Therapeutic agent for autoimmune diseases or allergy, and method for screening for the therapeutic agent

a technology for autoimmune diseases or allergies, applied in the field of pharmaceutical composition, can solve problems such as tissue damage and direct damage to tissues

Inactive Publication Date: 2012-12-20
OSAKA UNIV
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  • Summary
  • Abstract
  • Description
  • Claims
  • Application Information

AI Technical Summary

Problems solved by technology

As a result, the immune system acts on the body's own tissue, causing tissue damage.
For example, it is believed that in chronic rheumatoid arthritis and multiple sclerosis, activated T-cells specific to a self-antigen or self-MHC complex cause localized inflammation by activating macrophages, and may even damage tissues directly.

Method used

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  • Therapeutic agent for autoimmune diseases or allergy, and method for screening for the therapeutic agent
  • Therapeutic agent for autoimmune diseases or allergy, and method for screening for the therapeutic agent
  • Therapeutic agent for autoimmune diseases or allergy, and method for screening for the therapeutic agent

Examples

Experimental program
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Effect test

example 1

Methods

Mice

[0220]Plexin-A1− / −, Sema3K− / −, Sematic− / − and NP-1 knock-in mice with a C57BL / 6 background have already been established. OT-IITg mice were provided by Mr. W. R. Heath.

[0221]For the Sema6D− / −, a 0.6 kbp fragment comprising the second exon with start codon and the third exon were replaced with a neo resistance cassette, and a herpes simplex virus thymidine kinase (HSY-TK) gene was inserted for selecting a targeting vector from random integration. Linearized targeting plasmid DNA was transfected into embryonic stem (ES) cells by electroporation. After double selection with G418 and ganciclovir, 320 resistant clones were screened for homologous recombination of Sema6D alleles by PCR and Southern blot analysis. For the Southern blot analysis, genome DNA was isolated from wild-type and Sema6D-target ES cells and digested with EcoRI, and separated by agarose gel electrophoresis. The DNA was transferred to a nylon blotting membrane (HybondN) in accordance with the manufacturer's...

example 2

[0302]To evaluate the role of Plexin-A1 in cell migration in vivo, dendritic cells collected from wild-type or Plexin-A1 knockout mice and labeled with CFSE were adoptively transferred into the dermis of mice treated with oxazolone. The behavior of the transferred dendritic cells was then monitored.

[0303]Adoptive transfer was performed by the following methods. Dendritic cells from bone marrow were labeled for 10 minutes at 22° C. in 5 μl of CFSE (carboxyfluorescein diacetate succinimidyl ester). The cells were then washed with PBS. 1×106 dendritic cells suspended in PBS were subcutaneously injected into the foot pads of recipient mice. 24 and 48 hours after injection, the popliteal lymph nodes were collected. The lymph nodes were treated for 30 minutes at 37° C. with 1 mg / ml of collagenase D. The cell numbers were counted and analyzed by flow cytometry. As described in Cavanagh et al. (Nat. Immunol. (2005) 6, 1029-1037), the percentage of migrating dendritic cells corresponds to th...

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Abstract

Disclosed is a therapeutic agent for treating a cellular immune disease, comprising as an active ingredient a substance that inhibits binding between Sema3A and a Neuropilin-1 / Plexin-A1 heteroreceptor. The substance includes, for example, a Sema3A neutralizing antibody, a Neuropilin-1 neutralizing antibody, or a soluble Neuropilin-1 or derivative thereof. Also disclosed is a method for screening a therapeutic agent for treating a cellular immune disease utilizing a signal generated by the interactions of Neuropilin-1, Plexin-A1 and Sema3A as a marker.

Description

TECHNICAL FIELD[0001]1. Related Application[0002]This application claims priority from Japanese Patent Application No. 2009-254108 (filed on Nov. 5, 2009), contents of which are incorporated herein by reference.[0003]2. Technical Field[0004]The present invention relates to a pharmaceutical composition for preventing or treating autoimmune diseases or allergies, comprising as an active ingredient a substance effective for treating autoimmune diseases or allergies that inhibits binding between NP-1 and Sema3A, such as a Neuropilin-1-Fc (NP-1-Fc), Neuropilin-1 (NP-1) neutralizing antibody, Semaphorin3A (Sema3A) neutralizing antibody or the like. The present invention further relates to a therapeutic method using the pharmaceutical composition, and to a method for screening such inhibitors.BACKGROUND ART[0005]Autoimmune diseases involve a specific and continuous adaptive immune response to a self-antigen. Unlike natural immunity and adaptive immunity to external antigens, which ultimate...

Claims

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Application Information

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Patent Type & Authority Applications(United States)
IPC IPC(8): C07K16/28C07K14/705G01N21/76C12N5/0784G01N33/566C07K16/18C07K19/00
CPCC07K16/18C07K16/2863C07K2317/34G01N33/53G01N33/566G01N2500/04A61P1/02A61P1/04A61P1/16A61P11/00A61P15/08A61P17/00A61P17/06A61P19/02A61P19/08A61P25/00A61P27/02A61P29/00A61P37/00A61P37/02A61P37/06A61P37/08A61P5/14A61P7/04A61P7/06A61P9/00A61P3/10
Inventor KUMANOGOH, ATSUSHI
Owner OSAKA UNIV
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