I think there is a lot of validity to this therapy.
It seems that people that have MS have a defect in a certain type of immune cell that regulates the immune system and prevents autoimmunity.
These cells are known as regulatory Tcells or Tregs, and express a certain protein called FoxP3:http://www.jimmunol.org/cgi/content/meeting_abstract/182/1_MeetingAbstracts/99.3
Persistence of FOXP3 expression is impaired in RR-MS Tregs
Impaired Treg function may contribute to the development of Multiple Sclerosis (MS)....We examined the pSTAT5 levels of CD4+CD25+Treg from relapsing remitting MS and control subjects in response to low-dose IL-2. We found that, despite equivalent levels of CD25, pSTAT5 was lower in RR-MS subjects (p= 0.0013), indicating a mechanism by which FOXP3 expression and Treg function may be lost in MS.....Taken together we conclude that the impaired persistence of FOXP3 expression in aTreg may impact the number and function of Tregs in individuals with RR-MS.
So, the Helminth therapy appears to increase the development/function of these Tregs:http://www.plosntds.org/article/info%3Adoi%2F10.1371%2Fjournal.pntd.0001383
Induction of CD4+CD25+FOXP3+ Regulatory T Cells during Human Hookworm Infection Modulates Antigen-Mediated Lymphocyte Proliferation
Our results showed that hookworm infection induce an augmentation of Tregs in the peripheral blood, followed by the higher levels of circulating Treg cells expressing several markers and cytokines associated with cell regulation (CTLA-4, GITR, IL-10, TGF-β and IL-17). We also demonstrated that in vitro depletion of Tregs partially enhanced the naturally impaired cellular proliferation of lymphocytes from infected individuals after antigenic stimulation. Our results suggest that Treg cells may play an important role in hookworm-induced immunosuppression, contributing to the longevity of hookworm survival in infected people.