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PubMed1987

Unique epitopes of common acute lymphoblastic leukemia antigen detected by new monoclonal antibodies.

In the present study we have generated four new monoclonal antibodies (mAbs), termed SN5, SN5a, SN5b, and SN5c, which are directed toward the human common acute lymphoblastic leukemia antigen (CALLA). SN5 and SN5c were generated separately by immunizing two mice with a leukemia antigen preparation isolated from uncultured non-T-/non-B-acute lymphoblastic leukemia cells whereas SN5a and SN5b were generated by immunizing a third mouse with intact KM-3 (a cultured non-T-/non-B-acute lymphoblastic leukemia cell line) cells. It was found that the binding activities of mAbs SN5 and SN5c generated by using an isolated leukemia antigen preparation were approximately twice as large as those of mAbs SN5a and SN5b generated by using intact leukemia cells. All four of the present mAbs induced antigenic modulation of CALLA on the leukemia cells in vitro; subclasses of mAbs appear to be an important factor which influences the kinetics of antigenic modulation. SN5, SN5a, and SN5c immunoprecipitated a distinct Mr 100,000 component from detergent-solubilized cell membrane antigens but SN5b failed to do so. These four mAbs together with J5, another anti-CALLA mAb, were individually tested in a solid phase radioimmunoassay for reactivity with the detergent extracts of various human tissues, i.e., kidney, lymph node, spleen, brain, liver, pancreas, lung, and heart. SN5, SN5a, SN5c, and J5 showed reaction only with kidney whereas SN5b did not show significant reaction with any tissues including kidney. However, SN5b as well as SN5 showed a significant reaction with kidney in an immunoperoxidase-staining test. These results indicate that the interaction of SN5b with a unique epitope on the CALLA moleucle is strongly disturbed by relatively mild detergents (deoxycholate, taurocholate, and Nonidet P-450). These detergents did not significantly disturb the reaction between other mAbs (SN5, SN5a, and SN5c) and the corresponding epitopes on the CALLA molecule. Competitive binding experiments show that the three epitopes recognized by SN5, SN5b, and SN5c are sufficiently close to each other to allow complete or nearly complete reciprocal inhibition of binding to CALLA present on leukemia cells. Peculiar inhibition patterns, however, were observed between SN5a and the other three mAbs. SN5, SN5b, and SN5c inhibited only partially the subsequent binding of SN5a to the leukemia cells. Conversely, SN5a inhibited nearly fully the subsequent bindings of SN5, SN5b, and SN5c. These results suggest another unique epitope defined by SN5a.(ABSTRACT TRUNCATED AT 400 WORDS)

Antibodies, Monoclonal↗
PubMed1986

Immune response mediated by liposome-associated protein antigens. IV. Modulation of antibody formation by vesicle-encapsulated methotrexate.

Large unilamellar reverse-phase evaporation vesicles (REV) were used as a heterobifunctional carrier for a pharmacologically active agent and a protein antigen. Methotrexate (MTX) was encapsulated in the hydrophilic compartment of liposomal REV with or without surface-conjugated bovine serum albumin (BSA) antigen. The administration of MTX encapsulated within BSA-coated vesicles (MTX.REV-BSA) could either enhance or depress the anti-BSA plaque-forming cell (PFC) response in mice. On the other hand, the administration of MTX entrapped in plain vesicles (MTX.REV) produced essentially a suppressive effect on the PFC response stimulated by the simultaneous injection of a separate antigen, e.g. vesicle-conjugated BSA (REV-BSA). This suppression of the antibody response occurred, whether MTX.REV was injected 1 day before, during, or 1 day after the immunization with an antigen. These results indicate that liposome-encapsulation of a very limited drug dose can modify the immunobiological effect of the drug which, when presented in its free form at the same dose, exerts no appreciable action on the engendered immune response. Thus, the modulation of the immune response by a liposome-encapsulated drug appears to be influenced by the drug dose can modify the immunobiological effect of the drug which, when presented in its free form.

Animals↗
PubMed1991

Mixed blasts crisis following extramedullary involvement with the cytogenetic evidence of clonal evolutions in Philadelphia chromosome-positive chronic myelocytic leukemia.

