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Y H Chin

Publications and source records attributed to Y H Chin.

At least 37 records · Page 2Linked to original sources
PubMed1991

Tissue-specific homing receptor mediates lymphocyte adhesion to cytokine-stimulated lymph node high endothelial venule cells.

Lymphocytes bind to high endothelial venule (HEV) cells as the first step in the migration of these cells into lymph nodes (LN) and Peyer's patches (PP). In this study we isolated and cultured HEV cells from rat LN and investigated the effects of cytokines on the adhesiveness of these cells for lymphocytes. The results showed that lymphocytes from thoracic duct, spleen and LN adhered preferentially to the cultured LN HEV cells compared to cells isolated from the thymus and bone marrow. The adhesiveness of LN HEV cells for thoracic duct lymphocytes (TDL) was significantly increased in a dose- and time-dependent manner by pretreatment of the HEV cells with tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma) or interleukin-4 (IL-4). In contrast, pretreatment of HEV cells with IL-1, IL-6 or IL-7 did not alter the capacity of LN HEV cells to adhere lymphocytes. Furthermore, incubation of LN HEV cells with suboptimal doses of TNF and IL-4, IFN-gamma and IL-4, or TNF-alpha and IFN-gamma increased significantly the endothelial adhesiveness. Interestingly, although IL-1 alone did not promote the adhesiveness of HEV cells, the cytokine synergized with suboptimal doses of IL-4 and TNF-alpha to increase the adhesiveness. The adhesion of TDL to non-stimulated and IL-4-stimulated LN HEV cells could be blocked specifically by treatment of lymphocytes with the LN homing-receptor-specific A.11.5 monoclonal antibody (mAb). In contrast, lymphocytes pretreated with the PP-homing receptor-specific 1B.2.6 mAb or the antileucocyte common antigen (OX1) mAb adhered normally to the HEV cells. Taken together, these results indicate that the baseline and cytokine-stimulated bindings between lymphocytes and LN HEV cells are mediated by adhesive mechanisms that regulate lymphocyte migration into LN in vivo and provide strong evidence that cytokines are central mediators of organ-specific lymphocyte migration.

Animals↗
PubMed1991

Recruitment of mononuclear cells into wounded skin: mechanism and modulation.

In conclusion, we have shown that the development of specialized endothelium that supports lymphocyte and monocyte adherence may be a common biologic event associated with tissue injury or disease processes in the skin. We have shown that the adherence process is potentially regulated by cytokines that are secreted by infiltrating mononuclear cells. Studies are now in progress to identify the putative endothelial ligands, their interactions with the receptors and the factors that lead to the expression of the adhesion molecules.

Animals↗
PubMed1990

Lymphocyte adhesion to cultured Peyer's patch high endothelial venule cells is mediated by organ-specific homing receptors and can be regulated by cytokines.

Adhesion of lymphocytes to high endothelial venule (HEV) cells is the first step in the migration of these cells from blood into lymph nodes and Peyer's patches (PP). In the present study, we isolated and cultured HEV cells from PP of the rat and assessed their capacity to interact with lymphocytes. Flow cytometric analysis with a rat HEV-specific mAb KJ-4 revealed that greater than 90% of the cultured cells were stained by the antibody. Furthermore, confluent monolayers of PP HEV cells retained the capacity to support the adhesion of lymphocytes from spleen, thoracic duct, and lymph nodes but not binding of immature cells from thymus and bone marrow, which are deficient in cells capable of binding to HEV in vivo. In addition, intraepithelial lymphocytes that preferentially migrated into mucosal lymphoid tissues were also enriched in cells that adhered to the endothelial monolayers. The binding process required energy, was calcium-dependent, and could be inhibited by cytochalasin D, trypsin, and mixed glycosidase. Interestingly, pretreatment of PP HEV cells with rTNF, IFN-gamma, or granulocyte-macrophage CSF significantly increased the endothelial adhesiveness for thoracic duct lymphocytes in a time- and dose-dependent manner. In contrast, stimulation of lymphocytes with phorbol ester or TNF resulted in the rapid modulation of the surface expression of the PP homing receptor and decrease in lymphocyte binding to normal or TNF-stimulated HEV cells. The adhesion of lymphocytes to normal or cytokine-stimulated HEV cells can be blocked by pretreatment of lymphocytes, but not HEV cells, with the PP homing receptor-specific 1B.2.6 antibody. Taken together, these experiments provide strong evidence that the interaction between lymphocytes and cultured HEV cells are mediated by adhesive mechanisms that regulate lymphocyte entry into PP in vivo and that cytokines can promote HEV adhesiveness for lymphocytes through increased expression of organ-specific ligands on HEV cells.

