CXCL9

CXCL9
식별자
에일리어스	CXCL9, CMK, Humig, MIG, SKYB9, crg-10, C-X-C 모티브 케모카인 배위자 9
외부 ID	OMIM : 601704 HomoloGene : 1813 GenCard : CXCL9
유전자 위치(인간)
크르.	4번 염색체(인간)
끝.	76,007,509 bp
RNA발현패턴
	상단 표시 위치:
	부록; ; 림프절; ; 천측두동맥; ; 직장; ; 안검결막; ; 담낭; ; 두정 흉막; ; 흉선; ; 생식 상피; ; 흉선;
	없음
	추가 참조 표현식 데이터
	추가 참조 표현식 데이터
유전자 존재론
분자 함수	사이토카인 활성; CXCR3케모카인수용체결합; 케모카인 활성; 단백질 결합;
셀룰러 컴포넌트	세포외 영역; 혈장막외측; 세포외 공간; 세포내 해부학적 구조;
생물학적 과정	G단백질결합수용체신호경로; 케모카인결합신호경로; 세포신호; 세포에 격리된 칼슘 이온 방출의 양성 조절; cAMP 매개 시그널링의 양성 조절; 주화성; 백혈구 주화성 양성 조절; 세포방어반응; 근아세포융합양조절; 리포다당류에 대한 반응; 세포군 증식 조절; 근아세포 분화의 양성 조절; 바이러스에 대한 방어 반응; 면역 반응; 신호 변환; 방위 응답; 염증 반응; T세포주화성; 항균펩타이드에 의해 매개되는 항균성 체액 면역 반응; 신호수용체활성조절; 아데닐산시클라아제활성화G단백질결합수용체신호경로; 세균에 대한 반응; 호중구 주화성; 백혈구 주화성; 리포다당류에 대한 세포반응;
	출처:아미고 / QuickGO
맞춤법
	4283
	없음
	ENSG00000138755
	없음
	Q07325
	없음
	NM_002416
	없음
	NP_002407
	없음
	위키데이터
인간 보기/편집

케모카인(C-X-C 모티브) 리간드 9(CXCL9)는 CXC 케모카인 패밀리에 속하는 작은 사이토카인으로 감마인터페론(MIG)에 의해 유도되는 모노카인으로도 알려져 있다.CXCL9은 화학작용을 유도하고 백혈구의 분화와 증식을 촉진하며 조직발생을 ^[3]일으키는 역할을 하는 케모카인 중 하나이다.

CXCL9/CXCR3 수용체는 면역 세포의 이동, 분화 및 활성화를 조절합니다.면역반응성은 세포독성 림프구(CTL), 자연살해세포(NK), NKT세포, 대식세포와 같은 면역세포의 신병을 통해 발생한다.또한 Th1 분극은 IFN-α에 ^[4]반응하여 면역세포를 활성화시킨다.종양 투과 림프구는 체크포인트 억제제에 ^[5]대한 반응 예측과 임상 결과를 위한 핵심이다.생체 내 연구에 따르면 축은 종양 증식과 ^{[citation needed]}전이를 증가시킴으로써 종양 발생적 역할을 한다.CXCL9은 주로 림프구 침투를 국소 부위에 매개하고 종양 ^[6]성장을 억제한다.

그것은 CXCL10과 CXCL11이라고 불리는 두 개의 다른 CXC 케모카인과 밀접하게 관련되어 있다. CXCL9, ^[7]^[8]CXCL10, CXCL11은 모두 수용체 CXCRine과 상호작용함으로써 화학작용을 유도한다.

바이오마커

CXCL9, -10, -11은 심부전 및 좌심실 기능 장애의 발달에 유효한 바이오마커로 입증되었으며, 이는 이러한 화학 물질의 수치와 부정적인 ^[10]^[11]심장 리모델링의 발달 사이에 병태 생리학적 관계가 있음을 시사한다.

이 케모카인은 Q열 ^[12]감염을 진단하기 위한 바이오마커로도 알려져 있다.

