摘要:

AbstractMonoclonal anti‐Thy‐1.1 and anti‐Thy‐1.2 antisera selected for complement‐dependent cytotoxicity have high cytotoxic and binding titers on thymocytes and peripheral T cells of mouse strains bearing the appropriate Thy‐1 allele. The effect of both anti‐Thy‐1.1 and anti‐Thy‐1.2 monoclonal antisera plus complement on cytotoxic T cell effectors is to abrogate their activity. On the functional activity of precursor cytotoxic T cells, monoclonal antisera against the two alleles have different effects: anti‐Thy‐1.2 plus complement removes precursor activity of Thy‐1.2‐bearing strains, including (Thy‐1.1 × Thy‐1.2)F1heterozygotes. In contrast, six different anti‐Thy‐1.1 monoclonals, including four of the IgM class and two of the IgG class, failed to remove cytotoxic precursor activity from the splenic T cells of AKR, A. Thy‐1.1 or (CBA × AKR)F1mice. Analysis by fluorescence‐activated cell sorting ofin vitrocultured AKR spleen cells shows that Thy‐1.1 antigen appears on the cell

ISSN:0014-2980    

DOI:10.1002/eji.1830110402

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractA rat anti‐mouse monoclonal antibody, DNL 1.9, has been produced and shown to bind to all cells of the B lineage in mice. By quantitative immunofluorescence, DNL 1.9 binds to approximately 50% of spleen cells, 20–30% of lymph node cells, but not to thymocytes. In bone marrow and neonatal liver, 70–80% of the small cells and 10–20% of the large cells were identified by this antibody. Two‐color immunofluorescence studies showed that all immunoglobulin‐positive cells were also DNL 1.9‐positive, while Thy‐1.2‐positive cells did not bind the monoclonal antibody. All pre‐B cells in bone marrow, as identified by cytoplasmic IgM staining, were labeled by the DNL 1.9 antibody. A significant proportion of lymphocytes in the bone marrow which did not express cell surface immunoglobulin did bind DNL 1.9. Both direct and indirect plaque‐forming cells were also shown to bind DNL 1.9 antibody. The antigen recognized by this monoclonal antibody was not immunoglobulin nor was the antigen present in normal mouse serum. All seven mouse strains tested showed similar patterns of antigen expression. These results show that all of the cells identifiable as being of the B lineage were identified by this monoclonal antibody. It is possible that the cells which bind DNL 1.9 but do not express cell surface immunoglobulin may be very early precur

ISSN:0014-2980    

DOI:10.1002/eji.1830110403

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractVirgin mouse spleen cells culturedin vitrowithout antigen or mitogen produce a measurable amount of IgM bindingE. coliβ‐galactosidase (β‐gal). Lipopolysaccharide (LPS) and LPS plus antigen enhance this response, which cannot be considered truly polyclonal since it does not include the production of antibodies directed towards a conformation‐dependent determinant, responsible for the activation of a mutant β‐gal, and known otherwise to be highly immunogenic. By primingin vivowith alum‐treated β‐gal (unable to elicit activating antibodies), an activating response is obtainedin vitroby LPS plus antigen, but not by LPS alone.These results are compatible with a two‐signal requirement for the activation of B cells and may be explained as follows: (a) the mitogen, in absence of immunogen, stimulates those clones which have a specific signal from cross‐reacting structures in the environment; (b) instead, no cross‐reactions are available for the conformation‐controlled structure of the „activating”︁ determinant; thus, intact immunogen is required as well as mitogen. Because of this „uniqueness”︁, the molecule of β‐gal offers a highly specific tool to probe carrier

ISSN:0014-2980    

DOI:10.1002/eji.1830110404

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractCurrent concepts of activation of the alternative pathway of complement (APC) focus on the central role of an amplification mechanism triggered by C3b which is covalently bound to the surface of activating substances. Using sulfated polyanions as model substances, an efficient fluid‐phase activation of complement is demonstrated in contrast to solid‐phase activation.It is shown that particulate high‐molecular weight sulfated polyanions are capable of reversibly binding the guinea pig and human regulatory protein β1H. This fixation leads to an extensive activation of C3 and factor B because the regulatory function of β1H is blocked in the fluid‐phase C3b‐dependent amplification system of the APC. Addition of β1H to β1H‐depleted C4‐deficient guinea pig serum reconstitutes the physiological control mechanisms of the APC. Guinea pig β1H, purified to homogeneity, is described as a 160000 dalton protein of a single‐chain structure. In addition, highly specific and sensitive test systems f

ISSN:0014-2980    

DOI:10.1002/eji.1830110405

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractInjection of heterozygous (M‐13/M‐1b, G‐1g/G‐1i) B 14‐line chickens with antisera directed against either IgM‐1a or IgM‐1b induced suppression of the relevant IgM‐1 and genetically linked IgG‐1 allotypes, whereas a mixture of anti‐M‐1a and anti‐M‐1b antibodies failed to produce allotype suppression. Injection of anti‐M‐1 antiserum into M‐1 homozygous chickens induced only a transient delay of a few days in the appearance and rise of serum IgM‐1 levels. However, suppression of host allotypes was induced by injecting M‐1, G‐1 homozygous neonatal or embryonal recipients with anti‐M‐1 antisera together with B locus‐histocompatible allotype‐disparate spleen, bone marrow or bursal cells. The active cell type were donor B cells, which established chimerism in the injected hosts, whereas peripheral blood T lymphocytes from agammaglobulinemic donors were ineffective. Allotype suppression was attributed to a homeostatic control mechanism which is exerted by normal B cells (but not T cells) over B cell recruitment

