Dale L Greiner, Age 7298 Mount Jefferson Rd, Hubbardston, MA 01452

8431767, Apr 30, 2013

Nov 9, 2010

12/942666

Leonard D. Shultz - Bar Harbor ME, US
Dale L. Greiner - Hubbardston MA, US

The Jackson Laboratory - Bay Harbor ME
University of Massachusetts Medical School - Worcester MA

G01N 33/00
A01K 67/00
A01K 67/033
A01K 67/027

800 3, 800 13, 800 14, 800 18

Transgenic immunodeficient non-human animals according to embodiments of the present invention are described which include in their genome a nucleic acid encoding xenogeneic Stem Cell Factor operably linked to a promoter. Administration of xenogeneic hematopoetic stem cells to the inventive transgenic animals results in engraftment of the xenogeneic hematopoetic stem cells and xenogeneic leukocytes are produced in the animals, without conditioning such as without conditioning by irradiation and without conditioning by a radiomimetic agent.

2005011, May 26, 2005

Sep 2, 2004

10/933933

Dale Greiner - Hubbardston MA, US
John Mordes - Newton MA, US
Aldo Rossini - Sudbury MA, US
Edward Seung - Medford MA, US

A61K039/395

424144100, 424093700

The invention relates to the methods for producing hematopoietic chimerism and central tolerance by peripheral tolerance induction without myeloablative conditioning.

2005012, Jun 9, 2005

Jun 7, 2004

10/863012

Aldo Rossini - Sudbury MA, US
Rita Bortell - Shirley MA, US
Dale Greiner - Hubbardston MA, US
John Mordes - Waban MA, US
Silvia Corvera - Westborough MA, US
Malini Pandarpurkar - Farmington Hills MI, US
Helle Markholst - Charlottenlund, DK
Lars Hornum - Kirke Eskilstrup, DK

C12Q001/68
C07H021/04
C12N009/64
A61K039/00

424277100, 435006000, 435069100, 435226000, 435320100, 435325000, 536023200

The present invention relates, at least in part, to methods of modulating apoptosis in cells, comprising contacting the cell with a compound that modulates the expression, post-translational modification, or activity of Ian4, leucine-rich protein of 130 kD, GRP78, GRP94, or hsp60. The subject methods can be used to treat a variety of different disorders, for example, autoimmune disease and neoplasia. The invention also pertains to methods for identifying compounds that modulates the activity of Ian-4, leucine-rich protein of 130 kD, GRP78, GRP94, or hsp60.

5869049, Feb 9, 1999

Apr 25, 1994

8/232929

Randolph J. Noelle - Cornish NH
Teresa M. Foy - Federal Way WA
Fiona H. Durie - Seattle WA
David C. Parker - Grafton MA
Dale L. Greiner - Hubbardston MA
Aldo A. Rossini - Sudbury MA
John P. Mordes - Newton MA

Trustees of Dartmouth College - Hanover NH
University of Massachusetts Medical Center - Worcester MA

A61K 39395
A61K 3702
A61K 3704

4241541

Methods for inducing antigen-specific T cell tolerance are disclosed. The methods involve contacting a T cell with: 1) a cell which presents antigen to the T cell, wherein a ligand on the cell interacts with a receptor on the surface of the T cell which mediates contact-dependent helper effector function; and 2) an antagonist of the receptor on the surface of the T cell which inhibits interaction of the ligand on the antigen presenting cell with the receptor on the T cell. In a preferred embodiment, the cell which presents antigen to the T cell is a B cell and the receptor on the surface of the T cell which mediates contact-dependent helper effector function is gp39. Preferably, the antagonist is an anti-gp39 antibody or a soluble gp39 ligand (e. g. , soluble CD40). The methods of the invention can be used to induce T cell tolerance to a soluble antigen or to an allogeneic cell.

