Expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in colonic epithelial cells.

Dippold, Wolfgang; Wittig, B.; Schwaeble, Wilhelm; Mayet, W.‐J.; Büschenfelde, K H Meyer zum

doi:10.1136/gut.34.11.1593

Cited by 106 publications

(83 citation statements)

References 27 publications

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“…Moreover, several lines of evidence have demonstrated that IFN-␥ enhances ICAM-1 expression on intestinal epithelial cells (41)(42)(43)(44)(45). In line with this observation, we observed that ICAM-1 expression was enhanced in the ileum of WT, but not IFN-␥ KO, mice treated with toxin A.…”

Section: Discussionsupporting

confidence: 89%

Essential Involvement of IFN-γ in Clostridium difficile Toxin A-Induced Enteritis

Ishida

Maegawa

Kondo

et al. 2004

The Journal of Immunology

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Clostridium difficile has emerged as the important causative agent of antibiotics-associated pesudomembranous colitis; especially its toxin A is presumed to be responsible for the colitis. We examined the pathophysiological roles of IFN-γ in toxin A-induced enteritis using IFN-γ knockout (KO) mice. When toxin A of C. difficile was injected into the ileal loops of BALB/c wild-type (WT) mice, massive fluid secretion, disruption of intestinal epithelial structure, and massive neutrophil infiltration developed within 4 h after the injection. IFN-γ protein was faintly detected in some CD3-positive lymphocytes in the lamina propria and submucosa of the ileum of untreated WT mice. On the contrary, at 2 and 4 h after toxin A injection, IFN-γ protein was detected in infiltrating neutrophils and to a lesser degree in CD3-positive lymphocytes. In the ileum of WT mice, toxin A treatment markedly enhanced the gene expression of TNF-α, macrophage inflammatory protein-1α and -2, KC, and ICAM-1 >2 h after treatment. In contrast, the histopathological changes were marginal, without enhanced fluid secretion in the ileum of toxin A-treated IFN-γ KO mice. Moreover, toxin A-induced gene expression of TNF-α, neutrophil chemotactic chemokines, and ICMA-1 was remarkably attenuated in IFN-γ KO mice. Furthermore, pretreatment of WT mice with a neutralizing anti-IFN-γ Ab prevented toxin A-induced enteritis. These observations indicate that IFN-γ is the crucial mediator of toxin A-induced acute enteritis and suggest that IFN-γ is an important molecular target for the control of C. difficile-associated pseudomembranous colitis.

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Section: Discussionsupporting

confidence: 89%

Essential Involvement of IFN-γ in Clostridium difficile Toxin A-Induced Enteritis

Ishida

Maegawa

Kondo

et al. 2004

The Journal of Immunology

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“…31,36–38 Consistent with this, transfection of ICAM-1 into colorectal cancer cell lines inhibits tumor growth and metastasis. 39 In addition, the production of prostaglandin E2 in the tumor microenvironment downregulates the expression of ICAM-1 in tumor cells, reducing the cytotoxic effects of T cells.…”

Section: Discussionsupporting

confidence: 60%

Actin stabilizer TAGLN2 potentiates adoptive T cell therapy by boosting the inside-out costimulation via lymphocyte function-associated antigen-1

et al. 2018

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Correct temporal and spatial control of actin dynamics is essential for the cytotoxic T cell effector function against tumor cells. However, little is known whether actin engineering in tumor-targeted T cells can enhance their antitumor responses, thereby potentiating the adoptive T cell therapy. Here, we report that TAGLN2, a 22-KDa actin-stabilizing protein which is physically associated with lymphocyte function-associated antigen-1 (LFA-1), potentiates the OTI TCR CD8+ T cells to kill the intercellular adhesion molecule-1 (ICAM-1)-positive/OVA-presenting E0771 cells, but not ICAM-1-negative OVA-B16F10 cells, suggesting an ‘inside-out’ activation of LFA-1, which causes more efficient immunological synapse formation between T cells and tumor cells. Notably, recombinant TAGLN2 fused with the protein transduction domain (TG2P) overcame the disadvantages of viral gene delivery, leading to a significant reduction in tumor growth in mice. TG2P also potentiated the CD19-targeted, chimeric antigen receptor (CAR)-modified T cells to kill Raji B-lymphoma cells. Our findings indicate that activating the TAGLN2–actin–LFA-1 axis is an effective strategy to potentiate the adoptive T-cell immunotherapy.

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“…14,15 In contrast, ICAM-1 is expressed both by the tumor endothelium as well as by tumor cells themselves. 16,19,20 Increased expression of ICAM-1 has been seen in tissue samples of breast carcinomas and is associated with an improved prognosis. 36 The mechanisms by which ICAM-1 expression leads to decreased tumor size are unknown, but may involve localization of leukocytes to the tumor.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, ICAM-1 is expressed both by tumor endothelium as well as by tumor cells of epithelial origin. 16,19,20 This has been demonstrated using both tissue sections as well as tumor cell lines. Many have speculated that ICAM-1 and VCAM-1 expression may favor adhesive interactions with leukocytes, thus facilitating leukocyte tumor infiltration.…”

mentioning

confidence: 90%

Intercellular Cell Adhesion Molecule-1, Vascular Cell Adhesion Molecule-1, and Regulated on Activation Normal T Cell Expressed and Secreted Are Expressed by Human Breast Carcinoma Cells and Support Eosinophil Adhesion and Activation

Ali¹,

Kaur

Patel

2000

The American Journal of Pathology

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Eosinophils are usually associated with parasitic and allergic diseases; however, eosinophilia is also observed in several types of human tumors, including breast carcinomas. In this study we examined several human breast carcinoma cell lines for adhesion mol- Eosinophils represent a minor fraction of the circulating leukocytes; however, they are key mediators in diseases such as bronchial asthma, allergic dermatitis, and helminthic parasite infections.

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Expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in colonic epithelial cells.

Abstract: The expression of intercellular adhesion molecule-I (ICAM-1, CD54)

Cited by 106 publications

References 27 publications

Essential Involvement of IFN-γ in Clostridium difficile Toxin A-Induced Enteritis

Essential Involvement of IFN-γ in Clostridium difficile Toxin A-Induced Enteritis

Actin stabilizer TAGLN2 potentiates adoptive T cell therapy by boosting the inside-out costimulation via lymphocyte function-associated antigen-1

Intercellular Cell Adhesion Molecule-1, Vascular Cell Adhesion Molecule-1, and Regulated on Activation Normal T Cell Expressed and Secreted Are Expressed by Human Breast Carcinoma Cells and Support Eosinophil Adhesion and Activation

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