摘要:

AbstractA limiting dilution assay was used to compare the frequency of cytotoxic T lymphocyte precursors (CTL‐P) which respond to H‐2 antigens presented with additional background differences, with the frequency of CTL‐P which respond to H‐2 antigens on a self background. Individual cultures were divided and assayed for cytotoxic activity on the two targets sharing H‐2, but not the background; no cultures were seen which clearly killed one and not the other, and the same frequency of CTL‐P was measured on target cells that differed from the responder only at H‐2 and on target cells that differed also in the background, irrespective of the background of the stimulator. Thus, the assumption that allospecific cytotoxic T lymphocytes (CTL) recognize H‐2 plus minor histocompatibility antigens does not serve as an adequate explanation for the high frequency of allospecific CTL. The data also suggest that the two allelic forms of β2‐microglobulin do not contribute to the alloant

ISSN:0014-2980    

DOI:10.1002/eji.1830120202

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractThe metabolism of albumin and IgA was studied in normal and lactating mice. Lactation resulted in significant changes in the metabolism of these proteins. The serum albumin concentration was lowered from 47 mg/ml in normals to 24 mg/ml in lactating mice. However, only a slight decrease in the serum concentration of IgA was observed during lactation. The proportion of polymeric and monomeric IgA in serum and milk was evaluated by gel exclusion chromatography. The onset of lactation led to a rise in the proportion of polymeric IgA (P‐IgA) in serum from 37% to 51%. The proportion of P‐IgA in milk was 65% and remained constant throughout lactation. P‐IgA and albumin were shown to be efficiently transferred from the serum of lactating mice into their milk. Serum decay studies were performed to evaluate the turnover of the serum pools during lactation. The rates of disappearance from the serum of isotopically labeled albumin and P‐IgA were observed to increase dramatically during lactation, suggesting that both of these two milk proteins might be derived at least in part from the serum. The sites of synthesis of milk IgA (localvs. extra‐mammary gland) were evaluated by determining the extent of dilution of isotopically labeled serum IgA during transport through the mammary gland into the milk. Early in lactation, the majority of the IgA in mouse milk appeared to be derived from distant sites and transferred via the blood to the mammary gland. However, by day 8 of lactation, the isotopically labeled P‐IgA in milk was significantly.diluted by the IgA synthesized in the mammary gland. Albumin and IgG were not diluted by local synthesis indicating that these proteins were exclusively se

ISSN:0014-2980    

DOI:10.1002/eji.1830120203

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractThe expression and functional significance of idiotypic determinants on antigen‐specific helper T (Th) cell populations for responses to Staphylococcal nuclease (Nase) were evaluated in anin vitroantibody response system. Trinitrophenyl (TNP)‐specific plaque‐forming cell responses to TNP‐conjugates of Nase (TNP‐Nase) were shown to require the cooperation of Nase‐primed Thcells as well as unprimed B and accessory cells. The expression on these antigen‐primed Thcells of idiotypic determinants cross‐reactive with those on anti‐Nase antibodies was demonstrated by the specific elimination of Thcells for TNP‐Nase by treatment with affinity‐purified anti‐idiotypic antibodies plus complement. The susceptibility of Nase‐primed Thcells to elimination by such treatment was specific in that anti‐idiotypic antibodies affected Thcells only from strains normally expressing the same (or a cross‐reactive) idiotype on anti‐Nase antibodies. A functional role of the idiotypes expressed on Nase‐primed Thcells was suggested by the fact that anti‐idiotypic antibody present throughout the period of culture, in the absence of complement, suppressed responses to TNP‐Nase in an antigen‐ and strain‐specific manner. It was further shown, by cell mixing experiments, that this inhibition appeared to occur at the level of the Thcells and was not dependent on the strain of origin of the B cells. Thus, antigen‐specific Nase‐primed Thcells express strain‐specific idiotypic determinants cross‐reactive with, or identical to, those of anti‐Nase antibodies. These cell surface idiotypic determinants appear to be functionally involved in the activity of Thcells for the

