scholarly journals Mechanism of unresponsiveness to the alpha 1-6 epitope of dextran B512 in a C57BL substrain.

1983 ◽  
Vol 158 (1) ◽  
pp. 66-73 ◽  
Author(s):  
C Fernandez ◽  
G Möller

C57BL/10ScCr mice are low responders to the alpha 1-6 epitope of dextran B512, although other C57BL mice are high responders. Both thymus-independent and thymus-dependent forms of dextran failed to induce an immune response in C57BL/10ScCr mice, but dextran functioned as a good carrier for antihapten responses in this strain. Dextran is a potent polyclonal B cell activator for cells from C57BL/10ScCr mice, although such cells are not activated by LPS. The C57BL/10ScCr mice possess the Igh-V gene coding for antibodies against dextran and the antidextran antibodies induced in (A X C57BL/10ScCr)F1 hybrids share an idiotype with antidextran antibodies produced in C57BL/10 mice. Bone marrow cells from C57BL/10ScCr mice do not respond to dextran when transferred into lethally irradiated C57BL/10 mice and C57BL/10 cells transferred into C57BL/10ScCr mice give a strong antidextran response. Thus, B cells having both the Igh-V gene coding for antibodies against dextran and activation receptors for dextran cannot be activated into antibody synthesis against any form of this immunogen. This determinant specific immunodeficiency suggests the existence of as yet unknown regulatory influences on Igh-V gene expression or B cell activation.

1983 ◽  
Vol 158 (6) ◽  
pp. 2171-2176 ◽  
Author(s):  
L M Hutt-Fletcher ◽  
N Balachandran ◽  
M H Elkins

Human cytomegalovirus is shown to be a nonspecific polyclonal B cell activator. The B cell response is independent of virus replication and requires little, if any, T cell help.


1996 ◽  
Vol 26 (7) ◽  
pp. 1519-1526 ◽  
Author(s):  
Sanad Al-Balaghi ◽  
Erna Möller ◽  
Göran Möller ◽  
Manuchehr Abedi-Valugerdi

1975 ◽  
Vol 142 (6) ◽  
pp. 1564-1569 ◽  
Author(s):  
S Britton

Experimental amyloidosis in mice can be induced by repeated injections of casein. It has now been demonstrated that casein induces strong polyclonal antibody synthesis in mouse B spleen lymphocytes. This effect is much more pronounced in spleen cells from anyloid-susceptible mice (CBA/J) than amyloid-resistant mice (A/J). It is suggested that amyloidosis can be due in some instances to a constant exposure for molecules which induce polyclonal B-cell activation.


2004 ◽  
Vol 72 (9) ◽  
pp. 5412-5418 ◽  
Author(s):  
Daria Donati ◽  
Li Ping Zhang ◽  
Qijun Chen ◽  
Arnaud Chêne ◽  
Kirsten Flick ◽  
...  

ABSTRACT Polyclonal B-cell activation and hypergammaglobulinemia are prominent features of human malaria. We report here that Plasmodium falciparum-infected erythrocytes directly adhere to and activate peripheral blood B cells from nonimmune donors. The infected erythrocytes employ the cysteine-rich interdomain region 1α (CIDR1α) of P. falciparum erythrocyte membrane protein 1 (PfEMP1) to interact with the B cells. Stimulation with recombinant CIDR1α induces proliferation, an increase in B-cell size, expression of activation molecules, and secretion of immunoglobulins (immunoglobulin M) and cytokines (tumor necrosis factor alpha and interleukin-6). Furthermore, CIDR1α binds to Fab and Fc fragments of human immunoglobulins and to immunoglobulins purified from the sera of different animal species. This binding pattern is similar to that of the polyclonal B-cell activator Staphylococcus aureus protein A. Our findings shed light on the understanding of the molecular basis of polyclonal B-cell activation during malaria infections. The results suggest that the var gene family encoding PfEMP1 has evolved not only to mediate the sequestration of infected erythrocytes but also to manipulate the immune system to enhance the survival of the parasite.


1994 ◽  
Vol 14 (3-4) ◽  
pp. 221-238 ◽  
Author(s):  
Marilyn R. Kehry ◽  
Philip D. Hodgkin

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