Mechanisms of binding of cutaneous lymphocyte‐associated antigen‐positive and αeβ7‐positive lymphocytes to oral and skin keratinocytes

Brown, D J; Furness, J; Speight, PM; Thomas, Grunwald; Li, J; Thornhill, Martin H.; Farthing, Paula M.

doi:10.1046/j.1365-2567.1999.00855.x

Cited by 43 publications

(33 citation statements)

References 32 publications

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“…Intracellular granzyme B expression was assessed on BILs directly ex vivo, whereas intracellular IFN-␥ was assessed after BIL restimulation with 1 M gp [33][34][35][36][37][38][39][40][41] peptide or OVA 257-264 peptide for 6 h in the presence of 2 M monensin (BD Biosciences).…”

Section: Intracellular Stainingmentioning

confidence: 99%

“…with tumor cells. We chose an adoptive transfer strategy of naive P14-GFP TCR Tg CD8 ϩ T cells specific for the H-2D b -restricted gp [33][34][35][36][37][38][39][40][41] epitope of the lymphocytic choriomeningitis virus glycoprotein combined with i.c. injection of MC57-GP tumor cells expressing lymphocytic choriomeningitis virus glycoprotein.…”

Section: Ag-experienced P14 Cd8 ϩ T Cells Infiltrating the Brain Of Tmentioning

confidence: 99%

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Brain Microenvironment Promotes the Final Functional Maturation of Tumor-Specific Effector CD8+ T Cells

Masson

Calzascia

Berardino-Besson

et al. 2007

The Journal of Immunology

100

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During the priming phase of an antitumor immune response, CD8+ T cells undergo a program of differentiation driven by professional APCs in secondary lymphoid organs. This leads to clonal expansion and acquisition both of effector functions and a specific adhesion molecule pattern. Whether this program can be reshaped during the effector phase to adapt to the effector site microenvironment is unknown. We investigated this in murine brain tumor models using adoptive transfer of tumor-specific CD8+ T cells, and in spontaneous immune responses of patients with malignant glioma. Our data show proliferation of Ag-experienced tumor-specific T cells within the brain parenchyma. Moreover, CD8+ T cells further differentiated in the brain, exhibiting enhanced IFN-γ and granzyme B expression and induction of αE(CD103)β7 integrin. This unexpected integrin expression identified a subpopulation of CD8+ T cells conditioned by the brain microenvironment and also had functional consequences: αE(CD103)β7-expressing CD8+ T cells had enhanced retention in the brain. These findings were further investigated for CD8+ T cells infiltrating human malignant glioma; CD8+ T cells expressed αE(CD103)β7 integrin and granzyme B as in the murine models. Overall, our data indicate that the effector site plays an active role in shaping the effector phase of tumor immunity. The potential for local expansion and functional reprogramming should be considered when optimizing future immunotherapies for regional tumor control.

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Section: Intracellular Stainingmentioning

confidence: 99%

Section: Ag-experienced P14 Cd8 ϩ T Cells Infiltrating the Brain Of Tmentioning

confidence: 99%

Brain Microenvironment Promotes the Final Functional Maturation of Tumor-Specific Effector CD8+ T Cells

Masson

Calzascia

Berardino-Besson

et al. 2007

The Journal of Immunology

100

View full text Add to dashboard Cite

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“…Normal human melanocytes also express P-and E-cadherin, and adhesion to keratinocytes is mediated predominantly through E-cadherin (Tang et al, 1994). Adhesion of Langerhans cells is also mediated through E-cadherin (Tang et al, 1993), and mucosal T-lymphocytes recognize Ecadherin through the o-EP37 integrin receptor (Brown et al 1999). Soluble E-cadherins (sE-cad) have been identified in several skin diseases, including bullous pemphigoid, pemphigus vulgaris, psoriasis, and other inflammatory diseases (Matsuyoshi et al, 1995).…”

