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{{infobox gene|geneid=2833}}
'''趋化因子受体CXCR3'''是G蛋白偶连的七跨膜域受体，化学式为：C1844H2896O500N494S21<ref>{{Cite web |title=Expasy - ProtParam |url=https://web.expasy.org/cgi-bin/protparam/protparam_bis.cgi?P49682@1-368@ |website=web.expasy.org |access-date=2026-02-10}}</ref>，可选择性地与CXC[[趋化因子]]（[[CXCL9]]，[[CXCL10]]，和[[CXCL11]]）结合<ref name=leo>{{cite journal | last1=Clark-Lewis | first1=Ian | last2=Mattioli | first2=Ivan | last3=Gong | first3=Jiang-Hong | last4=Loetscher | first4=Pius | title=Structure-function relationship between the human chemokine receptor CXCR3 and its ligands | journal=The Journal of Biological Chemistry | volume=278 | issue=1 | date=2003-01-03 | issn=0021-9258 | pmid=12417585 | doi=10.1074/jbc.M209470200 | doi-access=free | pages=289–295 }}</ref>。 CXCR3又称G蛋白偶联受体9(GPR9)和CD183。有两种变异的CXCR3受体。CXCR3－A与CXCL9， CXCL10，CXCL11结合；而CXCR3-B除了与CXCL9， CXCL10，CXCL11结合外还可以与[[CXCL4]]结合<ref>{{cite journal | last1=Lasagni | first1=Laura | last2=Francalanci | first2=Michela | last3=Annunziato | first3=Francesco | last4=Lazzeri | first4=Elena | last5=Giannini | first5=Stefano | last6=Cosmi | first6=Lorenzo | last7=Sagrinati | first7=Costanza | last8=Mazzinghi | first8=Benedetta | last9=Orlando | first9=Claudio | last10=Maggi | first10=Enrico | last11=Marra | first11=Fabio | last12=Romagnani | first12=Sergio | last13=Serio | first13=Mario | last14=Romagnani | first14=Paola | title=An alternatively spliced variant of CXCR3 mediates the inhibition of endothelial cell growth induced by IP-10, Mig, and I-TAC, and acts as functional receptor for platelet factor 4 | journal=The Journal of Experimental Medicine | volume=197 | issue=11 | date=2003-06-02 | issn=0022-1007 | pmid=12782716 | pmc=2193908 | doi=10.1084/jem.20021897 | doi-access=free | pages=1537–1549 }}</ref>。

== 表达 ==
CXCR3主要表达在[[T细胞]]、[[自然杀伤细胞]]活性上<ref name=qin/>，有的[[上皮细胞]]和一些[[内皮细胞]]也表达CXCR3。 I型[[辅助T细胞]]（Th1）优先表达CXCR3及[[CCR5]]<ref name=qin>{{cite journal | last1=Qin | first1=S. | last2=Rottman | first2=J. B. | last3=Myers | first3=P. | last4=Kassam | first4=N. | last5=Weinblatt | first5=M. | last6=Loetscher | first6=M. | last7=Koch | first7=A. E. | last8=Moser | first8=B. | last9=Mackay | first9=C. R. | title=The chemokine receptors CXCR3 and CCR5 mark subsets of T cells associated with certain inflammatory reactions | journal=The Journal of Clinical Investigation | volume=101 | issue=4 | date=1998-02-15 | issn=0021-9738 | pmid=9466968 | pmc=508621 | doi=10.1172/JCI1422 | doi-access=free | pages=746–754}}</ref>，而II型辅助T细胞（Th2）表达[[CCR3]]和[[CCR4]]。 CXCR3与配体结合后在诱导I型辅助T细胞（Th1）迁移的同时又阻止II型辅助T细胞（Th2）的迁徙。从而增强T细胞的分化效应。

== 信号传递 ==
CXCR3与其配体CXCL9， CXCL10，CXCL11的结合，能引起细胞钙离子的内流，启动肌醇磷脂3-激酶和丝裂原活化蛋白激酶（MAPK）<ref>{{cite journal | last1=Smit | first1=Martine J. | last2=Verdijk | first2=Pauline | last3=van der Raaij-Helmer | first3=Elisabeth M. H. | last4=Navis | first4=Marjon | last5=Hensbergen | first5=Paul J. | last6=Leurs | first6=Rob | last7=Tensen | first7=Cornelis P. | title=CXCR3-mediated chemotaxis of human T cells is regulated by a Gi- and phospholipase C-dependent pathway and not via activation of MEK/p44/p42 MAPK nor Akt/PI-3 kinase | journal=Blood | volume=102 | issue=6 | date=2003-09-15 | issn=0006-4971 | pmid=12750173 | doi=10.1182/blood-2002-12-3945 | pages=1959–1965 }}</ref>。详细的信号通路尚未确立，但与其他的趋化因子受体的信号传递有类似的激酶。