We describe a unique case of a young girl with adult type chronic myelocytic leukemia (CML). Clinically she had an extramedullary blastic crisis (BC) prior to that in peripheral blood and in bone marrow. The blasts were primitive cells and always CD7, CD33, CD34 and HLA DR-positive. During the course of illness the blasts became negative for CD5 and positive for CD41a and for platelet-peroxidase. Additional chromosomal appearances and subsequently clonal evolution were seen during the clinical course. Surface antigen modulation and morphological changes, which were observed by microscopic examination and flow cytometry, were induced by in vitro incubation. Surface antigen modulation was more induced in the presence of phytohemagglutinine-conditioned media (PHA-CM) but the effects of PHA-CM on morphological changes were not clear.

Antigens, CD↗
PubMed1990

Marked difference in the in vivo antitumor efficacy between two immunotoxins targeted to different epitopes of common acute lymphoblastic leukemia antigen (CD10). Mechanisms involved in the differential activities of immunotoxins.

In the present study, two isotype-matching mAb, SN5d and SN5, which are directed toward two distinctively different epitopes of common acute lymphoblastic leukemia Ag (CD10) but show a very similar binding affinity to leukemia cells, were compared for their in vivo antitumor activity after conjugated to ricin A chain (RA). Our recently established nude mouse model carrying an ascitic tumor of NALM-6 human pre-B leukemia cells was used as the tumor model. A marked difference was observed in the in vivo antitumor efficacy between SN5d-RA and SN5-RA; SN5d-RA was much more effective than SN5-RA. Several experiments were carried out to gain information concerning the mechanisms involved in the different antitumor efficacy of the two immunotoxins. Although naked (unconjugated) mAb SN5d was much less effective than SN5d-RA conjugates in the in vivo tumor suppression, mAb SN5d was more effective than mAb SN5 in the in vivo tumor suppression. Additionally, marked differences were found between SN5d and SN5 in the induction of antigenic modulation and in the regulation of Ag biosynthesis and expression. Binding of SN5 to NALM-6 leukemia cells caused strong antigenic modulation (down-regulation of Ag expression) and strongly down-regulated Ag biosynthesis and cell surface expression of new Ag. In contrast, binding of SN5d to NALM-6 leukemia cells caused little modulation of overall cell surface expression of common acute lymphoblastic leukemia Ag; the decrease of old Ag by endocytosis after binding to mAb SN5d was compensated by newly exocytosed cell-surface expressed Ag. The present results appear to reveal a novel mechanism which regulates cytotoxic activities of antibodies and immunoconjugates.

Animals↗
PubMed1997

Immunoreceptor tyrosine-based activation motif (ITAM), a unique module linking antigen and Fc receptors to their signaling cascades.

Signal transduction by the T cell and B cell antigen receptors and by receptors for a variety of immunoglobulins' Fc region is strictly dependent on a receptor subunit cytoplasmic module termed immunoreceptor tyrosine-based activation motif (ITAM). This module exists in one or more copies in each of the receptor-associated signal-transducing molecules and it possesses two repeats of the consensus sequence Tyr-X-X-Leu/Ile spaced by six to eight amino acids. Receptor engagement is followed by a rapid and transient phosphorylation of tyrosine residues within their ITAMs, thereby creating temporary binding sites for Src homology 2 (SH2)-containing signaling molecules operating downstream of the activated receptor. The purpose of this review is to discuss recent findings on the functional role of ITAMs in antigen and Fc receptor-mediated signal transduction, with a particular emphasis on kinases operating upstream and downstream of the ITAMs.

Phosphorylation↗
PubMed2004

Modulation of antigenic phenotype by IL-1beta, IFNgamma and TGFbeta on cultured human decidual stromal cells.

Decidual stromal cells (DSC) constitute the most abundant population in normal human decidua together with leukocytes. Both populations may be involved in the immunological role of the decidua by favoring gestational functions, participating in physiological mechanisms to eliminate the fetus, or providing local defense against infection. Using flow cytometry, we investigated whether different cytokines modulate the expression on cultured DSC of antigen-presenting molecules. The treatment with IFNgamma or IL-1beta enhanced the expression of CD54. The percentage of expression of HLA-DR was enhanced by IL-1beta treatment but was not modified by IFNgamma. The expression of CD80 and CD86 was enhanced by IFNgamma treatment but was not modified by IL-1beta; the expression of CD86 and HLA-DR was reduced by TGFbeta1 treatment. The response of DSC and dendritic cells to these cytokines appears to be similar, suggesting a phenotypic and functional relationship between these cell types.

Antigen Presentation↗
PubMed1989

[Patterns in the antigen-nonspecific modulation of the B-cell activity in mice under the influence of a purified staphylococcal anatoxin].

