摘要:

AbstractMice were orally immunized by 4 daily intragastric (IG) intubations of 4 × 109sheep red blood cells (SRBC). The serum of such mice (OS), taken two weeks after the first intubation, was compared to normal mouse serum for its suppressive effect onin vitroprimary responses of normal spleen cells to SRBC. OS regularly depressed thein vitroresponse to less than 10% of the normal response. The suppressive effect was dose‐ dependent, antigen‐specific and removable by absorption with SRBC. When cultures were stimulated with SRBC pre‐exposed to OS, the response was also depressed. The suppression was less when the addition of OS was delayed. OS from BALB/c mice efficiently depressedin vitroresponses of spleen cells from other strains. Spleen cells, taken 2 weeks after IG immunization, responded normally toin vitrochallenge with SRBC. The suppressive factor had the molecular size of an IgG and could be removed by anti‐Ig and anti‐IgG1but not by anti‐α or anti‐μ immunosorbents. Purified IgG1was more suppressive than IgG2aand IgG2bdespite a similar anti‐SRB

ISSN:0014-2980    

DOI:10.1002/eji.1830091002

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractThe requirement for histocompatibility in the T lymphocyte killing of virus‐infected cells has led us to investigate the effect of influenza virus infection on mouse cell surface histocompatibility (H‐2) antigens. Monoclonal anti‐H‐2 antibody made it possible to develop equilibrium binding conditions for the assay of H‐2 antigen‐antibody interactions on intact cells. Scatchard analysis of anti‐H‐2 binding with normal and virus‐infected cells yielded linear curves indicating homogeneity of the interaction at varied concentrations of antibody through saturating levels. The estimated number of 2 × 105‐ 5 × 105H‐2 antigenic sites per mouse lymphoblast does not appear to change during the course of influenza virus infection.However, the Ka(binding affinity constant) of anti‐H‐2 binding is rapidly elevated by virus infection (“0” time), continues to increase for 3 h post infection, then decreases. Control cells, treated with normal egg allantoic fluid, show no change in Kaduring similar incubation.This change in Karequires the presence of active viral neuraminidase. Thermal denaturation of the neuraminidase of the virus particles abolishes their ability to induce Kaalteration, even though hemagglutinin activity is retained. Treatment of cells with neuraminidase of bacterial origin led to an elevation of Ka, but did not mimic the viral effect in time dependence and magnitude of peak responses. The time‐dependent lowering of Kafrom peak values appeared to relate to virus replication, since UV light‐inactivated virus‐induced Kaelevation, but did not produce the typical Kadecline at 4‐5 h post infection.The changes in Kaof anti‐H‐2 binding during influenza infection reflects a virus‐ induced alteration of the H‐2 molecule or its environment in the host cell membrane. The molecular basis of this change and its relation to H‐2‐restricted recognition of influenza virus‐infec

ISSN:0014-2980    

DOI:10.1002/eji.1830091003

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractHuman mononuclear cells from peripheral blood which were treated with phospholipase C (PLC), became cytotoxic against human or chicken red blood cells. PLC‐ induced cellular cytotoxicity against human red blood cells was further analyzed and compared to anti‐D‐mediated, antibody‐dependent cellular cytotoxicity (ADCC), using the same target cells. ADCC, but not cytotoxicity of PLC‐treated effector cells, was inhibited by free IgG. In addition, iodoacetate strongly enhanced PLC‐induced cytotoxicity, but blocked ADCC completely. Addition of fetal calf serum or human AB serum impaired PLC‐induced cytotoxicity. A similar inhibition was found by adding lecithin liposomes suggesting that the inhibitory effect of sera was also due to their phospholipid content. The data show that cytotoxicity of PLC‐treated effector cells can be clearly distinguished from cellular cytotoxicity, occurring spontaneously or induced by target cell antibodies. We favor the notion that cytotoxicity of PLC‐ treated effector cells against human erythrocytes is due to the action of PLC, adsorbed to t

