G. G. B. Klaus

Délégation Paris 6

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Manlio Ferrarini

University of Genoa

H. Robson MacDonald

University of Toronto

Michael Sela

Bar-Ilan University

J. Gergely

Institute for Plant Protection and Environment

Hartmut Wekerle

Max Planck Institute of Biochemistry

Stefan Meuer

Heidelberg University

Mary Holman

The Francis Crick Institute

Rolf M. Zinkernagel

University Hospital of Zurich

Michael Reth

University of Freiburg

N Mitchison

University College London

Cooperative Institutions

Délégation Paris 6

National Institute for Medical Research

Deutsche Nationalbibliothek

Johannes Gutenberg University Mainz

Inserm

University College London

University of Freiburg

Medical Research Council

European Writers' Council

Medizinisch Wissenschaftliche Verlagsgesellschaft (Germany)

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The generation of memory cells. I. The role of C3 in the generation of B memory cells.

PubMed (1977)

G. G. B. Klaus John Humphrey

Adult thymectomized, repopulated mice were chronically depleted of circulating C3 by treatment with cobra venom factor after primary immunization with dinitrophenylated haemocyanin (DNP-KLH). This treatment totally abrogated the development of B-cell memory in such mice, as assayed by a co-operative lymphocyte transfer. The failure of memory development appeared to involve impaired precursor proliferation following priming. It was further shown that the localization of DNP-KLH in splenic lymphoid follicles is both antibody and C3-dependent; thymus-deprived mice make sufficient antibody to DNP-KLH to effect follicular localization of the antigen. On the basis of these and earlier observations we suggest that the development of B-memory cells involves the formation of antigen-antibody-C3 complexes on dendritic cells in lymphoid follicles. C3 may serve to stabilize the antigen bridge between dendritic cells and virgin precursors. In complete contrast, C3 depletion had little effect on the functional expression of primed B cells, thus suggesting that only the early stages of B-cell triggering are C3 dependent.

Priming (agriculture)

Follicular dendritic cells

Precursor cell

Memory B cell

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Citations (235)

Transcriptomic and proteomic profiles of chronic kidney disease in pediatric arteriolar tissues: which pathways are involved in pro-calcifying processes?

Julie Bernardor Mária Bartošová Chao Zhang Ivana Marinović B Schaefer

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Activation and proliferation signals in mouse B cells. III. Intact (IGG) anti-immunoglobulin antibodies activate B cells but inhibit induction of DNA synthesis.

PubMed (1984)

G. G. B. Klaus Catherine M. Hawrylowicz Mary Holman K D Keeler

Intact (IgG) rabbit anti-immunoglobulin antibodies are generally not mitogenic for mouse B cells but, on the contrary, inhibit proliferation induced by either F(ab')2 anti-Ig or by lipopolysaccharide. We show here, however, that IgG anti-Ig activates mouse B cells, since it causes B cells to depolarize, to enlarge and to express increased levels of Ia antigens. In the continuing presence of IgG anti-Ig, B cells do not synthesise DNA. However, if cells cultured with IgG antibody are then washed, they start to proliferate earlier in response to F(ab')2 anti-Ig, i.e. they have become primed. We therefore conclude that IgG anti-Ig is an example of a 'step-one activator' for mouse B cells, which drives resting B cells out of Go, but actively prevents the cells from progressing into S. The latter effect appears to result from cross-linking of surface Ig and Fc receptors on B cells, although the mechanism is, as yet, unknown.

Surface Immunoglobulin

Immunoglobulin M

B-1 cell

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Antigen-specific T lymphocytes regulate lipopolysaccharide-induced apoptosis of dendritic cells in vivo.

