MadSci Network: Immunology
Query:

Re: Why does a B cells have B220 surface marker?

Date: Wed Feb 10 10:24:35 2010
Posted By: Djordje Miljkovic, Post-doc/Fellow, Imunology, Institute for Biological Research
Area of science: Immunology
ID: 1262141471.Im
Message:

CD45 is a tyrosine phosphatase that has an essential role in regulating T
and B cell antigen receptor-mediated signaling. CD45 is expressed on all
hematopoietic cells, and is also known as leukocyte common antigen (LCA).
Forms of CD45 with restricted cellular expression are designated CD45RO,
CD45RA, CD45RB (http://en.wikipedia.org/wiki/PTPRC). CD45R that has a
molecular weight of 220 kDa is commonly known as B220. Although B cells are
the predominant leukocyte expressing B220, this molecule is also displayed
by subsets of NK cells, activated T cells, and a subpopulation of dendritic
cells (Rolink A, ten Boekel E, Melchers F, Fearon DT, Krop I, and Andersson
J. (1996) J. Exp. Med. 183(1), 187-194).

"CD22 is a sugar binding transmembrane protein, which specifically binds
sialic acid with an immunoglobulin (Ig) domain located at its N-terminus.
The presence of Ig domains makes CD22 a member of the immunoglobulin
superfamily." (http://en.wikipedia.org/wiki/CD22). "CD22 is a member of the
immunoglobulin superfamily that is expressed only on B cells, and early
studies had suggested it to be a positive regulator of cellular activation.
However, the findings that (a) tyrosine phosphorylated CD22 recruits SHP-1
(14, 15), (b) coligating CD22 to mIg suppresses activation of
mitogen-activated protein (MAP) kinases, and (c) sequestering CD22 from mIg
enhances B cell activation have indicated that CD22 serves primarily as an
inhibitor. Although the precise role of CD22 in the biology of the B cell
is not yet understood in relation to its natural ligand (sialic acid in the
structure, Sia {alpha}2-6Gal β1-4GlcNAc; reference 17), the association of
CD22 with mIg in resting B cells suggests that it may constitutively
suppress signaling by the antigen receptor. The absence of this function
may account for the spontaneous, antigen-independent activation of
CD22-null B cells in vivo, and for their enhanced activation in vitro when
mIg is ligated." (Smith KG, Tarlinton DM, Doody GM, Hibbs ML, Fearon DT. J
Exp Med. 1998 Mar 2;187(5):807-11.).

Although I could not find data about interaction of CD22 and B220, if this
interaction would occur, it would not be a surprise or unexpected for me,
as this would be yet another way for B cell activation to be regulated.
B220 expressed on T cells could interact with CD22 on B cells, or even both
molecules could be expressed on B cells.

Finally, according to the current knowledge it does not seem that B cells
express B220 in order to interact with CD22. 



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