Purified staphylococcal toxoid (PST) has been shown to be an antigen-nonspecific immunomodulator, capable of inducing changes in the immune response of B-cells to unrelated antigens, such as sheep red blood cells (SRBC), in a wide range of doses (from 15 to 0.15 binding units per mouse). The manifestation of the immunomodulating effect depends on the conditions of the experiment: the doses of PST and SRBC, the age of mice, the sequence of the injections of the antigens and the intervals between the injections. The simultaneous injection of PST and SRBC induces, as a rule, an increase in immune response to the test antigen, while their separate injection induces mainly immunosuppression.

Adjuvants, Immunologic↗
PubMed2002

Germinal center B cells regulate their capability to present antigen by modulation of HLA-DO.

Peptide acquisition by MHC class II molecules is catalyzed by HLA-DM (DM). In B cells, HLA-DO (DO) inhibits or modifies the peptide exchange activity of DM. We show here that DO protein levels are modulated during B cell differentiation. Remarkably, germinal center (GC) B cells, which have low levels of DO relative to naive and memory B cells, are shown to have enhanced antigen presentation capabilities. DM protein levels also were somewhat reduced in GC B cells; however, the ratio of DM to DO in GC B cells was substantially increased, resulting in more free DM in GC B cells. We conclude that modulation of DM and DO in distinct stages of B cell differentiation represents a mechanism by which B cells regulate their capacity to function as antigen-presenting cells. Efficient antigen presentation in GC B cells would promote GC B cell-T cell interactions that are essential for B cells to survive positive selection in the GC.

Antigen Presentation↗
PubMed2004

Modulation of antigen presentation by autoreactive B cell clones specific for GAD65 from a type I diabetic patient.

We used a GAD65-specific human B-T cell line cognate system in vitro to investigate the modulation of GAD65 presentation by autoantibody, assessed in a proliferation assay. Generally, if the T cell determinant overlaps or resides within the antibody epitope, effects of presentation are blunted while if they are distant can lead to potent presentation. For three different autoreactive B-T cell line cognate pairs, the modulation of GAD65 presentation followed the mode of overlapping or distant epitopes with resultant potent or undetectable presentation. However, other cognate pairs elicited variability in this pattern of presentation. Notably, one B cell line, DPC, whose antibody epitope did not overlap with the T cell determinants, was consistently poor in presenting GAD65. Using the fluorescent dye Alexa Fluor 647 conjugated to GAD65 to study receptor-mediated antigen endocytosis showed that all the antigen-specific B cell clones were efficient in intracellular accumulation of the antigen. Additionally, multicolour immunofluorescence microscopy showed that the internalized GAD65/surface IgG complexes were rapidly targeted to a perinuclear compartment in all GAD-specific B cell clones. This analysis also demonstrated that HLA-DM expression was reduced strongly in DPC compared to the stimulatory B cell clones. Thus the capability of antigen-specific B cells to capture and present antigen to human T cell lines is dependent on the spatial relationship of B and T cell epitopes as well other factors which contribute to the efficiency of presentation.

Antibodies, Monoclonal↗
PubMed2002

Identification of growth factors that promote long-term proliferation of olfactory ensheathing cells and modulate their antigenic phenotype.

Olfactory ensheathing cells can develop into distinct subtypes in culture after incubation in serum-free medium conditioned by astrocytes, which have Schwann cell-like and astrocyte-like properties. It has not been possible so far to modulate and grow large numbers of these olfactory ensheathing cell subtypes. In this study, we have shown that astrocyte-conditioned medium, although promoting differentiation of the two olfactory ensheathing cell types, is growth-restrictive after 14 days, probably due to the upregulation of p16 and p27. Growth arrest can be overridden and cells maintained for a further 11 weeks, by a mitogen mix of fibroblast growth factor 2, forskolin, and heregulin (olfactory mitogen medium) combined with astrocyte-conditioned medium. In the absence of astrocyte-conditioned medium, combinations of the same factors can also override growth arrest but to a lesser extent. Olfactory mitogen medium combined with astrocyte-conditioned medium upregulates O4 and low-affinity nerve growth factor receptor expression on olfactory ensheathing cells, leading to a 100% Schwann cell--like phenotype. If cells are maintained in olfactory mitogen medium alone, or if they are treated with forskolin or fibroblast growth factor 2 diluted in serum-free medium, O4 and low-affinity nerve growth factor receptor expression remains at 100%, but there is also an increase in expression of E-NCAM, the astrocyte-like marker. Medium containing serum also overrides growth arrest, but for only 4 weeks, during which time most differentiation-specific markers disappear. These studies have allowed us to define conditions to modulate the olfactory ensheathing cell phenotype.