PubMed (1998)

Thibaut De Smedt Bernard Pajak G. G. B. Klaus Randolph J. Noelle Jacques Urbain

The potent accessory properties of dendritic cells (DC) develop sequentially during a process termed "maturation." Splenic DC undergo functional maturation in vivo in response to the bacterial product LPS and migrate from the marginal zone to the T cell areas. The redistribution of fully mature DC, which present Ags encountered in the periphery, in the T cell area is likely to result in T cell priming. Unexpectedly, we found that DC rapidly die by apoptosis once they have entered the T cell zone. Injection of OVA peptide in OVA-specific, TCR-transgenic mice strongly delays the LPS-induced apoptosis of DC in situ. We conclude that mature DC are programmed to die unless they receive a survival signal from T cells and that the regulation of DC survival may be a mechanism aimed at controlling the initiation and the termination of the immune response.

Priming (agriculture)

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Citations (133)

Masthead

European Journal of Immunology (1989)

N Mitchison London Von Boehmer Klaus Rajewsky Michael Sela M Séligmann

10.1002/eji.1830190701

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B cell tolerance induced by polymeric antigens V. Different avidities of primed and virgin precursor cells for paucivalent antigen

European Journal of Immunology (1976)

H. N. A. Willcox G. G. B. Klaus

We have compared the avidity of virgin and primed hapten-specific precursor cells for DNP-lys-S3 (dinitrophenylated type 3 pneumococcal polysaccharide) by measuring its capacity to prevent them from binding highly radioactive DNP-hemocyanin, and thereby protect them from committing hapten-specific "suicide". Moderately substituted conjugates (e.g. DNP-lys2.7S3) protected virgin and memory B cells impartially. In contrast, DNP-lys0.6S3 protected memory cells efficiently, but protected virgin cells only at considerably higher concentrations. These results are consistent with previous evidence - from this and other systems - that there is a higher density of receptors on primed than on unprimed B cells - the significance of which is discussed.

Priming (agriculture)

10.1002/eji.1830060514

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Citations (3)

EFFECTS OF CYCLOSPORINE ON THE IMMUNE SYSTEM OF THE MOUSE II. CYCLOSPORINE INHIBITS THE EFFECTOR FUNCTION OF PRIMARY T HELPER CELLS, BUT NOT HELPER CELL PRIMING

Transplantation (1983)

G. G. B. Klaus Annalisa Kunkl

Division of Immunology, National Institute for Medical Research, Mill Hill, London, NW7 1AA, England

Priming (agriculture)

Adoptive Cell Transfer

T helper cell

10.1097/00007890-198307000-00016

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Citations (43)

Vav Is Required for Cyclin D2 Induction and Proliferation of Mouse B Lymphocytes Activated via the Antigen Receptor

Journal of Biological Chemistry (2001)

Janet Glassford Mary Holman Lolita Banerji Elizabeth Clayton G. G. B. Klaus

B lymphocytes from mice null for the Rho-family guanine-nucleotide exchange factor, Vav, are defective in their ability to proliferate in response to BCR cross-linking, but are able to proliferate normally in response to LPS. In addition, they have a depletion of CD5(+) (B1) lymphocytes and defective IgG class switching. This phenotype is reminiscent of that observed in mice null for the cell cycle regulatory protein, cyclin D2. We demonstrate here that the inability of vav(-/-) B cells to proliferate in response to BCR ligation is due to an inability to induce cyclin D2. In addition, we show that the proliferative defect of these cells occurs after the cells have entered early G1 phase. Analyses of potential down-stream signaling intermediates revealed differential activation of the stress-activated MAP kinases in the absence of Vav, normal activation of the ERK, MAPK, and phosphatidylinositol 3-kinase pathways, and defective intracellular calcium mobilization. We further demonstrate that intracellular calcium homeostasis is required for cyclin D2 induction, implicating a possible link with the defective calcium response of vav(-/-) B cells and their inability to induce cyclin D2.

Cyclin D2

10.1074/jbc.m105305200

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Citations (33)

Masthead

European Journal of Immunology (1996)

Harald von Boehmer Douglas T. Fearon Diane Mathis Hidde Gunther Hammerling Lorenzo

10.1002/eji.1830261201

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Lymphocytes

Van Nostrand's Scientific Encyclopedia (2007)

G. G. B. Klaus

10.1002/9780471743989.vse10015

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