ISSN:0014-2980    

DOI:10.1002/eji.1830120204

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractThe primary antibody response in BALB/c mice to the T‐independent bacterial antigen dextran B1355S [α(l → 3)dextran] (Dex) was studied by means of isoelectric focusing, hemagglutination and immunodiffusion techniques. In response to a single immunization with 10 kg Dex all mice produce specific IgM antibodies. In addition, about 30% of conventionally raised BALB/c and BALB/c nu/+ mice, but 95% of germ‐free (GF)‐raised normal BALB/c and 100% of athymic BALB/c nu/nu mice produce specific IgG class anti‐Dex antibodies. These antibodies include all IgG subclasses, carry predominantly the λ light chain and the cross‐reactive J558 idiotype and are specific for the α(1 → 3)glucosidic linkage.As compared to athymic and GF‐raised mice, conventionally raised mice exhibit only a weak IgG response. The pronounced IgG production of GF‐raised mice was not altered when adult mice were removed from their GF environment and housed under conventional conditions for several weeks prior to immunization with Dex. Reconstitution with isolated splenic T cells from conventionally raised, unprimed BALB/c mice reduces the remarkable capacity of BALB/c nu/nu mice to produce IgG anti‐Dex antibodies.These findings suggest that the reduced capacity of conventionally raised BALB/c mice to mount an IgG response to the T‐independent antigen Dex is due to a T cell‐mediated suppressive mechanism which is neonatally induced by contact with environmenta

ISSN:0014-2980    

DOI:10.1002/eji.1830120205

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractThe infection of selected lymphocytes from a rheumatoid arthritis patient with Epstein‐Barr virus resulted in an immortalized cell line that secretes a monoclonal rheumatoid factor (RF). The cloned line has been growing for more than 24 months, and constantly produces a monoclonal IgM, λ, 19 S, RF (1‐2 μg/ml/l06cells).The RF agglutinates human and rabbit IgG (but not IgM) and also protein A‐coated erythrocytes, but fails to do so to mouse, goat and swine IgG‐coated erythrocytes. When bound to immune complexes, this monoclonal RF does not bind complement. In the cell supernatant RF is the only immunoglobulin and it comprises approximately 5% of the total proteins. The affinity of RF to aggregated human IgG, as detected in inhibition experiments, is higher than that of Fe receptors found on human non‐T lymphocytes, K562 and Daudi

ISSN:0014-2980    

DOI:10.1002/eji.1830120206

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractFour rat anti‐mouse macrophage monoclonal antibodies are described. Three of them are highly specific for macrophages, and one cross‐reacts with granulocytes. All 4 antibodies do not react with membrane antigens shared by all macrophages, but with antigens present only on subpopulations of 20‐50% of the cells. All antibodies are directly or indirectly cytotoxic for macrophages. The subpopulations defined by these antibodies can be correlated with certain macrophage functions. Thus, antibody M43 eliminates macrophages that are activated by lymphokine to cytotoxicity. Antibodies M43 and M57 eliminate macrophages that kill antibody‐coated tumor targets, and clone 102 (strictly macrophage‐specific) eliminates natural killer cells. Only M143, reacting with 10‐30% of macrophages, has not yet been correlated with any function. With the use of these antibodies, cells of the macrophage lineage with specific functions can be recognized and eliminated from a given

ISSN:0014-2980    

DOI:10.1002/eji.1830120207

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractMacrophages (Mϕ) isolated from the peritoneal cavity of C57BL/6 mice were either untreated or treated with various eliciting agents (thioglycollate, sodium caseinate) or with an activating agent bacillus Calmette Guérin (BCG). The various populations were assessed for their ability to release platelet‐activating factor (PAF‐acether), an ether phospholipid mediator, and slow‐reacting substance (SRS), a lipoxygenase arachidonic acid derivative. PAF‐acether was recovered in higher amounts from BCG Mϕ, than from resident Mϕ, whereas elicited Mϕ, exhibited a marked decreased ability to release this mediator. Such variations were only quantitative as evidenced by the similar enzyme sensitivity and high pressure liquid chromatography (HPLC) retention times of the various PAF‐acether‐containing supernatants. Resident, BCG‐and sodium caseinate‐induced Mϕ released similar amounts of SRS, whereas thioglycollate Mϕ, exhibited once again a marked decreased ability to release this mediator. Comparing retention times on HPLC of resident and BCG Mϕ, SRS with those of synthetic leukotrienes C and D, molecular variations were noted. Even though both Mϕ, populations released higher amounts of leukotrienes C than D, the DIC ratio was higher in BCG Mϕ, than in resident Mϕ,. These results show that different environmental factors can influence the release of PAF‐acet