Animals↗
PubMed1986

Decrease in acetylcholine-receptor content of human myotube cultures mediated by monoclonal antibodies to alpha, beta and gamma subunits.

One of the two main causes of acetylcholine-receptor loss in myasthenia gravis is antigenic modulation, i.e. accelerated internalization and degradation rate by antibody-crosslinking. This phenomenon has been studied only in animal tissues. Therefore, we tested antigenic modulation of the acetylcholine receptor on human embryonic myotubes in cultures. Several monoclonal antibodies to the alpha, beta and gamma subunits of the receptor reduced its concentration, in some cases down to one-third of the control. Some of these antibodies only form complexes of one antibody with two receptor molecules; consequently such small complexes are sufficient to accelerate internalization of the human acetylcholine receptor. This technique might be proved valuable for clinical screening of sera from myasthenic patients.

Animals↗
PubMed1995

Cell surface expression of major histocompatibility class I antigens is modulated by P-glycoprotein transporter.

P-glycoprotein (Mdr1), a member of the ABC superfamily, is a pump able to transport several compounds across plasma membranes. It displays a high level of similarity with the MHC-linked transporters TAP1 and TAP2 which are involved in the delivery of immunogenic peptides across the endoplasmic reticulum. In the present study we analyze the P-glycoprotein's ability to interfere with the biosynthetic pathway of the MHC class I molecules. Our results show that P-glycoprotein is involved in the modulation of the MHC class I expression in multidrug-resistant tumor cell lines, COS1 cells transfected with mdr1 gene, and human T lymphocytes. Epitope screening evokes the possibility that P-glycoprotein induces a modulation of the different MHC class I forms expressed on the cell surface. We propose that P-glycoprotein is involved in the transport of antigenic protein fragments from the cytosol into the endoplasmic reticulum. The suggested mechanism could be physiologically relevant in tissues displaying a high Mdr1 activity, where this transporter could contribute to the regulation of locoregional immune responses.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1983

Factors affecting expression of glycolipid tumor antigens: influence of ceramide composition and coexisting glycolipid on the antigenicity of gangliotriaosylceramide in murine lymphoma cells.

Gangliotriaosylceramide (Gg3Cer) was previously described as a tumor-associated antigen in murine L5178Y lymphoma [Young, W. W., Jr., and Hakomori, S., Science (Wash. D.C.), 211: 487-489, 1981]. This paper describes the major factors affecting the expression of Gg3Cer at the surface of various clones of L5178Y lymphoma. Of 26 sublines that were recloned, six cell lines showing different degrees of Gg3Cer expression at the cell surface were used for analysis of the glycolipid composition as related to its cell surface antigenicity. Three remarkable correlations between glycolipid composition and the antigenicity of Gg3Cer have been found: (a) high-expressor sublines were characterized by a large proportion of a unique molecular species of Gg3Cer having alpha-hydroxypalmitic acid in its ceramide moiety in striking contrast to low expressors which did not contain this molecular species; (b) low expressors contained a large quantity of ganglio-N-tetraosylceramide (Gg4Cer) and NeuAc alpha 2 leads to 3Gal beta 1 leads to 3GalNAc beta 1 leads to 4Gal beta 1 leads to 4Glc beta 1 leads to 1 Cer (GM1b) gangliosides, whereas these glycolipids were almost absent in high-expressor clones; and (c) nonexpressors, which were converted from the high expressors in vivo through immunotherapy with the monoclonal antibodies to Gg3Cer, contained a large quantity of ganglio-N-tetraosylceramide and NeuAc alpha 2 leads to 3Gal beta 1 leads to 3GalNAc beta 1 leads to 4Gal beta 1 leads to 4Glc beta 1 leads to 1Cer. The nonexpressors should have an induced enzyme system to metabolize Gg3Cer to ganglio-N-tetraosylceramide and NeuAc alpha 2 leads to 3Gal beta 1 leads to 3GalNAc beta 1 leads to 4Gal beta 1 leads to 4Glc beta 1 leads to 1Cer. Three factors, i.e., ceramide composition, coexisting glycolipids, and an antibody-dependent glycolipid change, are therefore important in determination of glycolipid antigenicity and antigen modulation by antibodies. The ceramide composition may affect glycolipid organization in membranes, and the coexisting glycolipid having a longer carbohydrate chain may mask the accessibility of antibody to the antigenic glycolipid. The antigenic modulation by the action of the antibody in vivo may be based on activation of a new glycosyltransferase.

