EA-1, a novel adhesion molecule involved in the homing of progenitor T lymphocytes to the thymus.

Imhof, Beat A.; Ruíz, Patricia; Hesse, B; Palacios, Ronald; Dunon, Dominique

doi:10.1083/jcb.114.5.1069

Cited by 46 publications

(21 citation statements)

References 61 publications

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“…Our data extend the data of Imhof et al (26), who demonstrated that the mAb EA-1 inhibits binding of progenitor T cells to the mouse endothelioma cell line eEnd.2. However, eEnd.2 cells express a6P8l and a6184 (27) and it has not yet been determined which of the two mediates the binding of progenitor T cells.…”

Section: Resultssupporting

confidence: 79%

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A monoclonal antibody against an activation epitope on mouse integrin chain beta 1 blocks adhesion of lymphocytes to the endothelial integrin alpha 6 beta 1.

Lenter¹,

Uhlig²,

Hamann³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

259

223

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We have generated a monoclonal antibody (mAb), 9EG7, against mouse endothelial cells that blocks adhesion of lymphocytes to endothelial cells. Sequencing offour tryptic peptides ofthe purified antigen revealed its identity with the integrin chain (3. The only Pu integrin that is known to mediate cell-cell adhesion is a4fi . This is not the integrin that is functionally dermed by the mAb 9EG7 on endothelial cells. First Antibodies. The following mAbs against mouse integrin chains were used: PS/2 (24) (anti-a4), R1-2 (16) (anti-a4), GoH3 (25) (anti-a6), and EA-1 (26, 27) (anti-a6). Other mAbs were K20 (28) (anti-human integrin chain (31) and (anti-mouse VCAM-1). Rabbit antibodies against a peptide corresponding to the C-terminal domain of the chicken integrin chain (31 were obtained from Richard 0. Hynes (MIT).The mAb 9EG7 (IgG2a) was produced by immunizing rats with TME cells in phosphate-buffered saline (PBS), using Alu-Gel-S (Serva) as adjuvant. Hybridoma production was done essentially as described (30) except that the mouse myeloma Sp2/0 was used for the fusion. Hybridoma supernatants were screened in cell-surface ELISA assays on TME Abbreviations: CAM, cell adhesion molecule; mAb, monoclonal antibody; PMA, phorbol 12-myristate 13-acetate.lTo whom reprint requests should be addressed. 9051

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Section: Resultssupporting

confidence: 79%

“…The following mAbs against mouse integrin chains were used: PS/2 (24) (anti-a4), R1-2 (16) (anti-a4), GoH3 (25) (anti-a6), and EA-1 (26,27) (anti-a6). Other mAbs were K20 (28) (anti-human integrin chain (31) and (29) (anti-mouse VCAM-1).…”

mentioning

confidence: 99%

A monoclonal antibody against an activation epitope on mouse integrin chain beta 1 blocks adhesion of lymphocytes to the endothelial integrin alpha 6 beta 1.

Lenter¹,

Uhlig²,

Hamann³

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

259

223

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“…After different migrations steps across the organ, mature T cells are generated and exit the thymus for the periphery (Scollay et al, 1980;Pénit, 1986). Migration and homing are partly dependent on adhesion molecules (Imhof et al, 1991;Aurrand-Lions et al, 1996). Virtually nothing is known about the precise thymic location from which mature thymocytes emigrate from the thymus to peripheral lymphoid organs.…”

Section: Introductionmentioning

confidence: 99%

Early Steps of a Thymic Tumor in SV40 Transgenic Mice: Hyperplasia of Medullary Epithelial Cells and Increased Mature Thymocyte Numbers Disturb Thymic Export

Nabarra

Martinon

Vasseur

et al. 2002

Journal of Immunology Research

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Bone marrow progenitors migrate to the thymus, where they proliferate and differentiate into immunologically competent T cells. In this report we show that mice transgenic for SV40 T and t antigens under the control of the L-pyruvate kinase promoter develop, in a first step, thymic hyperplasia of both thymocytes and epithelial cells. Morphological studies (histology, immunohistolabeling and electron microscopy) revealed modifications of the thymic microenvironment and gradual expansion of medullary epithelial cells in 1 month-old mice, taking over the cortical region. Then, a thymic carcinoma develops. Two-color labeling of frozen sections identified the transgene in medullary epithelial cells. Flow cytometry analysis demonstrated a marked increase in mature CD4þ and CD8 þ thymocytes in adult mice (39^10 £ 10 6 in transgenic mice and 12^5 £ 10 6 in age-matched controls). Furthermore, thymocyte export was disturbed.