ISSN:0014-2980    

DOI:10.1002/eji.1830120208

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractAnti‐idiotypic antibodies (a‐Id) were produced in syngeneic mice against two monoclonal IgM antibodies of BALB/c origin, TNP.11 and SP/603. In plaque inhibition tests, using IgM‐secreting hybridoma cells and anti‐idiotypic antibodies, these two IgM proteins, as well as the anti‐TNP myeloma protein MOPC 460 (IgA) were found to carry non‐cross‐reactive idiotypes.Analysis of the anti‐trinitrophenyl (TNP) plaque‐forming cells (PFC) in BALB/c mice, either normal or immunized with TNP‐horse red blood cells, revealed that in addition to the MOPC 460 Id, also the SP/603 Id is recurrent and expressed by a fraction of the anti‐TNP antibody‐secreting cells in all individuals tested. In contrast, the TNP.11 Id could not be detected in any BALB/c mouse studied.TNP.11 and SP/603 antibodies were then characterized by their ability to induce an antigen‐independent anti‐TNP response in normal BALB/c mice. While TNP.11 was found to be inactive, the same titers of SP/603 IgM induced antigen‐specific PFC all of which expressed the SPi603 Id, and increased titers of circulating IgM molecules carrying the same Id, suggesting that “recurrent” but not “nonrecurrent” Id are competent in this respect. A fraction of these SP/603‐induced, SP/603‐positive anti‐TNP antibodies also carried MOPC 460 Id, suggesting expression on the same molecule of idiotypic determinants found on independe

ISSN:0014-2980    

DOI:10.1002/eji.1830120209

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractThis is the first report describing the experimental induction of a full‐blown clinical syndrome strongly resembling systemic lupus erythematosus (SLE). The method used was the induction of a chronic graft‐vs.‐host reaction (GVHR) employing genetically nonautoimmune strains of mice. Many of the F1mice undergoing a GVHR (GVH F1mice) revealed the following pathological alterations: splenomegaly, periarteritis, immunecomplex glomerulonephritis accompanied by elevated proteinuria and ascites, dysgammaglobulinemia, persistently increased production of IgG in the spleen, and formation of autoantibodies to thymocytes, erythrocytes, nuclear antigens, double‐stranded DNA, and antibodies deposited along the basement membrane of skin.In spite of the excessive T cell help, the GVH F1animals failed to produce spontaneous serum antibodies to dextran and the bacteriophage fd. They also had no increased numbers of spontaneous indirect plaque‐forming cells to sheep red blood cells and trinitrophenyl. These negative findings indicate that antigen has to be present during the GVHR to trigger antibody formation. This in turn suggests that the persistent presence of self‐antigens was essential for the formation of IgG autoantibodies in GVH F1mice. However, whereas autoantibodies typical of SLE were readily produced, none of the GVH F1mice had autoantibodies to thyroglobulin, or other autoantibodies not typical of SLE.Conceivably, not only the presence of self‐antigens, but also their antigenic configuration, may determine whether or not autoreactive B cells are successfully triggered during abnormal T‐B cell cooperation. Given the lack of carrier‐specific T helper cells in abnormal T‐B cell cooperation, protein self‐antigens, such as thyroglobulin, may be intrinsically less apt than the self‐antigens involved in SLE to bind to the corresponding autoreactive B cells. The self‐antigens involved in SLE, such as DNA and cell‐surface epitopes, are assumed to be capable of multipoint high‐avidity binding to and cross‐linking of the Ig receptors of these B cells, thus

ISSN:0014-2980    

DOI:10.1002/eji.1830120210

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY

摘要:

AbstractTladmice have a distinct Qed‐1 allele, Qed‐1d. Its product is detected by cytotoxic T cells raised in C57BW6 (H‐2b, Tlab) mice against cells from a new recombinant, B6‐TL.123+(H‐2b, Tlad/b). Qed‐1dis also found on cells from B10.M, A.CA and B10.STC90 mice. It cross‐reacts weakly with Qed‐1b. (C57BL/6 X BALB/c) F1anti‐B10. A (SR) effectors discriminate Qed‐1aand Qed‐1d, while C3H/HeJ anti‐B10. BR effectors cross‐react extensively. CB6F1anti‐5R effector cells also discriminate between the Qed‐1 antigens of B6‐Tlaa(H‐2b, Tlaa) and those of B1

ISSN:0014-2980    

DOI:10.1002/eji.1830120211

出版商:WILEY‐VCH Verlag GmbH    

年代:1982

数据来源: WILEY