scholarly journals B-lymphocyte heterogeneity: development and characterization of an alloantiserum which distinguishes B-lymphocyte differentiation alloantigens.

1977 ◽  
Vol 145 (1) ◽  
pp. 101-110 ◽  
Author(s):  
A Ahmed ◽  
I Scher ◽  
S O Sharrow ◽  
A H Smith ◽  
W E Paul ◽  
...  

CBA/N mice and F1 male mice, which are hemizygous for the CBA/N X chromosome, have an immune defect which is associated with the absence (deficiency) of a subpopulation of mature or late developing B lymphocytes. This characteristic was utilized to develop an antiserum that was specific for this subclass of B cells. C57BL/L mice were immunized with DBA/2 spleen calls, and the resulting antisera was absorbed with lymphoid cells derived from immunologically abnormal (CBA/N female X DBA/2 male)F1 male mice. The absorbed antisera was cytotoxic for a subpopulation of lymphocytes that was present in the spleens of adult DBA/2 and (CBA/N female X DBA/2 male)F1 female mice. The cells killed by the absorbed antisera were Ig-bearing, complement receptor-bearing B lymphocytes, which had a low-to-intermediate density of total surface Ig. Moreover, the cells remaining after treatment of adult (CBA/N female X DBA/2 male)F1 female spleen cells with the absorbed antisera and C had a high ratio of surface IgM to IgD. The development of this cytotoxic alloantisera, which is specific for a late developing (mature) subpopulation of B lymphocytes, will allow the functional characterization of subclasses of B lymphocytes.

1975 ◽  
Vol 141 (4) ◽  
pp. 788-803 ◽  
Author(s):  
I Scher ◽  
A Ahmed ◽  
D M Strong ◽  
A D Steinberg ◽  
W E Paul

A study of the composition and functional properties of spleen cells from the immune deficient CBA/HN mice and their F1 progeny is reported. While abnormalities were seen in both the numbers and function of thymus-independent (B) lymphocytes, all studies involving thymus-dependent (T) lymphocytes were normal. The X-linked nature of the immune defect in these mice was therefore attributed to abnormal or absent B lymphocytes. The possible nature of this defect and the similarity of the immune defect in these mice to certain human X-linked immunodeficiency diseases are discussed.


1976 ◽  
Vol 144 (2) ◽  
pp. 494-506 ◽  
Author(s):  
I Scher ◽  
S O Sharrow ◽  
R Wistar ◽  
R Asofsky ◽  
W E Paul

The density of total Ig and of IgM, IgG1, IgG2, and IgA on the surface of adult murine splenic B lymphocytes was measured using the technique of rapid flow microfluorometry. In addition, the density of total surface Ig and of IgM on B lymphocytes derived from adult bone marrow, lymph nodes, and Peyer's patches, and from neonatal spleen was determined. Adult spleen and lymph node B lymphocytes are characterized by the presence of a large population of cells with a low-to-intermediate density of total surface Ig, which is seen as a peak in the fluorescence profiles when these cells are labeled with fluorescein-conjugated (F1) anti-Ig. This peak is not detected when neonatal spleen or adult bone marrow are examined; the development of this peak among spleen cells occurs during the first 4 wk of life. Although the characteristic fluorescence intensity peak is not seen when adult spleen cells are labeled with Fl anti-mu, changes in the density of surface IgM do occur during the first few weeks of life and are detected as a decrease in the frequency of cells which have relatively large amounts of surface IgM. The differences seen in the fluorescence patterns of adult spleen cells labeled with Fl anti-Ig and Fl anti-mu may be due to the appearance of IgD on the surface of mature splenic B lymphocytes. This is supported by the similarity of the fluorescence profiles of adult bone marrow cells stained with Fl anti-Ig and Fl anti-mu, as the latter population of cells is reported to lack surface IgD.


1989 ◽  
Vol 169 (5) ◽  
pp. 1693-1701 ◽  
Author(s):  
A G Rolink ◽  
F Melchers ◽  
R Palacios

The rat mAbs R52.120 and R52.625 inhibit the action of IL-5 on both IL-5-sensitive cell lines and freshly isolated splenic B lymphocytes. Neither antibody inhibits the proliferative cell responses promoted by IL-2, IL-3, or IL-4. Purified R52.120+ lymphoid spleen cells contain 15-20-fold higher numbers of B lymphocytes responding to IL-5 in the form of maturation into antibody-producing cells. By immunofluorescence staining and flow fluorocytometry, the R52.120 and R52.625 antibodies bound to all 12 IL-5-sensitive cell lines tested. Both antibodies react with 2-4% cells in the spleen, 5% lymphoid cells, and 10-15% myeloid cells in the bone marrow, and 10-14% in the peritoneum of C57BL/6, DBA/2, and BALB/c adult mice. No positive cells for either antibody were detected in the thymus and lymph nodes of these mice. Both R52.120 and R52.625 antibodies specifically inhibit the binding of radiolabeled IL-5 to its receptor. Finally, R52.120 and R52.625 antibodies precipitate from 35S-methionine-labeled IL-5-R+ cell lysates three proteins with Mr 46,000, 130,000, and 140,000. Taken together from these results, we conclude that the R52.120 and R52.625 mAbs recognize epitopes on the IL-5-R complex very close or identical to the IL-5 binding sites.


1999 ◽  
Vol 96 (17) ◽  
pp. 9797-9802 ◽  
Author(s):  
S. K. Cho ◽  
T. D. Webber ◽  
J. R. Carlyle ◽  
T. Nakano ◽  
S. M. Lewis ◽  
...  