Animals↗
PubMed2001

Modulation of CD8 and CD3 by HIV or HIV antigens.

To investigate whether human immunodeficiency virus (HIV)-1 and HIV-1 antigens modulate surface and cytoplasmic CD8 or CD3, as well as CD4, we used cell permeabilization reagents, surface/cytoplasmic fluorescent staining, multiparameter flow cytometric techniques and an in vitro culture system in which relatively few lymphocytes are actively infected with HIV. Human peripheral blood lymphocytes were: not stimulated, not stimulated but HIV-inoculated, phytohaemagglutinin (PHA)-stimulated, PHA/HIV-inoculated (PHA/HIV), or placed into media with soluble gp120, Rev or Nef. HIV inoculation and Nef had striking modulatory effects on CD8. The cytoplasmic CD8 median fluorescent intensity (MFI) of positive lymphocytes was lower for cells in unstimulated/HIV-infected cultures than unstimulated cultures (44 versus 62% of ex vivo value, P = 0.032) and lower for cells in PHA/HIV cultures than in PHA cultures (56 versus 100% of ex vivo, P = 0.041). The surface CD8 MFI values for Nef were significantly lower than the ex vivo value (75% of ex vivo, P = 0.006). At days 2-7 of culture, Rev was associated with slight reductions in surface CD4 MFI (58% of ex vivo versus 78% of ex vivo for unstimulated cultures, P = 0.047) and greater effects on cytoplasmic CD3 MFI (131 versus 179% of ex vivo for unstimulated cultures, P = 0.035), and surface CD8 MFI (70% of ex vivo, P = 0.006 versus ex vivo value). The globality of Rev's effects suggests these are related to a shared processing pathway, i.e. not due to direct interaction with CD3, CD4 and CD8; the effects of HIV inoculation and Nef on CD8 expression appear to be more CD8 specific. Because CD8 is essential for cytotoxic T-cell function, its down-modulation could inhibit this activity, including anti-HIV cytotoxicity. Given the critical roles of CD3 and CD8 in T-lymphocyte signal transduction and antigen responsiveness, the effects of HIV, Rev and Nef on these molecules have clinically significant implications concerning the pathogenesis and treatment of HIV.

Brefeldin A↗
PubMedDate not supplied

Lung injury mediated by antibodies to endothelium. III. Effect of chlorpromazine in rabbits.

In rabbits intravenous administration of antibodies to lung angiotensin converting enzyme (ACE) results in a rapid redistribution of ACE on the plasma membrane of pulmonary endothelium with fixation of complement and development of fatal pulmonary edema. In survivors given daily injections of antibodies, ACE disappears from the lung ("antigenic modulation") and the rabbits become resistant to further immune injury. To test the hypothesis that these events depend on a functionally intact mechanism of cell activation, rabbits received, in addition to anti-ACE antibodies, chlorpromazine, a drug that inhibits calmodulin and protein kinase C and decreases plasma membrane fluidity. Initially, chlorpromazine inhibited antigen redistribution, fixation of complement, and development of pulmonary edema. In rabbits maintained on chlorpromazine and receiving daily anti-ACE antibodies this effect became attenuated and the rabbits eventually developed ACE redistribution, complement fixation, and pulmonary edema. We conclude that chlorpromazine temporarily inhibits antigenic modulation in vivo, presumably through its action on calcium-mediated antibody-cell surface antigen interaction.

Animals↗
PubMed1994

Lymphocyte-activation gene 3/major histocompatibility complex class II interaction modulates the antigenic response of CD4+ T lymphocytes.