2020035, Nov 19, 2020

May 28, 2020

16/886289

- Bar Harbor ME, US
- Boston MA, US
Dale L. Greiner - Hubbardston MA, US
Michael A. Brehm - Dudley MA, US

The Jackson Laboratory - Bar Harbor ME
University of Massachusetts - Boston MA

A01K 67/027
C12N 15/90
C07K 14/47
A61K 49/00

The present invention relates generally to genetically modified non-human animals and immunodeficient non-human animals characterized by restored complement-dependent cytotoxicity, as well as methods and compositions for assessment of therapeutic antibodies in the genetically modified immunodeficient non-human animals. In specific aspects, the present invention relates to immunodeficient non-obese diabetic (NOD), A/J, A/He, AKR, DBA/2, NZB/B1N, B10.D2/oSn and other mouse strains genetically modified to restore complement-dependent cytotoxicity which is lacking in the unmodified immunodeficient mice. In further specific aspects, the present invention relates to NOD.Cg-PrkdcIL2re/SzJ (NSG), NOD.Cg-Rag1Il2rg/SzJ (NRG) and NOD.Cg-PrkdcIl2rg/JicTac (NOG) mice genetically modified to restore complement-dependent cytotoxicity which is lacking in unmodified NSG, NRG and NOG mice. Methods for assessment of therapeutic antibodies or putative therapeutic antibodies in the genetically modified immunodeficient mice characterized by an intact complement system are provided according to specific aspects of the present invention.

2020023, Jul 30, 2020

Aug 9, 2018

16/637621

- Bar Harbor ME, US
- Worcester MA, US
Dale L. Greiner - Hubbardston MA, US

The Jackson Laboratory - Bar Harbor ME
University of Massachusetts Medical School - Worcester MA

A01K 67/027
A61K 49/00

An immunodeficient mouse is provided which is useful as a model of functions and regulation of human natural killer (NK) cells and other interleukin 15 (IL-15)-dependent cell populations and processes in studies of human immunity, cancer, infectious diseases, and other areas. According to specific aspects, an immunodeficient mouse is provided which is genetically modified to express human interleukin 15, wherein the mouse does not have or produce functional mouse natural killer cells, and wherein the mouse is modified to include human natural killer cells. Methods of identifying anti-tumor activity of a test substance using a mouse of the present invention are described along with methods of making the mouse.

2020006, Feb 27, 2020

May 14, 2018

16/612450

- Bar Harbor ME, US
- Boston MA, US
Dale L. Greiner - Hubbardston MA, US
Leonard D. Shultz - Bar Harbor ME, US

The Jackson Laboratory - Bar Harbor ME
University of Massachusetts - Boston MA

A01K 67/027

A NOD.Cg-PrkdcH2rg/SzJ.(NOD-scid-IL2rγ, NSG) mouse which is genetically modified such that the en NSG mouse lacks functional major histocompatibility complex I (MHC I) and lacks functional major histocompatibility complex II (MHC II) is provided according to aspects of the present, invention. According to specific aspects the genetically modified NSG mouse, is a NOD.Cg-PrkdcH2-K1H2-Ab1H2-D1H2rg/SzJ (NSG-KD)(IA)) mouse, NSG-RIP-DTR (KD)(IA) mouse, or a NOD.Cg-B2mPrKdcH2H2rg/SzJ (NSG-B2M(IA IE)) mouse. Human, immune cells and/or human: tumor cells are administered to a genetically modified immunodeficient mouse according to aspects described herein and assays of one or more test substances can be performed using the provided mice.

2019032, Oct 24, 2019

Nov 30, 2017

16/465006

- Bar Harbor ME, US
- Boston MA, US
Dale L. Greiner - Hubbardston MA, US
Michael A. Brehm - Dudley MA, US

The Jackson Laboratory - Bar Harbor ME
University of Massachusetts - Boston MA

A01K 67/027
A61K 49/00

A genetically-modified, immunodeficient mouse is provided along with methods of use, wherein the mouse includes (a) a nucleotide sequence encoding human stem cell factor (hSCF); (b) a nucleotide sequence encoding human granulocyte-macrophage colony-stimulating factor (hGM-CSF); (c) a nucleotide sequence encoding human interleukin-3 (hIL-3); and (d) a nucleotide sequence encoding human colony-stimulating factor 1 (hCSF1), wherein each of the nucleotide sequences is operably linked to a promoter, and wherein the genetically-modified, immunodeficient mouse expresses hSCF, hGM-CSF, hIL-3, and hCSF1, wherein the genetically-modified, immunodeficient mouse allows engraftment of human hematopoietic stem cells along with engraftment of human-patient derived tumor xenografts and/or human tumor cell lines to enable in vivo investigation of the interactions between the human immune system and human cancer.