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“…In situ binding of IRBCs was performed in analogy to a leukocyte binding assay described previously (21). Freshly prepared frozen sections (brain and lung) of LPS-primed and control SCID mice were preincubated with binding medium and placed in a humid chamber, before IRBCs were allowed to adhere for 1 h at room temperature with gentle agitation.…”

Section: Adhesion Of Irbcs On Frozen Sectionsmentioning

confidence: 99%

In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria.

Willimann

Matile

Weiss

et al. 1995

The Journal of Experimental Medicine

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SummaryCerebral malaria is a fatal complication of infection by Plasmodiumfakiparum in man. The neurological symptoms that characterize this form of malarial disease are accompanied by the adhesion of infected erythrocytes to the vasculature of the brain. To study this phenomenon in vivo, an acute phase severe combined immunodeficiency (SCID) mouse model was developed in which sequestration of P.fakiparum-infected human erythrocytes took place. During acute cerebral malaria in humans, the expression of intercellular adhesion molecule-1 (ICAM-1) is induced in vascular endothelium by inflammatory reactions. Acute phase ICAM-1 expression can also be obtained in SCID mice. The endothelium of the midbrain region was the most responsive to such inflammatory stimulus. It is noteworthy that the reticular formation in the midbrain controls the level of consciousness, and loss of consciousness is a symptom of cerebral malaria. We found that infected human erythrocytes were retained 24 times more than normal erythrocytes in ICAM-1-positive mouse brain. Sequestration to the brain was reduced by anti-ICAM-1 antibodies. These in vivo results were confirmed by the binding of P. fakiparum-infected erythrocytes to the ICAM-l-positive endothelium in tissue sections of mouse brain. We conclude that the SCID mouse serves as a versatile in vivo model that allows the study ofP.fakiparum-infected erythrocyte adhesion as it occurs in human cerebral malaria. Upregulation of ICAM-1 expression in the region of the midbrain correlates with increased retention of malaria-infected erythrocytes and with the symptoms of cerebral malaria.p , lasmodium falciparum, one of the four plasmodium spedes that infect man, produces a fulminant disease that can lead to severe cerebral symptoms. Every year, this parasite causes about 250 million clinical cases of malaria (1). Approximately 2 million individuals, mainly children under 5 years of age, die from the main complications, which are cerebral malaria and severe anemia. A special feature of P. falciparum pathology is the absence of mature intraerythrocytic stages of the parasite in the circulating blood. Mature forms are found attached to the lining of microvessels in peripheral organs. This adhesion of infected erythrocytes to the vascular endothelium is called sequestration. Clinically severe neurological symptoms correlate with a much higher frequency of sequestered parasitized erythrocytes in the brain vasculature compared to other organs (2).Sequestration is thought to depend on differences between P.fakiparum strains leading to the expression of different erythrocyte surface molecules mediating adhesion to endothelia, as well as variation in the production of endotoxins eliciting a TNF-ot response by host macrophages (3). Thus, sequestration depends also on the susceptibility of the host to endotoxins, the subsequent regulation of adhesion molecules, and the host's level of immunity (4). A key role is played by TNF. Its plasma concentration levels are elevated in patients with fatal cerebral m...

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EA-1, a novel adhesion molecule involved in the homing of progenitor T lymphocytes to the thymus.

Cited by 46 publications

References 61 publications

A monoclonal antibody against an activation epitope on mouse integrin chain beta 1 blocks adhesion of lymphocytes to the endothelial integrin alpha 6 beta 1.

A monoclonal antibody against an activation epitope on mouse integrin chain beta 1 blocks adhesion of lymphocytes to the endothelial integrin alpha 6 beta 1.

Early Steps of a Thymic Tumor in SV40 Transgenic Mice: Hyperplasia of Medullary Epithelial Cells and Increased Mature Thymocyte Numbers Disturb Thymic Export

In vivo sequestration of Plasmodium falciparum-infected human erythrocytes: a severe combined immunodeficiency mouse model for cerebral malaria.

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