상호 작용

CXCL9은 CXCR3과 ^[13]^[14]상호작용하는 것으로 나타났습니다.

면역반응에서의 CXCL9

면역세포 분화의 경우 CXCL9가 CXCR3를 ^[15]통해 Th1 분극으로 이어진다는 보고도 있다.Zohar 등의 생체내 모델에서는 CXCL9가 T-bet 및 RORγ의 전사를 증가시켜 STAT1, STAT4, STAT5 ^[15]인산화 과정을 통해 순진한 T세포로부터 Foxp3⁻ 타입 1 조절세포(Tr1) 또는 T 도우미 17(Th17)의 분극으로 이어졌다.

여러 연구에서 종양 관련 대식세포(TAM)가 TME에서 조절 활동을 하고 CXCL9/CXCR3 축이 TAMs 분극에 영향을 미치는 것으로 나타났다.TAMs는 항종양 활성의 경우 M1, 항종양 활성의 경우 M2 등 반대의 효과가 있습니다.오구무 외 연구진은 CXCR3 결핍 생쥐가 쥐 유방암 모델에서 IL-4 생성과 M2 분극이 증가하고 선천적 및 면역세포 매개 항종양 반응이 ^[16]감소했음을 명확히 했다.

면역세포 활성화를 위해 CXCL9은 Th1 분극과 활성화를 통해 면역세포를 자극한다.Th1 세포는 IFN-γ, TNF-α, IL-2를 생성하며 CTL, NK 세포 및 ^[17]대식세포를 자극하여 항종양 면역력을 강화한다.IFN 의존성 면역 활성화 루프는 CXCL9 방출도 ^[3]촉진합니다.

Th1, CTLs, NK 세포, NK 세포와 같은 면역 세포는 종양 ^[6]모델에서 파라크린 CXCL9/CXCR3를 통해 암세포에 대한 항종양 효과를 보인다.암세포의 자가분비 CXCL9/CXCR3 시그널링은 암세포의 증식, 혈관신생 및 ^{[citation needed]}전이를 증가시킨다.

CXCL9/CXCR3 및 PDL-1/PD-1

CXCL9/CXCR3와 PDL-1/PD-1의 관계는 중요한 연구 영역이다.프로그램 세포사망-1(PD-1)은 말초혈액에 존재하는 T세포보다 종양부위의 T세포에서 많이 발현되며 항PD-1 치료는 면역탈출 및 면역활성화를 ^[18]억제할 수 있다.Peng 등은 항PD-1이 T세포 매개 종양 퇴행뿐만 아니라 골수 유래 ^[18]세포에 의한 IFN-γ의 발현을 증가시킬 수 있다는 것을 보여주었다.T세포에서 PDL-1/PD-1 축을 차단하면 CXCL9/CXCR3 축을 통해 종양 부위에서 양성 피드백 루프를 트리거할 수 있다.또한 항CTLA4 항체를 사용하여 이 축은 ipilimumab 투여 ^[19]후 임상 반응이 양호한 환자의 전처리 흑색종 병변에서 유의하게 상향 조절되었다.

CXCL9 및 흑색종

또한 CXCL9은 전이성 ^[20]흑색종에서 T세포 전이 요법의 후보 바이오마커로 확인되었다.TME에서 CXCL9/CXCR3의 역할과 면역반응 - 이는 파라크린 시그널링을 통한 면역활성화에 중요한 역할을 하며 암 ^[3]치료의 효과에 영향을 미친다.

레퍼런스

^ ^a ^b ^c GRCh38: 앙상블 릴리즈 89: ENSG00000138755 - 앙상블, 2017년 5월
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추가 정보

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외부 링크

UCSC 게놈 브라우저의 인간 CXCL9 게놈 위치 및 CXCL9 유전자 세부 정보 페이지.

[refGRCh38Ensembl-1] GRCh38: 앙상블 릴리즈 89: ENSG00000138755 - 앙상블, 2017년 5월

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