Role of Interleukin-1 in Human B-Cell Activation

1985 ◽  
pp. 195-217
Author(s):  
Peter E. Lipsky
Author(s):  
Gábor Koncz ◽  
Israel Pecht ◽  
János Gergely ◽  
Gabriella Sármay

2001 ◽  
Vol 167 (11) ◽  
pp. 6132-6139 ◽  
Author(s):  
Isaac R. Blanca ◽  
Earl W. Bere ◽  
Howard A. Young ◽  
John R. Ortaldo

1985 ◽  
Vol 82 (6) ◽  
pp. 1766-1770 ◽  
Author(s):  
E. A. Clark ◽  
G. Shu ◽  
J. A. Ledbetter

1983 ◽  
Vol 157 (5) ◽  
pp. 1529-1543 ◽  
Author(s):  
M Howard ◽  
S B Mizel ◽  
L Lachman ◽  
J Ansel ◽  
B Johnson ◽  
...  

In this report we describe conditions for polyclonal activation of small numbers of highly purified mouse B lymphocytes. Three signals are required for induction of DNA synthesis by the particular subset of small B lymphocytes investigated: a signal delivered by antibodies specific for the IgM receptor expressed on the B cell membrane; a signal delivered by a T cell-derived factor (B cell growth factor [BCGF]); and a signal delivered by the macrophage-derived factor interleukin 1 (IL-1). The conclusion that IL-1 has B cell co-stimulator activity is based on the findings that highly purified preparations of mouse and human IL-1 have the capacity to cause proliferation in B cells treated with anti-IgM and BCGF. Such cultures show an absolute dependence on exogenously added IL-1 when 2-mercaptoethanol is omitted from the medium. BCGF and IL-1 each act in a non-antigen-specific, non-H-2-restricted, synergistic manner. Their requirement is not observed when B cells are cultured at high density, presumably reflecting accessory cell contamination and endogenous factor production under these conditions. The B cell activation induced by these three signals is restricted to proliferation without the production of antibody-forming cells.


1989 ◽  
Vol 29 (3) ◽  
pp. 353-361 ◽  
Author(s):  
M. WIKEN ◽  
P. BJORCK ◽  
B. AXELSSON ◽  
P. PERLMANN

1994 ◽  
Vol 179 (1) ◽  
pp. 221-228 ◽  
Author(s):  
G Fischer ◽  
S C Kent ◽  
L Joseph ◽  
D R Green ◽  
D W Scott

Treatment of the WEHI-2131 or CH31 B cell lymphomas with anti-mu or transforming growth factor (TGF)-beta leads to growth inhibition and subsequent cell death via apoptosis. Since anti-mu stimulates a transient increase in c-myc and c-fos transcription in these lymphomas, we examined the role of these proteins in growth regulation using antisense oligonucleotides. Herein, we demonstrate that antisense oligonucleotides for c-myc prevent both anti-mu- and TGF-beta-mediated growth inhibition in the CH31 and WEHI-231 B cell lymphomas, whereas antisense c-fos has no effect. Furthermore, antisense c-myc promotes the appearance of phosphorylated retinoblastoma protein in the presence of anti-mu and prevents the progression to apoptosis as measured by propidium iodide staining. Northern and Western analyses show that c-myc message and the levels of multiple myc proteins were maintained in the presence of antisense c-myc, results indicating that myc species are critical for the continuation of proliferation and the prevention of apoptosis. These data implicate c-myc in the negative signaling pathway of both TGF-beta and anti-mu.


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