Antibodies to Hen Egg Lysozyme

Jorg Kirberg kirberg at
Mon Jan 20 12:22:13 EST 1997

In article <5bvu2f$re0 at>,
bunka at (Sebastian Bunka) wrote:
> In article <1997Jan14.153933.5812 at>,
>         ttha at (Tom Thatcher) writes:
> > I'm looking for polyclonal and/or monoclonal antibodies against hen
> > egg lysozyme.  So far I've found one commercial source of a polyclonal
> > (Biodesign) and no sources of monoclonals.  Any help would be appreciated.
> > 
> To my best knowledge there is no (commercial available) monoclonal.
> But another good source of polyclonal rabbit-anti-HEL, IgG fraction
> is: Rockland, Gilbertsville, PA; Order-Nr. 200-4172. (Don't have
> the phone number anymore ...).
> I've found the IgG fraction quite good (don not buy the whole serum).
> Much better was immunizing a sheep w/ HEL !! (Well, I don't
> have any more of that serum - in case you ask ;-))
> -- 
Dear Sebastian and Tom,

as there are transgenic mice with a HEL specific B cell receptor,
there must be somewhere the hybridoma from which the genes
were taken. That will be a good source for your monoclonal:

%A Eris, J. M.
%A Basten, A.
%A Brink, R.
%A Doherty, K.
%A Kehry, M. R.
%A Hodgkin, P. D.
%D 1994
%T Anergic self-reactive B cells present self antigen and respond normally
to CD40-dependent T-cell signals but are defective in
antigen-receptor-mediated functions
%B Proc Natl Acad Sci U S A
%V 91
%N 10
%P 4392-6
%X B-cell tolerance to soluble protein self antigens such as hen egg
lysozyme (HEL) is mediated by clonal anergy. Anergic B cells fail to mount
antibody responses even in the presence of carrier-primed T cells,
suggesting an inability to activate or respond to T helper cells. To
investigate the nature of this defect, B cells from tolerant HEL/anti-HEL
double-transgenic mice were incubated with a membrane preparation from
activated T-cell clones expressing the CD40 ligand. These membranes,
together with interleukin 4 and 5 deliver the downstream
antigen-independent CD40-dependent B-cell-activating signals required for
productive T-B collaboration. Anergic B cells responded to this stimulus
by proliferating and secreting antibody at levels comparable to or better
than control B cells. Furthermore, anergic B cells presented HEL acquired
in vivo and could present the unrelated antigen, conalbumin, targeted for
processing via surface IgD. In contrast, the low immunoglobulin receptor
levels on anergic B cells were associated with reduced de novo
presentation of HEL and a failure to upregulate costimulatory ligands for
CD28. These defects in immunoglobulin-receptor-mediated functions could be
overcome in vivo, suggesting a number of mechanisms for induction of
autoantibody responses.
%O May 10

%0 Journal Article
%A Hartley, S. B.
%A Crosbie, J.
%A Brink, R.
%A Kantor, A. B.
%A Basten, A.
%A Goodnow, C. C.
%D 1991
%T Elimination from peripheral lymphoid tissues of self-reactive B
lymphocytes recognizing membrane-bound antigens
%B Nature
%V 353
%N 6346
%P 765-9
%X The long-standing hypothesis that tolerance to self antigens is
mediated by either elimination or functional inactivation (anergy) or
self-reactive lymphocytes is now accepted, but little is known about the
factors responsible for initiating one process rather than the other. In
the B-cell lineage, tolerant self-reactive cells persist in the peripheral
lymphoid organs of transgenic mice expressing lysozyme and anti-lysozyme
immunoglobulin genes, but are eliminated in similar transgenic mice
expressing anti-major histocompatibility complex immunoglobulin genes. By
modifying the structure of the lysozyme transgene and the isotype of the
anti-lysozyme immunoglobulin genes, we demonstrate here that induction of
anergy or deletion is not due to differences in antibody affinity or
isotype, but to recognition of monomeric or oligomeric soluble antigen
versus highly multivalent membrane-bound antigen. Our findings indicate
that the degree of receptor crosslinking can have qualitatively distinct
signalling consequences for lymphocyte development.



Joerg Kirberg                              Tel. 0031 - 20 - 512 19 98
The Netherlands Cancer Institute           FAX  0031 - 20 - 512 20 11
Div. Molecular Genetics (H4)               E_mail kirberg at
Plesmanlaan 121
NL - 1066 CX Amsterdam
The Netherlands

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