Surface immunoglobulin phenotype of murine spleen cells which form B cell colonies in agar

The proliferative response of mouse B lymphocytes induced by Fc fragments was found to be dependent upon an adherent cell population. The adherent cell is esterase positive, irradiation resistant, and not susceptible to lysis by anti-thymus serum and complement. The mechanism(s) by which Fc fragments induce B-cell proliferation could be the result of the interaction of Fc with both B cells and adherent cells or with adherent cells which then release factors that trigger the B cells to proliferate. Spleen cells from the C3H/HeJ mouse were shown to be unable to respond to Fc fragments. The addition of adherent cells from either C3H/St or C3H/HeN mice to adherent cell depleted C3H/HeJ cells enabled them to respond to Fc, indicating the defect was in the adherent cell population.

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Obligatory role of gamma interferon in T cell-replacing factor-dependent, antigen-specific murine B cell responses.

Journal of Experimental Medicine ◽

10.1084/jem.161.5.953 ◽

1985 ◽

Vol 161 (5) ◽

pp. 953-971 ◽

Cited By ~ 28

Author(s):

M Brunswick ◽

P Lake

Keyword(s):

T Cell ◽

B Cell ◽

Cell Activation ◽

Human Peripheral Blood ◽

Gamma Interferon ◽

Spleen Cells ◽

Ifn Gamma ◽

Murine Spleen

The role of gamma interferon (IFN-gamma) in T cell-replacing factor (TRF) activity for antigen-specific plaque-forming cell (PFC) responses in vitro was studied using antibodies to murine IFN-gamma (Mu IFN-gamma). TRF activity was present in supernatants (Sn) of Con A- or mixed leukocyte reaction-stimulated murine spleen cells as well as in an IL-2-rich fraction of phytohemagglutinin-stimulated human peripheral blood lymphocyte Sn and in the Sn of the Gibbon T lymphoma MLA-144. The human TRF was highly active with cells from nu/nu mice and normal mice but not with cells from animals with the xid immunologic defect, similar to the activity of murine TRF. Antibodies to IFN-gamma consisted of hyper-immune rabbit antisera, IFN-gamma affinity-purified rabbit immunoglobulin and an interspecies hybridoma specific for Mu IFN-gamma. The results show that the activities of all preparations of TRF are markedly diminished or abrogated by antibody to Mu IFN-gamma but not by antibodies to human IFN-gamma (Hu IFN-gamma), nor by normal rabbit sera or purified rabbit Ig. The degree of inhibition was dose dependent and was quantitatively reversed by the addition to the cultures of recombinant-derived Mu IFN-gamma (Mu rIFN-gamma) but not Hu rIFN-gamma. This reversal was fully antigen specific and thus not attributable to polyclonal B cell activation by IFN-gamma, which is inactive alone in the TRF assay. Kinetic analysis shows that IFN-gamma must act by 24-48 h to produce PFC responses at 4 d. Together, the data demonstrate that IFN-gamma is a necessary mediator for TRF effects and that IFN-gamma is induced by TRF from T-depleted murine spleen cells in sufficient quantity to support large antibody responses. The source of this IFN-gamma may be the potent natural killer cells that are induced in cultures stimulated with TRF.

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Control of B-lymphocyte function. I. Inactivation of mitogenesis by interactions with surface immunoglobulin and Fc-receptor molecules.

Journal of Experimental Medicine ◽

10.1084/jem.144.4.882 ◽

1976 ◽

Vol 144 (4) ◽

pp. 882-896 ◽

Cited By ~ 83

Author(s):

C L Sidman ◽

E R Unanue

Keyword(s):

B Cells ◽

B Cell ◽

B Lymphocyte ◽

Regulatory Mechanism ◽

Fc Receptor ◽

Mouse Spleen ◽

Lymphocyte Function ◽

Spleen Cells ◽

Surface Immunoglobulin

Mouse spleen cells were incubated with anti-Ig antibodies for 1 h, washed, exposed to LPS for 1 h, washed, and their DNA synthetic responses assayed 2 days later. It was shown that the 1-h incubation with anti-Ig antibodies produced a profound, internal, and long lasting state of inactivation in the B cells. Experiments with anti-Ig fragments and other ligands showed that the inactivation occurred optimally when both surface Ig molecules and Fc receptors were bound simultaneously. The role of the classical capping and clearing cycle was also investigated. It was shown that capping and clearing were neither necessary nor sufficient for the inactivation to occur, and that the signals, but only secondarily the ligands themselves, were transmitted across the membrane. Capping and clearing were viewed as a natural regulatory mechanism by which the B cell attempts to clear its membrane of perturbations and signals from the exterior.

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H-40, an antigen controlled by an Igh linked gene and recognized by cytotoxic T lymphocytes. I. Genetic analysis of H-40 and distribution of its product on B cell tumors.