The activation requirements for antigen-dependent proliferation of CD4+ T cells are well documented, while the events leading to the inactivation phase are poorly understood. Here, we tested the hypothesis that the lymphocyte-activation gene 3 (LAG-3), a second major histocompatibility complex (MHC) class II ligand, plays a regulatory role in CD4+ T lymphocyte activation. CD4+ class II-restricted T cell clones were stimulated by their relevant antigen (hemagglutinin peptide or diphteria toxoid) and antigen-presenting cells with or without anti-LAG-3 monoclonal antibody (mAb). Kinetic studies were performed to monitor different activation parameters, including the measurement of thymidine incorporation, expression of activation antigens and cytokine secretion. Results showed that the time course from the initial time points up to the peak time point was not modified in the presence of anti-LAG-3 mAb. However, addition of these antibodies, either as whole IgG or as Fab fragments, led to increased thymidine incorporation values for late time points and, hence, to a shift in the decreasing proliferation curve. We also showed that expression of activation antigens, such as CD25, was higher in the presence of anti-LAG-3 mAb, and that cytokine concentrations, i.e. of interferon-gamma or interleukin-4, were higher in the corresponding culture supernatants. In addition, we tested whether the effects of anti-LAG-3 mAb were limited to antigen-dependent, MHC class II-restricted responses. The proliferative responses of CD4+ T cell clones following stimulation with either interleukin-2, mitogens, a combination of anti-CD2 mAb, immobilized anti-CD3 or anti-T cell receptor mAb were not altered by anti-LAG-3 mAb. The allogeneic proliferative response of a CD8+ T cell clone was also not affected. Overall, the present analysis reveals a modulating effect of anti-LAG-3 mAb, mediated specifically on antigen-dependent, MHC class II-restricted responses of CD4+ T cell lines. These results support the view that LAG-3/MHC class II interaction down-regulates antigen-dependent stimulation of CD4+ T lymphocytes.

Antigens, CD↗
PubMed1971

Immunoglobulin and other surface antigens of cells of the immune system.

Immunoglobulins (Ig) on cells of the immune system: The cytotoxicity test, with class-specific and type-specific anti-Ig sera, identifies kappa and micro determinants on mouse lymphocytes. The proportion of kappa(+) cells is characteristic for each source of cells: 30% of bone marrow cells, 40% of cells from peripheral lymph nodes, 45% of lymphocytes from peripheral blood or peritoneal cavity, and 50% of spleen cells. No Ig was demonstrable on thymocytes or on leukemia cells (most of which arise from thymus-derived [T] cells). Cytotoxicity tests were performed on various myelomas secreting different Ig; the only positive reactions were given by kappagamma1 myelomas (all four kappagamma1 myelomas tested were sensitive to both anti-kappa and anti-gamma1). Hemolytic plaque-forming cells (PFC) of IgG type had no demonstrable surface Ig, but a proportion of IgM PFC were kappa(+)micro(+). Virtually all rosette-forming cells (RFC) have surface Ig, more than 90% of them being inhibited by anti-kappa, 50% by anti-micro, and 10-30% by antisera to other heavy chains. Anti-lambda sera gave no positive reactions with any cell type, which is in keeping with the low level of this light chain in mouse serum. Ig and other differentiation antigens as markers for T and B cells: Thymocytes are hallmarked by the alloantigens TL, theta, and the Ly series, and it is generally held that extrathymic lymphoid cells that bear them are derived from thymocytes. There is one alloantigen marker for the thymus-independent (B) cell, and that is PC, which appears late in differentiation. (The mouse-specific lymphocyte (MSLA) and mouse-specific bone marrow-derived lymphocyte (MBLA) antigens recognized by heteroantisera, not used in the present study, are other candidates for T and B cell markers.) Making use of antisera to these surface antigens to inhibit the function of cells that carry them, we find the following: Approximately 30% of RFC, 60% of IgM PFC, and 90% of IgG are PC(+) and so are identified as B cells. No T markers were demonstrable on these cell populations. Thus if T cells do become RFC or PFC they presumably lose their T surface markers in the process (cf. the quantitative reduction of T markers accompanying the thymocyte --> lymphocyte transition). Cells that have the potential to initiate graft-versus-host (GVH) reactions have the T cell surface phenotype theta(+)Ig(-). Adoptive transfer of thymus-dependent antibody-forming capacity (response to sheep erythrocytes) required theta(+) cells but transfer of a thymus-independent immune response to Brucella antigen did not. Cells with surface Ig were involved in both types of adoptive transfers. Thus the presently available T markers do not provide evidence for T cells carrying surface Ig. Suppression of the Ig phenotype by antibody: antigenic modulation? A phenotypic change from Ig(+) to Ig(-) occurs when Ig(+) lymphocytes or myeloma cells are incubated with anti-Ig sera in vitro in the absence of complement (C). As with antigenic modulation in the TL system, which it resembles, this phenomenon is temperature dependent and in the case of lymph node cells (LNC) can be inhibited by high doses of actinomycin D.

Animals↗