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<h2>New FOXP3Δ2 (Exon 2 Deleted) Specific Antibody</h2>by Stephen Jones 
 
FOXP3 
is a master regulator of immune homeostasis expressed specifically in CD4+ 
CD25+ T regulatory cells controlling their growth, development and 
function.  FOXP3 significance in the 
normal development of Tregs is better elucidated with the fact that mutated 
FOXP3 results in a rare and fatal early onset autoimmune disorder in humans 
called XLAAD/IPEX (human immune dysregulation, polyendocrinopathy, enteropathy, 
X-linked syndrome), a condition phenotypically similar to Scurfy in 
mice.  <o:p /> 
 
 
 
FOXP3 
is primarily an oligomeric, transcriptional repressor protein that belongs to 
the P subfamily of forkhead (FKH)-winged helix family of transcriptional factors. 
Members of this subfamily are forkhead (FKH) box proteins characterized by the 
presence of a highly conserved C-terminal winged-helix/FKH DNA binding domain 
(DBD) and centrally-located C2H2 zinc finger domain and leucine zipper domain.  Apart from these, an additional N-terminal 
proline rich region is present in FOXP3, whose function is yet to be 
understood. Studies have shown that FOXP3 is a nuclear-localized protein that 
specifically trans-represses NF-AT-induced expression of cytokines and other transcriptional 
factors in Tregs including IL-2, IL-4, IFN-gamma and NF-κB.<o:p /> 
 
 
 
However, 
FOXP3 is not the sole master switch regulating the origin and development of 
CD4+ CD25+ Tregs. Studies have confirmed the existence of 
splice variant forms FOXP3 that are specifically expressed in humans but are 
lacking in mouse. Cloning and RT-PCR analysis from mRNA of CD4+ CD25+ 
T regulatory cells (Allan et. al, Smith et. al) has shown that these cells 
express two different alternatively spliced variant forms of FOXP3. While the 
FOXP3Δ2 variant had a deleted 105bp exon2 region, there was another FOXP3Δ2, Δ7 
variant that had an additional 81bp exon7 deletion apart from exon2 deletion. 
The predicted molecular weight of this FOXP3Δ2 is ~4KDa lower than the 
molecular weight of FOXP3.  Transient 
transfection assays using Jurkat cells suggest that the FOXP3Δ2 is novel splice 
variant that functions as a transcriptional repressor protein and acts in 
cohort with FOXP3 causing a significant suppression of cytokines and 
up-regulating the expression of various Treg-associated markers. <o:p /> 
 
 
 
The 
existence of the splice variant forms of FOXP3 protein suggests an additional 
level of complexity related to the biology of FOXP3.  A lot research needs to be done so as to 
elucidate the physiological and functional importance of FOXP3 splice variant 
forms towards maintaining immune homeostasis in Tregs and preventing autoimmune 
disorders. <o:p /> 
 
 
 
Continuing 
its efforts towards supporting research on FOXP3, IMGENEX has come up with an 
antibody that specifically recognizes the FOXP3Δ2 splice variant. <o:p /> 
 
 
<h3>About the Author</h3>

IMGENEX India Pvt Ltd. the only biotech company in Orissa
and one of its kinds in <st1:place w:st="on">Eastern India</st1:place>. IMGENEX
India started in Oct as an outsourcing branch of <a href="http://www.imgenex.com">IMGENEX
Corporation</a> , <st1:place w:st="on"><st1:city w:st="on">San Diego</st1:city>,
 <st1:country-region w:st="on">USA</st1:country-region></st1:place>.  Find out more information about  <a href="http://www.imgenex.com/sa_details.php?id=17">FOXP3</a> .

<o:p> </o:p>

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