1976 ◽  
Vol 144 (2) ◽  
pp. 507-518 ◽  
Author(s):  
I Scher ◽  
S O Sharrow ◽  
W E Paul

CBA/N mice have an X-linked defect in B-lymphocyte function characterized by a failure to respond to certain thymus-independent antigens. When studied by rapid flow microfluorometry, adult CBA/N splenic B lymphocytes labeled with either fluorescein-conjugated (Fl) anti-Ig or Fl anti-mu had fluorescence profiles which were considerably different from those of B lymphocytes derived from normal mice. By studying progeny of crosses of CBA/N and normal mice, it was shown that the abnormal fluorescence profiles of CBA/N B cells were determined by an X-linked gene. The fluorescence profile of adult CBA/N splenic B lymphocytes labeled with anti-mu were very similar to the patterns of neonatal normal and of neonatal CBA/N splenic B lymphocytes suggesting that the defect of CBA/N mice is due to a failure in the development of a mature B-lymphocyte population. The fluorescence profiles of adult CBA/N splenic B lymphocytes labeled with Fl anti-Ig also had immature characteristics in that the frequency of cells with large amounts of surface immunoglobulin was increased in comparison to that of normal strains and the population of cells with low-to-intermediate density of total surface immunoglobulin, which appear characteristic of normal adult splenic B lymphocytes, was markedly diminished.


1975 ◽  
Vol 142 (3) ◽  
pp. 637-650 ◽  
Author(s):  
I Scher ◽  
A D Steinberg ◽  
A K Berning ◽  
W E Paul

The mechanisms underlying the X-linked thymus-independent (B) lymphocyte functional defect in the CBA/N (CN) mice and their F1 progeny were studied. Immune defective mice were unable to respond to the T-independent antigen 2,4-dinitrophenyl-lysyl-derivative of Ficoll (DNP-lys-Ficoll) but were able to form antibody against the highly cross-reactive hapten (trinitrophenyl) when it was coupled to an erythrocyte carrier. Immune defective CN X DBA/2N (DN) F1 male mice, which do not normally respond to T-independent antigens, were able to respond to both polyribosinic-polyribocytidylic acid and DNP-lys-Ficoll after the administration of CN X DN F1 female spleen cells even if these cells had been depleted of T lymphocytes. In addition, it was shown that the inability of the CN mice and their F1 progeny to respond to T-independent antigens was not due to an intrinsic abnormality of their microenvironment or the suppressive actions of a T lymphocyte. Our data present evidence that the X-linked defect in the CN mice is due to an intrinsic defect in B-lymphocyte development.


2021 ◽  
Author(s):  
Ra&uacutel Pi&ntildeeiro-Salvador ◽  
Eduardo Vazquez-Garza ◽  
José Antonio Cruz-Cardenas Cruz-Cardenas ◽  
Gerardo de Jes&uacutes Garc&iacutea-Rivas ◽  
Jorge Moreno-V&aacutesquez ◽  
...  

Breastmilk is a dynamic fluid which initial goal is to provide the most adapted nutrition to the neonate. Additional functions have been recently attributed to breastmilk, with the evidence of a specific microbiota and the presence of a variety of components of the immune system, such as cytokines and leukocytes. The composition of breastmilk varies through time, according to the health status of mother and child, and altogether contributes to future health of the infant. Obesity is a rising condition worldwide, that creates a state of systemic, chronic inflammation including leukocytosis. Here, we asked whether colostrum, the milk produced within the first 48 h post-partum, would contain a distinct leukocyte composition depending on the body mass index (BMI) of the mother. We applied a panel of 6 antibodies plus viability marker to the peripheral blood and colostrum obtained from obese (BMI > 30) and lean (BMI < 25) mothers to characterize 10 major leukocyte subpopulations using flow cytometry. While lymphoid cells were otherwise unaffected by their tissue of origin, the phenotypes of granulocyte and monocyte populations significantly contrasted between blood and colostrum, including variations in morphology and surface expression of CD45 and CD16. These differences recapitulated across groups, which suggests a generalized cell-specific phenotype alteration caused by trafficking to colostrum. The B lymphocyte compartment was significantly reduced in obese colostrum and these cells did not exhibit enhanced CD16 shedding in this tissue, unlike B lymphocytes from lean mothers colostrum. This is the first exhaustive characterization of major leukocyte subsets in obese mothers colostrum, and the first report of leukocyte subpopulations from Latin-American womens colostrum. This pioneering study is a steppingstone to further investigate active immunity in human breastmilk.


2009 ◽  
Vol 422 (3) ◽  
pp. 553-561 ◽  
Author(s):  
Daniela Marasco ◽  
Romania Stilo ◽  
Annamaria Sandomenico ◽  
Simona Maria Monti ◽  
Barbara Tizzano ◽  
...  

The molecular complex containing BCL10 and CARMA [CARD (caspase recruitment domain)-containing MAGUK (membrane-associated guanylate kinase)] proteins has recently been identified as a key component in the signal transduction pathways that regulate activation of the transcription factor NF-κB (nuclear factor κB) in lymphoid and non-lymphoid cells. Assembly of complexes containing BCL10 and CARMA proteins relies on homophilic interactions established between the CARDs of these proteins. In order to identify BCL10-inhibitory peptides, we have established a method of assaying peptides derived from the CARD of BCL10 in binding competition assays of CARD–CARD self-association. By this procedure, a short peptide corresponding to amino acid residues 91–98 of BCL10 has been selected as an effective inhibitor of protein self-association. When tested in cell assays for its capacity to block NF-κB activation, this peptide represses activation of NF-κB mediated by BCL10, CARMA3 and PMA/ionomycin stimulation. Collectively, these results indicate that residues 91–98 of BCL10 are involved in BCL10 self-association and also participate in the interaction with external partners. We also show that blocking of the CARD of BCL10 may potentially be used for the treatment of pathological conditions associated with inappropriate NF-κB activation.


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