Section: Cadherin Expression and Functionmentioning

confidence: 99%

Cell Adhesion Molecules and Oral Cancer

Thomas

Speight

2001

Critical Reviews in Oral Biology & Medicine

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Cell adhesion molecules (CAMs) are found on the surfaces of all cells, where they bind to extracellular matrix molecules or to receptors on other cells. As well as having a structural role, CAMs function as signaling receptors, transducing signals initiated by cellular interactions which regulate many diverse processes, including cell division, migration, and differentiation. Cell adhesion molecules are essential for maintaining stable tissue structure. However, cell adhesion must be dynamic to facilitate the mobility and turnover of cells. In dynamic situations, cells alter their cell-cell and cell-matrix interactions by virtue of altered expression and function of CAMs. The expression of CAMs is normally tightly regulated, thereby controlling cell proliferation, mobility, differentiation, and survival. Many of these processes are misregulated in malignant tumors, and it has been shown that many of the characteristics of tumor cells are attributable to the aberrant expression or function of CAMs.Integrins and E-cadherin are the most important CAMs expressed by stratified squamous epithelium. Altered expression of these molecules has been found in oral carcinoma, where loss of CAM expression is often seen in poorly differentiated lesions.However, up-regulation of certain integrins, such as av16, has consistently been found in oral cancer, suggesting that it may play an active role in disease progression.Key words. Oral cancer, cell adhesion molecules, integrins, cadherins, selectins, immunoglobulin superfamily, CD44. (I) IntroductionCell adhesion molecules (CAMs) are found on the surfaces of all cells, where they bind to extracellular matrix molecules or to receptors on other cells. Cell adhesion is critical in the dynamic processes necessary for tissue morphogenesis in development and the maintenance of complex differentiated tissues in adult organisms. CAMs serve in these roles by virtue of their capacity to connect the exterior of the cell with the interior. They form structural linkages between the cell cytoskeleton and the extracellular matrix or between cells, and also function as signaling receptors, transducing signals initiated by cellular interactions which regulate many diverse processes, including cell division, migration, and differentiation ( Fig. 1).Cell adhesion molecules are essential for maintaining the stable structure of stratified squamous epithelium. In normal epithelium, keratinocytes are attached to each other and to the underlying basement membrane. Cell adhesion, however, must be dynamic to facilitate the mobility and turnover of cells. In dynamic situations, keratinocytes alter their cell-cell and cell-ECM interactions by virtue of altered expression and function of CAMs.The expression of cell adhesion molecules is normally tightly regulated-forming, persisting, or declining in an ordered fashion. This allows for controlled cell proliferation, mobility, differentiation, and survival. Many of these processes are misregulated in malignant tumors, and it has been shown that man...

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“…Recent findings on the role of cytokines, chemokines, and their receptors in migration of lymphoid cell subsets with affinity to a particular organ suggest that a variety of clinical manifestations as reflected by multiple organ involvements are attributed to T cell subsets expressing different organspecific homing molecules (8). Thus, it is possible that cutaneous lymphocyte Ag (CLA) ϩ and ␣E␤7 ϩ T cells induce skin damage and mucous membrane injuries, respectively (9). Another concern is the mechanism in which the multiple subsets of pathogenic T cells with different immunological characteristics are generated in response to phenobarbital.…”

mentioning

confidence: 99%

Characterization of Drug-Specific T Cells in Phenobarbital- Induced Eruption

Hashizume

Takigawa

Tokura

2002

The Journal of Immunology

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Phenobarbital has a high potential to elicit adverse reactions including severe skin eruptions and systemic involvements among the worldwide-prescribed drugs. Although phenobarbital hypersensitivity is thought to be mediated by T cells specific to the drug, its precise mechanism remains not fully elucidated. To characterize T cells reactive with phenobarbital, we generated drug-specific T cell clones and lines from PBMCs of patients with phenobarbital hypersensitivity showing various degrees of cutaneous and extracutaneous involvements. Although the TCR Vβ repertoire and phenotype in the T cell clones/T cell lines were heterogeneous among the patients, Vβ13.1+ and Vβ5.1+ clones or lines were raised from the individuals examined who possessed different HLA haplotypes. Histopathological examination suggested that Vβ5.1+CD8+ T cells and Vβ13.1+ T cells played a role in cutaneous and extracutaneous involvements, respectively. A Vβ13.1+CD4+ clone was found to proliferate in response to the Ag with processing-impaired, fixed APCs. Most of the clones and lines belonged to the Th2 phenotype, producing IL-4 and IL-5 but not IFN-γ upon phenobarbital stimulation. Clones/lines with Th1 or Th0 phenotypes also constituted minor populations. These observations clearly indicate the heterogeneity and a marked individual deviation of reactive T cell subsets among the patients in terms of CD4/8 phenotype, Vβ repertoire, Ag recognition pattern, and cytokine production; and thus provide evidence whereby each pathogenic T cell subset contributes to special elements of clinical presentation.

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Mechanisms of binding of cutaneous lymphocyte‐associated antigen‐positive and αeβ7‐positive lymphocytes to oral and skin keratinocytes

Cited by 43 publications

References 32 publications

Brain Microenvironment Promotes the Final Functional Maturation of Tumor-Specific Effector CD8+ T Cells

Brain Microenvironment Promotes the Final Functional Maturation of Tumor-Specific Effector CD8+ T Cells

Cell Adhesion Molecules and Oral Cancer

Characterization of Drug-Specific T Cells in Phenobarbital- Induced Eruption

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