IP Library Granted Patent US 9,872,905
Granted Patent B2
US 9,872,905 · App. 13/512,754 · Granted Jan 23, 2018

Modulation of NK cell antigen specific effector activity by modulation of CXCR6 (CD186)

Inventors: Ulrich Von Andrian (Chestnut Hill, MA); Silke Paust (Jamaica Plain, MA)
Assignee: President and Fellows of Harvard College
A61K45/06A61K38/177A61K38/195A61K39/3955C07K16/2866C12Q1/025A61K2039/505
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Quick Facts
Patent No.
US 9,872,905
App. No.
13/512,754
Granted
Jan 23, 2018
Kind
B2
Abstract

The instant invention is based, at least in part, on the discovery that CXCR6 plays a critical role in antigen-specific effector function of NK cells. Accordingly, the invention provides, among other things, methods for modulation of antigen-specific NK cell effector function, methods for identifying modulators of antigen-specific NK cell effector function.

Claims (22)

1. A method of decreasing antigen-specific NK cell function in a subject comprising:

measuring antigen-specific NK cell function in the subject and comparing the level of antigen-specific NK cell function to an appropriate control; and

administering to the subject having an increased level of antigen-specific NK cell function a composition comprising an antibody, or antigen-binding fragment thereof, that binds to an extracellular domain of human CXCR6 and blocks the binding of CXCR6 to the extracellular domain of CXCL16, such that antigen-specific NK cell function is decreased.

2. A method of decreasing antigen-specific NK cell function in a subject having unwanted immune cell activation, comprising:

measuring antigen-specific NK cell function in the subject and comparing the level of antigen-specific NK cell function to an appropriate control; and

administering to the subject having an increased level of antigen-specific NK cell function a composition comprising an antibody, or antigen-binding fragment thereof, that binds to the extracellular domain of CXCL16 and blocks the binding of CXCL16 with an extracellular domain of CXCR6, such that antigen-specific NK cell function is decreased.

3. The method of claim 1 or 2 , wherein the subject has delayed-type hypersensitivity to an antigen or is at risk for developing delayed-type hypersensitivity to an antigen.

4. The method of claim 3 , wherein the antigen is a hapten.

5. The method of claim 3 , wherein the step of administering is performed after secondary exposure to the antigen and prior to the onset of a delayed-type hypersensitivity reaction.

6. The method of claim 3 , wherein the step of administering is performed after secondary exposure to the antigen and after onset of a delayed-type hypersensitivity reaction.

7. The method of claim 3 , wherein the step of administering is performed prior to secondary exposure to the antigen.

8. The method of claim 1 or 2 , wherein the subject suffers from an occupational allergy.

9. The method of claim 1 or 2 , wherein the step of administering is performed more than once.

10. The method of claim 1 or 2 , further comprising administration of an immunosuppressive agent that inhibits activation of T cells and/or B cells.

11. The method of claim 10 , wherein the subject does not respond adequately to said immunosuppressive agent when administered alone.

12. The method of claim 1 or 2 , wherein the subject has or is at risk for developing a deleterious immune response to an infectious agent.

13. The method of claim 12 , wherein the infectious agent is a virus.

14. The method of claim 12 , wherein the infectious agent is a bacteria.

15. The method of claim 12 , wherein the infectious agent is a virus selected from the group consisting of: hepatitis B virus, influenza virus, hepatitis C virus, varicella zoster, herpes virus, HIVI and HIV2.

16. A method of treating a subject having delayed-type hypersensitivity to an antigen, comprising:

administering to the subject (i) a composition comprising an antibody, or antigen-binding fragment thereof, wherein the antibody, or antigen-binding fragment thereof, is selected from the group consisting of an antibody, or antigen-binding fragment thereof, that binds to the extracellular domain of CXCR6 and blocks the binding of CXCR6 to CXCL16, and an antibody, or antigen-binding fragment thereof, that binds to the extracellular domain of CXCL16 and blocks the binding of CXCL16 to CXCR6; and (ii) a composition comprising an immunosuppressive agent that inhibits activation of T cells and/or B cells, wherein the immunosuppressive agent is not an antibody, or antigen-binding fragment thereof, that binds CXCR6 or CXCL16, such that hypersensitivity to the antigen is reduced.

17. The method of claim 16 , wherein the delayed-type hypersensitivity is due to an occupational allergy.

Assignments (3)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Aug 8, 2013
From: PAUST, SILKE; VON ANDRIAN, ULRICH H.
To: PRESIDENT AND FELLOWS OF HARVARD COLLEGE
Reel/Frame 030971/0541 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 5, 2013
From: PAUST, SILKE; VON ANDRIAN, ULRICH H.
To: PRESIDENT AND FELLOWS OF HARVARD COLLEGE
Reel/Frame 030741/0806 →
CONFIRMATORY LICENSE Recorded Aug 21, 2012
From: HARVARD UNIVERSITY
To: NATIONAL INSTITUTES OF HEALTH (NIH), U.S. DEPT. OF HEALTH AND HUMAN SERVICES (DHHS), U.S. GOVERNMENT
Reel/Frame 028819/0326 →
Continuity (2)
Provisional Application 61265669 · Dec 1, 2009
Related Publication 20130101597A1 · Apr 25, 2013