ISSN:0014-2980    

DOI:10.1002/eji.1830091004

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractDextran ligands, modified to increase epitope reactivity with receptors, were more effective in suppressing BALB/c mouse plasmacytomas MOPC 104 E and J‐558, which bind α(1 → 3) dextran and have an idiotype (Id) in common, than autoantibody (Ab) against the Id unique to each of the proteins secreted by the two tumors (the Idl). BALB/c immunized with 104 E myeloma protein and expressing an antibody response to the 104 E Idl exhibited a specific, anti‐104E Idl transplantation resistance to lethal grafts of 104E, but not J‐558, tumors notwithstanding the shared common Id and similar ability to bind a(1 → 3) dextran. This autoantibody did not prevent modulation of the 104 E tumor to variant forms or the growth of the variants. On challenge with a(1 → 3) dextran, the immunized mice expressing the anti‐104E Idl responses failed to express the 104E Idl‐like antibody clone present in the normal, anti‐α(1 → 3) dextran antibody repertoire. Passive, iso‐anti‐104E Idl antibody had a transitory suppressive effect on the normal, 104E Idl‐like antibody clone but failed to circumvent 104 E tumor growth. It is apparent that the greater effectiveness of ligands strongly reactive in a nonphysiological manner with the tumor receptors lies in the stabilization of the tumor load without inducing variant escape or a disturbance of the immune network, and that receptor expression and malignancy state are not necessa

ISSN:0014-2980    

DOI:10.1002/eji.1830091005

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractT lymphocyte hybrid lines have been produced by fusion of the thymoma BW 5147 with spleen cells of C57BL/10 mice primed to sheep red blood cells (SRBC). The supernatant (culture fluid) of a T hybrid designated A1 was able to suppress the primary (IgM) and secondary (IgM and IgG) antibody responses to SRBCin vitro.The suppressive activity of supernatants could be titrated to 50% end points at final dilutions of up to 1:270. The suppression affected only SRBC and haptens coupled to SRBC, except when used at high concentration when some nonspecific suppression was observed. Absorption of the A1 supernatant with SRBC removed all activity, while several other species of red cells failed to do so. The suppressor factor present in A1 supernatant was not removed by anti‐Ig adsorbents, but was removed by anti‐H‐2 antibodies reacting specifically with the haplotype of the spleen cells used in the fusion (H‐2b). The cellular target of action of the factor was apparently a B cell, based on absorption with different cell populations. No genetic restrictions in the activity of the factor were found. Al cells carried H‐2 and Thy‐1 alleles of both parental cells and formed rosette

ISSN:0014-2980    

DOI:10.1002/eji.1830091006

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractThe extent to which VHframework determinants are represented on T cell receptors is unresolved and controversial. We have studied this question in the rabbit using antia (VHframework) allotype antisera and a goat anti‐rabbit VHantiserum. Flow micro‐ fluorometric analysis of spleen lymphocytes from hyperimmune animals (Freund's adjuvant plus picryl chloride) demonstrated closely similar frequencies of cells stained with the anti‐VHframework antisera compared to anti‐light chain antisera. To search for potentially hidden molecules, additional studies were performed with radioiodinated, detergent‐solubilized plasma membranes derived from immune spleen and lymph node cells. The membranes were analyzed by standard immunoprecipitation techniques. Absorption with anti‐Ig constant region immunoabsorbents removed all radioactivity precipitable by specific anti‐VHframework antisera compared to controls, whereas after absorption with control (normal goat globulin) immunosorbents, VH‐bearing surface IgM and putative surface IgD (presumably of B cell origin) were readily demonstrated by immunoprecipitation. Thus, no evidence for a population of cells or a class of molecule(s) bearing VHin the absence of light or heavy chain constant region determinants was obtained. Although these studies do not support the concept of similar VHframework determinants on T and B cell receptors, they do not exclude a much more limited sharing of determinants or a very minor T cell subpopulation which expresses VHframework that would not be detectable by the methods used i

