The patent badge is an abbreviated version of the USPTO patent document. The patent badge does contain a link to the full patent document.

The patent badge is an abbreviated version of the USPTO patent document. The patent badge covers the following: Patent number, Date patent was issued, Date patent was filed, Title of the patent, Applicant, Inventor, Assignee, Attorney firm, Primary examiner, Assistant examiner, CPCs, and Abstract. The patent badge does contain a link to the full patent document (in Adobe Acrobat format, aka pdf). To download or print any patent click here.

Patent No.:

US 9546207 B1

PDF
Full Text
Expired
Date of Patent:
Jan. 17, 2017

Filed:

Sep. 16, 2013
Applicant:

Yissum Research Development Company of the Hebrew University of Jerusalem Ltd., Jerusalem, IL;

Inventors:

Raymond Kaempfer, Jerusalem, IL;

Gila Arad, Mevasseret Zion, IL;

Attorney:
Primary Examiner:
Int. Cl.
CPC ...
C07K 16/28 (2006.01); C07K 14/74 (2006.01); A61K 39/395 (2006.01); C07K 14/705 (2006.01);
U.S. Cl.
CPC ...
C07K 14/70521 (2013.01);
Abstract

Disclosed are methods and compositions for the inhibition of modulation of T cell costimulatory pathway by a pathogenic agent, particularly, the inhibition of activation of a T cell costimulatory pathway by a pyrogenic exotoxin. The direct interaction of a superantigen with a specific site within the dimer interface of a CD28 family member is inhibited using immunomodulatory peptides. Specific antagonist immunomodulatory peptides comprise amino acid sequences derived from a dimer interface of a T cell co-stimulatory pathway member, or peptides which comprise an amino acid sequence which specifically binds to an amino acid sequence within the dimer interface of a T cell co-stimulatory pathway member. Compositions comprising said peptides and methods for the treatment of immune-related disorders are also disclosed. Such molecules may be used in screening for a test substance which specifically binds to the CD28 molecule and is capable of antagonizing pyrogenic exotoxin-mediated activation of Th1 lymphocytes.


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