Antibody‐mediated blockade of the CXCR3 chemokine receptor results in diminished recruitment of T helper 1 cells into sites of inflammation

@article{Xie2003AntibodymediatedBO,
  title={Antibody‐mediated blockade of the CXCR3 chemokine receptor results in diminished recruitment of T helper 1 cells into sites of inflammation},
  author={Jenny H. Xie and Naomi Nomura and Min Lu and Shiow-Ling Chen and G E Koch and Youmin Weng and Raymond L Rosa and Jerry Di Salvo and John Stuart Mudgett and Laurence B. Peterson and Linda S. Wicker and Julie A Demartino},
  journal={Journal of Leukocyte Biology},
  year={2003},
  volume={73}
}
Naïve T cells, when activated by specific antigen and cytokines, up‐regulate adhesion molecules as well as chemokine receptors on their surface, which allows them to migrate to inflamed tissues. Human studies have shown that CXCR3 is one of the chemokine receptors that is induced during T cell activation. Moreover, CXCR3‐positive T cells are enriched at inflammatory sites in patients with autoimmune diseases such as rheumatoid arthritis and multiple sclerosis. In this study, we use a mouse… 
Blockade of Chemokine Receptor CXCR3 Inhibits T Cell Recruitment to Inflamed Joints and Decreases the Severity of Adjuvant Arthritis1
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How the balance, timing and pattern of CXCR3 ligand expression appears to regulate the generation of effector T cells in the lymphoid compartment and subsequent migration into peripheral sites of Th1‐type inflammation is discussed.
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CXCR3 has a non‐redundant role in T’cell migration to dermal inflammation and is critical for activated T“lymphoblast recruitment, but memory T cells are less dependent on CXCR 3 for their infiltration.
A fully humanized IgG-like bispecific antibody for effective dual targeting of CXCR3 and CCR6
TLDR
It is proposed that dual targeting of CXCR3 and CCR6 with a fully humanized BsAb may display a potent interventional approach for the treatment of inflammatory and autoimmune diseases.
Regulatory T cells control endothelial chemokine production and migration of T cells into intestinal tumors of APCmin/+ mice
TLDR
This study demonstrates that Treg reduce endothelial CXCL10 production, inhibit T-cell migration into tumors and that CXCR3 mediated signalling is crucial for lymphocyte accumulation in intestinal tumors.
T-bet is required for optimal proinflammatory CD4+ T-cell trafficking.
TLDR
It is shown that in the absence of T-box expressed in T cells (T-bet), selective migration of T cells in vivo is completely abrogated and that T-bet regulates the binding of CD4(+) T cells to P-selectin.
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Results demonstrate that the chemokine receptor CXCR3 and CCR5 are markers for T cells associated with certain inflammatory reactions, particularly TH-1 type reactions, and appear to identify subsets of T cells in blood with a predilection for homing to these sites.
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