ISSN:0014-2980    

DOI:10.1002/eji.1830091007

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractMice infected with an aerosol of influenza virus or immunized with purified UV‐ inactivated whole virus or viral subunits developed delayed‐type hypersensitivity (DTH) to influenza virus. The level of DTH was greatly enhanced when mice were injected intraperitoneally 2 days prior to immunization with 200 mg/kg of cyclophosphamide. The reaction peaked at 24 h after elicitation, had the classical DTH histology, and was transferable by immune cells but not by immune serum. DTH induced in cyclophosphamide‐pretreated mice persisted for at least 40 days after sensitization. DTH induced by deoxycholate‐treated subviral particles (DC particles) or the matrix protein of the influenza virus was type‐specific,i.e.DTH induced by DC particles or matrix protein of type A virus cross‐reacted only with type A virus and not with type B virus. DTH induced by purified hemagglutinin (HA) subunits, on the other hand, showed subtype specificty. Thus, DTH induced by HA of X 31 virus (H3) did not cross‐react with PR 8 virus (H 0). However, DTH induced by HA of one subtype cross‐reacted significantly with the variants of the same subtype. Thus, it appears that the effector T cells of DTH do not discriminate between the antigenic variants of influenza virus that are distinguishable by serology. DTH induced by purified, UV‐ inactivated whole virus showed extensive cross‐reactivity. This nonspecific reaction was shown to be due to host‐derived material, the lipid bilayer. ‐ The theoretical and practical implications of these

ISSN:0014-2980    

DOI:10.1002/eji.1830091008

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractMonkey erythrocyte (Mk) rosette formation is described as an exquisitely sensitive method for the detection of complement (C) components on the membrane of human leukocytes. Blocking of the immune adherence receptor on Mk blocked subsequent rosette formation as did pretreatment of leukocytes with antiserum to the C components C3 and C4.In vitroC deposition by immune complex formation with normal human lymphocytes enhanced Mk rosette formation, and this could be inhibited with antiserum to C3. The use of Mk rosette formation revealed that cells from a wide variety of human lymphoid and myeloid leukemias carry membrane‐bound C. It was also shown that several lymphoblastoid cell lines, including a T cell line, probably synthesize both C3 and C4. Mk rosette formation is not dependent on metabolic activity of the resetting leukocyte, and it is suggested that this technique will be of value in detecting C deposition in a variety of situation

ISSN:0014-2980    

DOI:10.1002/eji.1830091009

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractA rosette assay for the identification of cells with receptors for C 1q is described. Glutaraldehyde‐treated bovine erythrocytes bound C 1q specifically, and the reagent thus prepared provided a valid indicator for rosette formation mediated by C 1 q receptors. The presence of these receptors on the membrane of a subset of human peripheral lymphocytes (mainly non‐T cells) and on B‐derived lymphoblastoid cells was confirmed. Rosette formation was dependent on the number of C 1 q molecules bound per indicator cell and was specifically inhibited by soluble native C 1 q and pepsin‐resistant C 1 q fragments. These data, together with the reduced binding activity of C 1r‐C 1s‐associated C 1q, indicated that the C 1 q binding sites for lymphoid membranes are expressed on the collagen‐like moiety, C 1q rosette formation provided a simple new procedure for fractionation of human lymphocyte populations and separation from phagocytes that do not express recept

ISSN:0014-2980    

DOI:10.1002/eji.1830091010

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY

摘要:

AbstractIn this report, a model of xenogeneic education is described, whereby cytotoxic mouse spleen cells are generated against human target cell antigens. To generate a significant response, a primaryin vivoimmunization followed by anin vitroboosting 4 to 8 weeks later is required.Lysis is totally abrogated after treatment of the effector cells by anti‐Thy‐1.2 antiserum plus complement confirming the T origin of these effectors. Such cytotoxic T lymphocytes (CTL) do not discriminate between two lymphoblastoid cell lines carrying different HLA‐A and HLA‐B specificities, either by direct assay or by competition assay with unlabeled target cells. Moreover, Daudi cells which lack the serologically defined (SD) HLA antigens, are susceptible to CTL specifically raised against Daudi. However, CTL raised against another B line do not lyse Daudi, and, reciprocally, anti‐Daudi CTL do not lyse other B lines thus suggesting a polymorphic distribution of xenogeneic determinants on human lymphoid lines. A third specificity is revealed when mouse spleen cells are educated against human T lines. The CTL generated under these conditions lyse not only the line used for sensitization but the three other human T lines of the panel. On the other hand, they affect none of the B cell lines (including Daudi) nor phytohemagglutinin or concanavalin A‐induced T blasts. In conclusion, the mouse T cell repertoire is capable of recognizing a polymorphic system of antigens expressed on human lymphoblastoid cell lines that is not related to the expression of HLA‐SD antigens nor to that of the Epstein‐Ba

ISSN:0014-2980    

DOI:10.1002/eji.1830091011

出版商:WILEY‐VCH Verlag GmbH    

年代:1979

数据来源: WILEY