Why Im excited!

In a nutshell ...basically research has stumbled upon why 1102 was so effective and the significance of its reduction of B cells.
Believe it or not this new body of evidence has just pushed 1102 to the forefront of this field of focus.

The company has given us enough clues to understand this significant development but this has been missed by most when you consider people are selling sub 5c and we are soooo close to a major licensing transaction, imo.

http://www.neurology.org/content/early/2014/09/19/WNL.0000000000000926.full.html

ATL1102 treatment reduced the number of circulating
CD191 (pre) B cells (53%) and granulocytes
(43%) at 8 weeks compared to treatment with placebo;
T cells were less significantly reduced (;25%), but
ATL1102 treatment had no effect on monocyte or
NK lymphocyte numbers14 (appendix e-2). VLA-4
has a role in the maturation, apoptosis, activation,
adhesion, and migration of B and T cells.20–25
ATL1102 may be having an effect on one or more
of these activities on CD191 (pre) B and T cells
within the lymphoid tissues of patients with RRMS,
thereby reducing leukocyte number and activity in
blood, and in turn the CNS, and subsequently reducing
the number and volume of MS brain lesions in this
RRMS study.
Natalizumab interferes with transmigration of
VLA-41 leukocytes and disproportionately increases
circulating B cells more than other lymphocytes and
monocytes in blood of patients with RRMS.26,27 The​

44% of disease-free natalizumab-treated patients with

RRMS are characterized by a substantial reduction of
CD191 B cells, particularly the CD51 subset, and
plasmablasts in the CNS.28 The therapeutic effects of
CD20 antibodies that deplete CD201 blood B cells
also point to the importance of reducing proinflammatory​

B cells in CNS in RRMS.29"

B Cells Can Drive Inflammation in MS
http://www.the-scientist.com/?artic...9/title/B-Cells-Can-Drive-Inflammation-in-MS/

A type of B cell that produces the inflammation-inducing cytokine granulocyte macrophage–colony stimulating factor (GM-CSF) may be key to driving disease-causing inflammation and relapses in multiple sclerosis (MS), according to research published today (October 21) in Science Translational Medicine. The results of the study, in which researchers examined blood samples from MS patients, suggest a possible mechanism as to why B cell-targeted therapies have been found to be efficacious for the disease.
“This is an important paper and among the first to study the role of B cells in MS, which has predominantly been studied from a T cell perspective,” said Claudia Mauri, a professor of immunology at the University College London who was not involved in the work.