Suppression of B Cell Development and Antibody Responses in Mice with Polyclonal Rabbit and Monoclonal Rat Anti-IgM Antibodies

Cerny, Andreas; Hugin, A. W.; Sutter, S.; Heusser, C H; Bos, Nicolaas A.; Izui, Shozo; Hengartner, Hans; Rm, Zinkernagel

doi:10.1159/000163327

Cited by 9 publications

(2 citation statements)

References 10 publications

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“…Female DBA/2, BALB/c, ICR, (B10.D2 X C57BL/10)F| or C57BL/6 mice were obtained from the Institut für Zuchthygiene, Abteilung Labortier kunde, Tierspital Zürich (Switzerland); they were used at the age of 7-15 weeks. B cell-deprived mice were raised exactly as described [8,10].…”

Section: Methodsmentioning

confidence: 99%

“…VSV induces an early T cell-independent B cell response in mice [6][7][8] which around day 6-8 is switched to a T cell-dependent IgG response [7,9], The present study set out to characterize the dose-response parameters of the neutralizing antibody response to live, UV-inactivated VSV or purified VSV glyco protein G in mice. We found that priming of mice with vesicular stomatitis virus (VSV) required doses greater than 10-100 plaque forming units (pfu) of virus.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Antibodies in Natural and Acquired Resistance of Mice to Vesicular Stomatitis Virus

Gobet¹,

Cerny²,

Rüedi³

et al. 1988

Pathobiology

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Mice infected with live vesicular stomatitis virus (VSV) produced primary antibody responses more efficiently (with doses > 10² pfu) than those injected with UV-inactivated VSV ( > 10⁶ pfu) or purified VSV glycoprotein G (equivalent to 10⁷ pfu) by producing neutralizing antibodies. Very low doses of live VSV ( < 10² pfu) failed to prime mice. Normal mouse serum had the capacity to inactivate VSV by heat-labile and immunoglobulin-mediated mechanisms in vitro independently of specifically induced antibodies. Studies using B cell-depleted agammaglobulineamic mice showed that their serum lacked VSV-neutralizing capacity in vitro and that naturally resistant mice became susceptible to VSV-induced paralytic disease which could be prevented by adoptive transfer of immune but also of normal serum.

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Role of Antibodies in Natural and Acquired Resistance of Mice to Vesicular Stomatitis Virus

Gobet¹,

Cerny²,

Rüedi³

et al. 1988

Pathobiology

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Development of follicular dendritic cells in lymph nodes of B-cell-depleted mice

1988

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We have studied follicular dendritic cells (FDC) in lymph nodes of normal and thymus dysgeneic nude mice depleted of B-cells by chronic treatment with anti-IgM antibodies. We found that B cell depletion was accompanied by the absence of mature FDC as defined morphologically at the ultrastructural level. Only precursor FDC (p-FDC) could be demonstrated. Upon release of B-cell suppression, the repopulation of lymph nodes with B-cells was associated with the reappearance of fully differentiated FDC in primary follicles of nude mice and in secondary follicles of T-cell competent mice. We conclude that mature B-cells and/or B-cell products are required for the development of mature follicular dendritic cells in the mouse lymph node.

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Anti-Listeria monocytogenes immunity in μ-suppressed mice: a comparison of treatment with conventional hyperimmune rabbit anti-mouse IgM and affinity-purified, monoclonal rat anti-mouse IgM

Cerny¹,

Hugin²,

Bazin³

et al. 1988

Med Microbiol Immunol

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The capacity of anti-IgM treated, B-cell-depleted mice to control infection by Listeria monocytogenes was evaluated. Suppression was achieved with a hyperimmune rabbit anti-mouse-IgM antiserum (IRS), with affinity-purified IRS (IRP), or with an affinity-purified, monoclonal, rat anti-mouse-IgM antibody (LO-MM-9). B-cell depletion in specifically treated mice was judged to be complete by the following criteria: absence of significant response to a B-cell mitogen lipopolysaccharide, absence of B-cells with detectable IgM or kappa light chain on their surface, absence of detectable IgM, and presence of free anti-IgM antibodies in serum. BALB/c mice, conventionally treated from birth with IRS, had an increased capacity to clear L. monocytogenes from the blood during the first 5 min after intravenous infection. Furthermore, control of infection seemed to be enhanced during the first 24 h but was found to be impaired when assessed 3 and 4 days after initiation of infection. These effects were, however, not IRS specific, because control mice treated with normal rabbit serum behaved comparably. Mortality caused by 2 x 10(3) L. monocytogenes injected intraperitoneally into BALB/c mice susceptible to L. monocytogenes was increased more in NRS-than in IRS-treated mice when both were compared with untreated control mice. Therefore, chronic injection of IRS or NRS seemed to disturb anti-L. monocytogenes immunity, rendering an evaluation of the role of antibodies impossible.(ABSTRACT TRUNCATED AT 250 WORDS)

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Suppression of B Cell Development and Antibody Responses in Mice with Polyclonal Rabbit and Monoclonal Rat Anti-IgM Antibodies

Cited by 9 publications

References 10 publications

The Role of Antibodies in Natural and Acquired Resistance of Mice to Vesicular Stomatitis Virus

The Role of Antibodies in Natural and Acquired Resistance of Mice to Vesicular Stomatitis Virus

Development of follicular dendritic cells in lymph nodes of B-cell-depleted mice

Anti-Listeria monocytogenes immunity in μ-suppressed mice: a comparison of treatment with conventional hyperimmune rabbit anti-mouse IgM and affinity-purified, monoclonal rat anti-mouse IgM

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