View source for 18273579. MODULATION OF A PATHOGENIC PHENOTYPE IN TH1 CELLS simplified abstract (THE REGENTS OF THE UNIVERSITY OF CALIFORNIA)

=MODULATION OF A PATHOGENIC PHENOTYPE IN TH1 CELLS=


==Organization Name==

[[:Category:THE REGENTS OF THE UNIVERSITY OF CALIFORNIA|THE REGENTS OF THE UNIVERSITY OF CALIFORNIA]]


[[Category:THE REGENTS OF THE UNIVERSITY OF CALIFORNIA]]

==Inventor(s)==

[[:Category:Vijay K. Kuchroo of Boston MA (US)|Vijay K. Kuchroo of Boston MA (US)]][[Category:Vijay K. Kuchroo of Boston MA (US)]]

[[:Category:Ramnik Xavier of Cambridge MA (US)|Ramnik Xavier of Cambridge MA (US)]][[Category:Ramnik Xavier of Cambridge MA (US)]]

[[:Category:Mathias Pawlak of Boston MA (US)|Mathias Pawlak of Boston MA (US)]][[Category:Mathias Pawlak of Boston MA (US)]]

[[:Category:David Detomaso of Oakland CA (US)|David Detomaso of Oakland CA (US)]][[Category:David Detomaso of Oakland CA (US)]]

[[:Category:Nir Yosef of Oakland CA (US)|Nir Yosef of Oakland CA (US)]][[Category:Nir Yosef of Oakland CA (US)]]

==MODULATION OF A PATHOGENIC PHENOTYPE IN TH1 CELLS - A simplified explanation of the abstract==


This abstract first appeared for US patent application 18273579 titled 'MODULATION OF A PATHOGENIC PHENOTYPE IN TH1 CELLS

==Simplified Explanation==

The subject matter of this patent application is focused on pathogenic Th1 cells that rely on IL-23R signaling for their phenotype. The application discloses specific therapeutic targets and gene programs for Th1 cells, with a particular emphasis on the inhibition of CD160 to reduce Th1 cell pathogenicity.

* Th1 cells are a type of T helper cell involved in immune responses.
* IL-23R signaling plays a crucial role in determining the phenotype of pathogenic Th1 cells.
* The patent application identifies CD160 as a potential therapeutic target for reducing Th1 cell pathogenicity.

== Potential Applications ==
The technology described in this patent application could be applied in the development of new therapies for autoimmune diseases and inflammatory conditions where pathogenic Th1 cells play a role.

== Problems Solved ==
This technology addresses the need for more targeted and effective treatments for conditions involving pathogenic Th1 cells, by identifying specific therapeutic targets and gene programs that can modulate their pathogenicity.

== Benefits ==
The benefits of this technology include the potential for more precise and personalized treatments for autoimmune diseases and inflammatory conditions, leading to improved patient outcomes and reduced side effects compared to current therapies.

== Potential Commercial Applications ==
One potential commercial application of this technology could be the development of novel therapeutics targeting pathogenic Th1 cells for autoimmune diseases and inflammatory conditions.

== Possible Prior Art ==
Prior research has identified various signaling pathways and molecules involved in the regulation of Th1 cell function and pathogenicity, but the specific targeting of CD160 to reduce Th1 cell pathogenicity may be a novel aspect of this patent application.

=== Unanswered Questions ===

== How does the inhibition of CD160 specifically reduce Th1 cell pathogenicity? ==
The mechanism by which CD160 inhibition leads to a reduction in Th1 cell pathogenicity is not clearly explained in the abstract. Further research or data may be needed to elucidate this mechanism.

== Are there any potential side effects or unintended consequences of targeting CD160 in Th1 cells? ==
The abstract does not mention any potential side effects or unintended consequences of inhibiting CD160 in Th1 cells. Additional studies or clinical trials may be necessary to assess the safety and efficacy of this approach.


==Original Abstract Submitted==

The subject matter disclosed herein is generally directed to pathogenic Th1 cells whose phenotype is dependent on IL-23R signaling. Th1 cell specific therapeutic targets and gene programs are disclosed herein. In particular, inhibition of CD160 reduces Th1 cell pathogenicity.



[[Category:A61K38/17]]
[[Category:A61P37/02]]
[[Category:C12N5/0783]]
[[Category:C12N9/22]]