== 功能 ==
CXCR3调节[[白细胞]]迁徙。CXCR3与配体相互作用引起I型辅助T细胞（Th1）的迁移，并促进I型辅助T细胞（Th1）成熟。

== 疾病 ==
CXCR3可能在下列疾病中起作用，包括[[动脉粥样硬化]]<ref>{{cite journal | last1=Mach | first1=F. | last2=Sauty | first2=A. | last3=Iarossi | first3=A. S. | last4=Sukhova | first4=G. K. | last5=Neote | first5=K. | last6=Libby | first6=P. | last7=Luster | first7=A. D. | title=Differential expression of three T lymphocyte-activating CXC chemokines by human atheroma-associated cells | url=https://archive.org/details/sim_journal-of-clinical-investigation_1999-10_104_8/page/1040 | journal=The Journal of Clinical Investigation | volume=104 | issue=8 | date=1999 | issn=0021-9738 | pmid=10525042 | pmc=408576 | doi=10.1172/JCI6993 | doi-access=free | pages=1041–1050 }}</ref>、[[多发性硬化]]<ref>{{cite journal | last1=Sørensen | first1=T. L. | last2=Tani | first2=M. | last3=Jensen | first3=J. | last4=Pierce | first4=V. | last5=Lucchinetti | first5=C. | last6=Folcik | first6=V. A. | last7=Qin | first7=S. | last8=Rottman | first8=J. | last9=Sellebjerg | first9=F. | last10=Strieter | first10=R. M. | last11=Frederiksen | first11=J. L. | last12=Ransohoff | first12=R. M. | title=Expression of specific chemokines and chemokine receptors in the central nervous system of multiple sclerosis patients | url=https://archive.org/details/sim_journal-of-clinical-investigation_1999-03_103_6/page/806 | journal=The Journal of Clinical Investigation | volume=103 | issue=6 | date=1999 | issn=0021-9738 | pmid=10079101 | pmc=408141 | doi=10.1172/JCI5150 | doi-access=free | pages=807–815}}</ref>、[[肺纤维化]]<ref>{{cite journal | last1=Jiang | first1=Dianhua | last2=Liang | first2=Jiurong | last3=Hodge | first3=Jennifer | last4=Lu | first4=Bao | last5=Zhu | first5=Zhou | last6=Yu | first6=Shuang | last7=Fan | first7=Juan | last8=Gao | first8=Yunfei | last9=Yin | first9=Zhinan | last10=Homer | first10=Robert | last11=Gerard | first11=Craig | last12=Noble | first12=Paul W. | title=Regulation of pulmonary fibrosis by chemokine receptor CXCR3 | url=https://archive.org/details/sim_journal-of-clinical-investigation_2004-07_114_2/page/290 | journal=The Journal of Clinical Investigation | volume=114 | issue=2 | date=2004 | issn=0021-9738 | pmid=15254596 | pmc=449741 | doi=10.1172/JCI16861 | doi-access=free | pages=291–299}}</ref>、I型[[糖尿病]]<ref>{{cite journal | last1=Frigerio | first1=Simona | last2=Junt | first2=Tobias | last3=Lu | first3=Bao | last4=Gerard | first4=Craig | last5=Zumsteg | first5=Urs | last6=Holländer | first6=Georg A. | last7=Piali | first7=Luca | title=Beta cells are responsible for CXCR3-mediated T-cell infiltration in insulitis | journal=Nature Medicine | volume=8 | issue=12 | date=2002 | issn=1078-8956 | pmid=12415259 | doi=10.1038/nm1202-792 | pages=1414–1420 }}</ref>、重症肌无力、急性心脏移植排斥<ref>{{cite journal | last1=Hancock | first1=W. W. | last2=Lu | first2=B. | last3=Gao | first3=W. | last4=Csizmadia | first4=V. | last5=Faia | first5=K. | last6=King | first6=J. A. | last7=Smiley | first7=S. T. | last8=Ling | first8=M. | last9=Gerard | first9=N. P. | last10=Gerard | first10=C. | title=Requirement of the chemokine receptor CXCR3 for acute allograft rejection | journal=The Journal of Experimental Medicine | volume=192 | issue=10 | date=2000-11-20 | issn=0022-1007 | pmid=11085753 | pmc=2193193 | doi=10.1084/jem.192.10.1515 | doi-access=free | pages=1515–1520 }}</ref>。开发阻断CXCR3与其配体相互作用的药物可提供治疗这些疾病的新途径。

== 参见 ==
*[[趋化因子受体]]
*[[趋化因子]]

== 参考文献 ==
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<references />
</div>

== 外部链接 ==
*[http://content.nejm.org/cgi/content/extract/354/6/610 Charo IF, Ransohoff RM. The many roles of chemokines and chemokine receptors in inflammation. N Engl J Med. 2006 Feb 9;354(6):610-21.]{{Wayback|url=http://content.nejm.org/cgi/content/extract/354/6/610 |date=20070110225703 }}

{{细胞因子受体}}

[[Category:细胞因子受体]]
[[Category:免疫学]]

CXCR3 - 版本历史

2026年2月10日 (二) 10:08 imported>曦城星月