expression of the Ia-antigen required continual presence of bioactive IFN. However, cells that reverted from the Ia+ to the Ia- state did not become refractory to reinduction, and induction was possible even after several days (at least 96 h) in culture, despite the in vitro maturation and modulation of the AM that occurred. Treatment of calves with rBoIFN-gamma also resulted in increased numbers of Ia(H34A)+ cells, but in a decline of B18A+ cells. In contrast to the in vitro findings, rBoIFN-alpha 1 appeared to have some modulatory effect in vivo. The latter effect may be indirect rather than direct as for rBoIFN-gamma. As previously shown for rBoIFN-alpha 1, in vitro treatment of the AM with rBoIFN-gamma "activated" the AM as judged by enhanced cytotoxicity, enhanced accessory cell activity in mitogen-driven lymphocyte-proliferation, enhanced IgG Fc- and C3b-receptor expression and content of some enzymes. The fact that the two IFNs have very similar effects on cell functions, but differ markedly in their Ia-inducing immunoregulatory activity, supports the notion that the Ia-antigen expression may be irrelevant as a surface marker for macrophage activation, and may rather be a marker for a certain functional stage of the macrophage. Moreover, the acquisition of this stage appears to be, at least in the AM, a reversible event.

Animals↗

PubMed1991

Granulomatous hypersensitivity to Schistosoma mansoni egg antigens in human schistosomiasis. III. In vitro granuloma modulation induced by immune complexes.

Granulomatous hypersensitivity to parasite eggs of Schistosoma mansoni is an important factor in the development of morbidity in chronic schistosomiasis. It has been demonstrated previously that the chronic, well-tolerated, intestinal form of schistosomiasis is associated with the establishment and maintenance of a variety of immunoregulatory mechanisms. We have used an in vitro model of granuloma formation for the purpose of studying the regulation of granulomatous hypersensitivity to S. mansoni egg antigens, mediated by immune complexes (IC). Our results show that the peripheral blood mononuclear cells (PBMCs) from patients with active schistosome infections, when treated with sera from chronic schistosomiasis patients, were able to induce an inhibitory activity on in vitro granuloma formation. Significant modulation of the in vitro granuloma reaction remained after treatment of PBMCs with isolated IC or manufactured IC with soluble egg antigen (SEA) and purified IgG from pooled chronic schistosomiasis sera. In contrast to granuloma modulation stimulated with whole molecule IgG-SEA IC, the incubation of PBMCs with F(ab')2 IgG-SEA IC did not induce any suppression of the granulomatous hypersensitivity to SEA. It appears in this model system that IC may inhibit the activity of granuloma formation by stimulating macrophages to release suppressive mediators. We have demonstrated this possibility by inhibition of prostaglandin activity using indomethacin. The addition of indomethacin to the granuloma culture significantly reduced in vitro granulomatous hypersensitivity to S. mansoni eggs in patients with chronic intestinal schistosomiasis and do so by inducing macrophages to secrete prostaglandins.

Alprostadil↗

PubMedDate not supplied

Immunological responses to bacterial plaque in the mouth.

A heavy load of bacteria, referred to as dental plaque, accumulates at the junction between the teeth and gum. Bacterial plaque may be considered to have three functional components: (a) cariogenic organisms, (b) organisms inducing gingival inflammation and periodontal disease, and (c) adjuvant and tolerizing agents, such as lipopolysaccharides, dextrans and levans. Sequential investigation of plaque accumulation in man has shown a correlation between gingival inflammation and both lymphocyte transformation and macrophage migration inhibition. An adjuvant effect of in vivo plaque accumulation was manifested by the enhancement of T lymphocytes in the mixed leucocyte culture reaction and of B lymphocytes, as shown by the increased response to lipopolysaccharide. It may be significant that a substantial component of bacterial plaque consists of dextrans and levans, produced by certain streptococci and actinomyces, and lipopolysaccharides from Gram-negative bacteria. These bacterial products are B cell mitogens which may have an adjuvant or tolerizing effect on immune responses. The relationships between immunogenicity, mitogenicity, adjuvanticity and tolerogenicity of lipopolysaccharides, levan and dextran have not been clearly defined. However, important variables of the polyglycans are the molecular weight, type of branching, negative charge, epitope density, degradability, dosage and the sequence between mitogen and antigen. Dental plaque in man is a focus of B cell mitogens and T cell antigens which may modulate the immune responses in such a way as to induce a protective response in the development of caries and a damaging response in periodontal disease.

Antigens, Bacterial↗

PubMed1987

Modulation of expression of class II histocompatibility antigens by secretion of a cellular inhibitor in K562 leukemic cells.

