Finding and treatment of inflammation after birth in chimeric animal

US11856927B2 · US · B2

Patent metadata
FieldValue
Publication numberUS-11856927-B2
Application numberUS-201816480169-A
CountryUS
Kind codeB2
Filing dateJan 25, 2018
Priority dateJan 25, 2017
Publication dateJan 2, 2024
Grant dateJan 2, 2024

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  1. Title

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  2. Abstract

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  3. Assignees and inventors

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  4. Key dates

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  5. First independent claim

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  6. CPC / IPC classifications

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  7. Citations and related patents

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Abstract

Official abstract text for this publication.

The present invention has found that chimeric animals suffer from noticeable inflammation after birth, though neither immune response nor inflammation in the fetal period of these animals has been reported hitherto. This is an unexpected finding since chimeric animals in the fetal period were exclusively analyzed in prior studies and thus it is deemed that immunotolerance has been theoretically established therein. The present invention provides a composition for suppressing immune response or inflammation in the fetal period of a born chimeric animal.

First claim

Opening claim text (preview).

The invention claimed is: 1. A method for obtaining an adult individual from a xenogeneic or allogeneic chimeric animal fetus individual, the method comprising: providing a xenogeneic or allogeneic chimeric animal fetus individual that shows no substantial inflammation; obtaining an adult individual from the fetus individual by growing the fetus individual; and administering an effective amount of an anti-inflammatory agent or an immunosuppressive agent to the individual before the birth of the individual and/or after the birth, wherein the effective amount is sufficient to suppress inflammation after the birth of the individual. 2. The method according to claim 1 , wherein the anti-inflammatory agent or the immunosuppressive agent is administered before occurrence of immune response or inflammation in the individual. 3. The method according to claim 1 , further comprising: confirming that the immune response or the inflammation has occurred in the epidermis of the born individual; and administering the anti-inflammatory agent or the immunosuppressive agent to the individual thus confirmed to have the immune response or the inflammation. 4. The method according to claim 1 , wherein the individual induces inflammation after its birth. 5. The method according to claim 1 , wherein the individual is immunodeficient. 6. The method according to claim 5 , wherein the immunodeficiency is associated with a genetic modification or an abnormality in any one or more members selected from Interleukin 2 receptor subunit gamma (IL2Rg), recombination-activating gene 1 (RAG1), recombination-activating gene 2 (RAG2), forkhead box protein N1 (Foxn1), protein kinase, DNA-activated, catalytic subunit (PRKDC), major histocompatibility complex (MHC) and signal-regulatory protein alpha (SIRPa). 7. The method according to claim 2 , wherein the individual induces inflammation after its birth. 8. The method according to claim 2 , wherein the individual is immunodeficient. 9. The method according to claim 8 , wherein the immunodeficiency is associated with a genetic modification or an abnormality in any one or more members selected from Interleukin 2 receptor subunit gamma (IL2Rg), recombination-activating gene 1 (RAG1), recombination-activating gene 2 (RAG2), forkhead box protein N1 (Foxn1), protein kinase, DNA-activated, catalytic subunit (PRKDC), major histocompatibility complex (MHC) and signal-regulatory protein alpha (SIRPa). 10. The method according to claim 3 , wherein the individual induces inflammation after its birth. 11. The method according to claim 3 , wherein the individual is immunodeficient. 12. The method according to claim 11 , wherein the immunodeficiency is associated with a genetic modification or an abnormality in any one or more members selected from Interleukin 2 receptor subunit gamma (IL2Rg), recombination-activating gene 1 (RAG1), recombination-activating gene 2 (RAG2), forkhead box protein N1 (Foxn1), protein kinase, DNA-activated, catalytic subunit (PRKDC), major histocompatibility complex (MHC) and signal-regulatory protein alpha (SIRPa).

Assignees

Inventors

Classifications

  • Chimeric vertebrates, e.g. comprising exogenous cells · CPC title

  • substituted in position 21, e.g. cortisone, dexamethasone, prednisone or aldosterone · CPC title

  • Immunosuppressants, e.g. drugs for graft rejection · CPC title

  • Animals comprising random inserted nucleic acids (transgenic) · CPC title

  • inducing loss of function, i.e. knock out · CPC title

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What does patent US11856927B2 cover?
The present invention has found that chimeric animals suffer from noticeable inflammation after birth, though neither immune response nor inflammation in the fetal period of these animals has been reported hitherto. This is an unexpected finding since chimeric animals in the fetal period were exclusively analyzed in prior studies and thus it is deemed that immunotolerance has been theoretically…
Who is the assignee on this patent?
Univ Tokyo
What technology area does this patent fall under?
Primary CPC classification A01K67/0271. Mapped technology areas include Human Necessities.
When was this patent published?
Publication date Tue Jan 02 2024 00:00:00 GMT+0000 (Coordinated Universal Time) (B2). Legal status and post-grant events are not shown on this page.
What related patents are in patentsdb?
We list 1 related publication on this page (citations in our corpus or others sharing the same primary CPC).