Journal of Experimental Medicine ◽

10.1084/jem.159.6.1724 ◽

1984 ◽

Vol 159 (6) ◽

pp. 1724-1740 ◽

Cited By ~ 12

Author(s):

J Forman ◽

R Riblet ◽

K Brooks ◽

E S Vitetta ◽

L A Henderson

Keyword(s):

T Lymphocytes ◽

Genetic Analysis ◽

B Cell ◽

Cytotoxic T Lymphocytes ◽

Target Antigen ◽

Spleen Cells ◽

Competition Assay ◽

Linked Gene ◽

Surface Immunoglobulin ◽

Gene Maps

C.B-20 ( Ighb ) mice challenged with BALB/c ( Igha ) spleen cells (or vice-versa) generate cytotoxic T lymphocytes (CTL) that recognize an antigen, H-40, controlled by an Igh-linked gene. The gene maps to the Igh-C region end of the Igh complex, telomeric to Tsu in the region of Pre-1. At least three alleles, a, b, and c, can be defined. Using a cold target competition assay, no polymorphism of the a allele was detected. Both surface Igh-5a positive and negative spleen cells from (C.B-20 X BALB/c)F1 animals express the a allele of the antigen, indicating that this gene is not allelically excluded. Recognition of the target antigen by CTL is restricted by the D-end of H-2d. The tissue distribution of H-40 was explored using both bulk-cultured and cloned CTL. The antigen is expressed on surface immunoglobulin positive (sIg+) cells and correlates with the expression of sIgM. This was determined by analysis of several B lymphomas as well as of other tumors that varied in their extent of expression of sIg. Four subclones of BCL1 were analyzed. Two of the subclones are sIg+ and express H-40, while two other subclones are sIg- and H-40-. Thus, these data define an Igh-linked gene, separate from immunoglobulin structural loci, that controls an antigen expressed on sIg+ cells. Possible mechanisms to account for this finding are discussed.

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A Trypanosoma cruzi Alkaline Antigen Induces Polyclonal B-Cell Activation of Normal Murine Spleen Cells by T-Cell-Independent, BCR-Directed Stimulation

Scandinavian Journal of Immunology ◽

10.1046/j.1365-3083.1999.00577.x ◽

1999 ◽

Vol 50 (2) ◽

pp. 159-166 ◽

Cited By ~ 10

Author(s):

Montes ◽

Zuniga ◽

Minoprio ◽

Vottero-Cima ◽

Gruppi

Keyword(s):

T Cell ◽

Trypanosoma Cruzi ◽

B Cell ◽

Cell Activation ◽

B Cell Activation ◽

Spleen Cells ◽

Murine Spleen

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In vivo effects of dialyzable leukocyte lysates (DLL): Changes in the responses of murine spleen cells to T- and B-cell mitogens, spleen weight, and morphology of splenic tissue

Clinical Immunology and Immunopathology ◽

10.1016/0090-1229(78)90046-6 ◽

1978 ◽

Vol 11 (2) ◽

pp. 229-244 ◽

Cited By ~ 8

Author(s):

Thomas K. Huard ◽

Tawfik Sabet ◽

Peter Baram

Keyword(s):

B Cell ◽

Splenic Tissue ◽

Spleen Weight ◽

Spleen Cells ◽

Murine Spleen ◽

In Vivo Effects

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SPECIFIC MURINE B-CELL ACTIVATION BY SYNTHETIC SINGLE- AND DOUBLE-STRANDED POLYNUCLEOTIDES

Journal of Experimental Medicine ◽

10.1084/jem.138.6.1545 ◽

1973 ◽

Vol 138 (6) ◽

pp. 1545-1563 ◽

Cited By ~ 27

Author(s):

Irwin Scher ◽

Douglas M. Strong ◽

Aftab Ahmed ◽

Richard C. Knudsen ◽

Kenneth W. Sell

Keyword(s):

Molecular Structure ◽

B Cell ◽

Cell Activation ◽

Thymidine Incorporation ◽

Inbred Strains ◽

B Cell Activation ◽

Spleen Cells ◽

Functional Interaction ◽

Murine Spleen ◽

Cell Mitogen

The synthetic single- and double-stranded polynucleotides, poly I, poly C, and poly I·C, were shown to induce thymidine incorporation in six inbred strains of murine spleen cells. This stimulation was shown to be secondary to B-cell activation and not due to contamination of the polynucleotides with bacterial lipopolysaccharide (LPS). The ability of poly I·C to act as a B-cell mitogen, in addition to its behavior as a thymic-independent antigen, suggested that these two phenomena may be related. The similarity of the molecular structure of poly I·C to LPS, a material which also acts as a thymic-independent antigen and a B-cell mitogen, supports the hypothesis that the polyvalent nature of these materials accounts for their functional interaction with murine B cells.

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