In this report we show that it is possible to induce the expression of HLA-DR antigens on K562 cells, previously reported to be unresponsive to interferon-gamma (IFN-gamma). However, only low cell concentrations and a high dose of IFN-gamma allowed the induction of HLA-DR antigens. Furthermore, the recombinant glycosylated IFN-gamma is 100-fold more efficient than the unglycosylated form. This induction of HLA-DR antigens on K562 was not related to a stage of differentiation or to the presence of cells subsets specifically sensitive to IFN-gamma, since repeated sorting of K562 HLA-DR-positive and negative cells did not lead to the selection of a cell subset with a different potential of induction for HLA-DR. The difficulty in obtaining induction is due to the production of a soluble endogenous inhibitor of proteic nature, whose action is not restricted to the K562 cell line since it operates also on both epithelial and fibroblastic cells. Treatment of normal human epithelial and fibroblastic cells with conditioned medium from K562 cultures caused a marked decrease in the expression of HLA class II antigens (DR and DP) induced by IFN-gamma (10,000 U/ml), but had no effect on cell growth; however, it also affected expression of HLA class I antigens. This inhibition is not mediated by prostaglandin or an IFN-alpha or IFN-beta-dependent mechanism. Production of this inhibitor by pluripotent human leukemic cells could cause an unbalance in the complex control exerted by the immunological system during hematopoietic differentiation or leukemic progression.

Antibodies, Monoclonal↗

PubMed1995

Interleukin-2 down-modulates memory T helper lymphocyte development during antigenic stimulation in vitro.

Using an in vitro antigenic stimulation model of murine spleen cells in the presence of the immunosuppressor cyclosporin A (CSA) we have previously reported that not only does this drug not interfere with the differentiation of T lymphocytes into memory cells it appears to favor this differentiation (Motta, I. et al., Eur. J. Immunol. 1991. 21:551). Because CSA blocks interleukin-2 (IL-2) gene expression, we have analyzed the effect of this cytokine on memory T helper cell development. Murine splenic cells were primed for 6 days with sheep red blood cells (SRBC) in protocols in which either IL-2 was not produced or its biological activity was neutralized by anti-IL-2 receptor (R) antibodies. The helper function of the recovered T cells was revealed by their capacity to help virgin B splenocytes produce anti-SRBC antibodies upon challenge in vitro. We found that CD4+ cells primed in the absence of IL-2, provoked either by IL-2 gene transcription blockade by CSA or by treatment with anti-IL-2R antibodies, afford the best helper functions. These cells exhibit a memory-type phenotype characterized by the low expression of the MEL-14 marker and the high expression of the CD44 marker. Evidence is also presented that memory T helper cells originate in part from naive subset displaying the MEL-14hi phenotype. The pattern of expression of the genes encoding different cytokines (IL-2, IL-4, IL-5 and interferon-gamma) following a secondary antigenic stimulation shows that the helper function of the cells primed in the absence of IL-2 correlates with the up-regulation of the IL-2 and the IL-5 genes. From these data, we conclude that IL-2 plays a major role in the control of memory T helper cell induction.

Animals↗

PubMed1984

Modulation of production of hepatitis B surface antigen by a human hepatoma cell line.

Three drugs were assayed for their capacity to inhibit hepatitis B surface antigen (HBsAg) production by the PLC/PRF/5 human hepatoma cell line. The effect on cell growth and HBsAg production of Cordycepin, 6-azauridine, and Hygromicin B is reported. Hygromicin B, a translation inhibitor unable to penetrate normal cells, greatly reduced HBsAg production by growing and confluent cells.

Anti-Bacterial Agents↗

PubMed1989

Modulation of antibody responses by conjugates of antigens with monomethoxypolyethylene glycol.

The use of tolerogenic conjugates of monomethoxypolyethylene glycol (mPEG) and diverse antigens, including xenogeneic monoclonal immunoglobulins, is reviewed with respect to the induction of specific abrogation of antibody responses. Evidence is presented for activation of specific suppressor T (Ts) cells by antigen-mPEG conjugates and for the release of suppressor lymphokines (TsFs) from these cells; both Ts cells and TsFs are able to suppress antigen-specific immune responses on transfer to syngeneic mice. The therapeutic potential of tolerogenic mPEG conjugates is discussed with respect to IgE-mediated allergies and diseases which could be ameliorated by administration of xenogeneic monoclonal antibodies and of their respective immunotoxins, as would be the case for suppression of rejection of organ transplants, localization and destruction of tumors, and in vivo annihilation of the human immunodeficiency virus (HIV).

Animals↗