ISSN:0014-2980    

DOI:10.1002/eji.1830110406

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractInjection of M‐1 (Cμ), G‐1 (CμgM) heterozygous chickens on the day of hatch with anti‐IgM‐1 antiserum induced allotype suppression from which chickens recovered over a period of approximately 4 months. The suppression of the serum IgM‐1 levels was matched by a decrease in the number of splenic and peripheral blood B cells bearing the relevant IgM‐1 allotype, and a compensatory increase in the number of cells bearing the alternative nonsuppressed IgM‐1 allotype. However, the proportion of IgM‐1‐bearing bursal cells was only marginally altered. The recovery from suppression was due to B cell recruitment and could be abrogated by bursectomy. Allotype suppression inducedin ovoor maintained by repeated injections of anti‐IgM‐1 anti‐serum resulted in chronic suppression and depletion of the relevant peripheral as well as bursal IgM‐1‐bearing cells. Antibody titers of the relevant allotype in partially suppressed chickens generally correlated with serum allotype levels without clonal restriction in antibody respon

ISSN:0014-2980    

DOI:10.1002/eji.1830110407

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractEmbryonally induced allotype suppression in M‐1, G‐1 heterozygous chickens was stable for at least 18 months after hatching. Suppression was established rapidly since injection of antigen only 4 days after anti‐IgM‐1 antiserum failed to abrogate its effect. Injected chickens had undetectable serum levels (i.e.less than 40 μg/ml) of the suppressed IgM‐1 and low (0.3–0.6 mg/ml) levels of the linked IgG‐1 allotype. This correlated with a complete depletion of cells bearing the relevant IgM‐1 allotype and a compensatory increase in the alternative nonsuppressed IgM‐1 allotype‐bearing cells in the spleen, peripheral blood and bursa. Cell transfer studies suggested that suppression could not be attributed to allotype‐spe

ISSN:0014-2980    

DOI:10.1002/eji.1830110408

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractGenetic control has been studied of the response to the encephalitogenic nonapeptide (NP) determinant of myelin basic protein (BP) in inbred guinea pigs of strains resistant or susceptible to induction of experimental autoimmune encephalomyelitis (EAE). By studying bone marrow‐reconstituted animals, we found that susceptibility to induction of EAE was a function of the genotype of the cells of the lymphohematopoietic system and not of the physiological environment or target organ. Analysis of the T cell response showed that susceptible strain 13 or (2 × 13)F1hybrid guinea pigs recognized the NP determinant when injected with whole BP in adjuvant. Resistant strain 2 guinea pigs responded to undefined determinants on BP, but not to the NP moiety. We investigated the cells involved in regulating the response to the NP determinant by injecting susceptible F1hybrids with BP‐pulsed macrophages of either parental strain. Susceptible strain 13 macrophages triggered a response to the NP determinant and induced clinical EAE. In contrast, F1animals injected with resistant strain 2 macrophages failed to respond to the NP determinant, although the macrophages were capable of presenting other undefined determinants present on whole BP. Therefore, genetic control of the immune response to the NP determinant appears to be exerted at the level of antigen presentation by macrophages to T lymphoc

ISSN:0014-2980    

DOI:10.1002/eji.1830110409

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractThe rat basophilic leukemia (RBL) cell lines were cloned and the various sublines compared for their chromosome number, IgE‐mediated histamine release and for IgE surface receptors. It was found that cell lines started from tumors at different times vary in both their chromosome number and their ability to release histamine by an IgE‐mediated reaction. RBL‐I and III have ∼ 44 chromosomes and did not respond to an IgE‐mediated reaction, whereas RBL‐II and RBL‐IV have 68–73 chromosomes and showed moderate levels of histamine release (percent release x̄ = 5 ± 2 and 10 ± 4, respectively). The cloning of the RBL‐IV line resulted in some sublines which were excellent histamine releasers (range 39–100%) and some which were relatively refractory (<10%) to IgE‐mediated histamine release. These clones did not differ significantly in chromosome number. Recloning the releasing lines gave rise to poor releasers, whereas the recloning of poor releasers did not produce good releasers indicating that the mutational drift in culture is toward loss of histamine‐releasing capacity. The number of IgE receptors and the rate of IgE association and dissociation were similar for the different cell lines. The study failed to disclose significant molecular weight differences in the IgE receptor from the various clones and sublines indicating that the failure to release probably does not reside in the receptor. The various cloned sublines are phenotypically stable, and the isolation of excellent histamine‐releasing sublines are useful for studies of the complex phe

ISSN:0014-2980    

DOI:10.1002/eji.1830110410

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY

摘要:

AbstractThe control of the immunogenic antigen‐presenting capacity of different subpopulations of thioglycollate‐induced peritoneal macrophages has been investigated. The experiments revealed the existence of two major subpopulations of macrophages, only one of which was highly efficient in educating antigen‐specific T cells. The other subpopulation, while highly phagocytic, was devoid of antigen‐presenting capacity. Further analysis, using specific antisera directed at H‐2I region gene products, revealed that the immunogenic antigen‐presenting population expressed H‐2I region‐controlled membrane antigens. Searching for cellular elements which control the differentiation of this antigen‐presenting macrophage subpopulation, it was found that its function was strictly controlled by T cells. T cell‐deficient mice (nu/nu) failed to generate a functional antigen‐presenting macrophage subpopulation. Transplantation of mature T lymphocytes to T cell‐deprived mice restored the immunogenic function of their antigen‐presenting macrophages. The results obtained suggest the existence of heterogeneity of functions among macrophage subpopulations and add a new regula

ISSN:0014-2980    

DOI:10.1002/eji.1830110411

出版商:WILEY‐VCH Verlag GmbH    

年代:1981

数据来源: WILEY