Animals↗
PubMed1990

Lymphocyte adhesion to psoriatic dermal endothelium: mechanism and modulation.

Psoriasis is characterized by the hyperproliferation of keratinocytes in the epidermis and the accumulation of activated CD4+ T lymphocytes in the upper dermis. We have recently rested the hypothesis that the abnormal endothelial proliferation in the dermal papillae of psoriatic lesions may be mechanistically linked to the expression of endothelial ligands capable of promoting lymphocytes binding and extravasation. The results indicated that specialized endothelial cells lining the post-capillary venules of psoriatic lesions are capable of promoting the selective adherence of human CD4+ T cells and its memory subset. In contrast, B cells, CD8+ T cells, and CD45RA+ T cells are deficient in their capacities to bind. The adhesion process is energy and calcium dependent and involves tissue-specific lymphocyte receptors, with LFA-1 molecules playing an accessory role. We concluded that transformation of the dermal endothelium into a lymphocyte-receptive phenotype by defined growth factors or cytokines may represent a positive feedback mechanism promoting lymphocyte migration into the diseased sites.

Cell Adhesion↗
PubMed1990

Recruitment of mononuclear cells by endothelial cell binding into wounded skin is a selective, time-dependent process with defined molecular interactions.

Wound healing involves a complex series of interactions between cells in the dermis and epidermis, and important relationships exist between keratinocytes and resident dermal cells. Monocytes and lymphocytes secrete cytokines that are capable of stimulating dermal repair and influencing keratinocyte and fibroblast migration and proliferation, although the mechanism by which mononuclear cells are recruited into the wound is unknown. We have tested the hypothesis that in wounded skin specialized endothelial cells are induced to mediate peripheral blood mononuclear cell (PBMC) emigration from the vasculature into the dermis. For this purpose, partial-thickness wounds made with a keratome on the backs of domestic pigs were excised 0 to 9, 12, 15, and 21 d after wounding. The biopsies were then tested for the capacity to adhere selectively to PBMC. The results indicated that PBMC overlaid onto sections of wounds from day 4 to 15 adhered selectively to dermal endothelium, with two distinct peaks of adherence observed on day 7 and day 12. In contrast, PBMC did not adhere to the tissue sections when overlaid onto frozen sections of normal skin or 0-, 1-, 2-, 3-, and 21-d-old wounded skin. Additional studies on the binding properties of PBMC subsets revealed that monocytes adhered maximally at day 7, whereas T cells adhered optimally at day 12 post-wounding. Furthermore, the adhesion process was energy and magnesium dependent but not calcium dependent and involved surface protein and carbohydrate moieties on PBMC surface. Pre-treatment of PBMC with monoclonal antibodies against the LFA-1 adhesive receptors inhibited the binding by greater than 80%, suggesting that LFA-1 adhesive receptors play an important role in the binding process. These studies provide evidence that the recruitment of monocytes and lymphocytes into wounds is an active, dynamic, and regulated process mediated at least in part by specific adhesive interactions between mononuclear leukocytes and dermal endothelial cells.

Animals↗
PubMed1990

Adherence of human helper/memory T-cell subsets to psoriatic dermal endothelium.

Dermal lymphocytic infiltrates are characteristic features of psoriasis and may be involved in the pathogenesis of the disease. We have previously shown that specialized endothelial cells are present in the dermis of psoriatic skin and are capable of supporting lymphocyte adherence and promoting lymphocyte extravasation. In this study, we investigated the dermal endothelial binding properties of human lymphocyte subsets and the role of LFA-1 molecules in the adhesion process. It was found that both human T cells and B cells adhered to frozen sections of psoriatic plaques, but with different cell dose-response relationships. In addition, quantitative assessment of lymphocyte adhesion demonstrated that human CD4+T cells and the CDw29+ (helper-inducer) subset adhered preferentially to the papillary dermis as compared with CD8+ T cells or the CD45R+ (suppressor-inducer) subset. Moreover, human lymphocytes adhered to untreated psoriatic plaques, but not to uninvolved skin or to steroid-treated, clinically and histologically resolved lesions. Preincubation of T lymphocytes with saturating amounts of monoclonal antibody 60.3 against the surface membrane CD18 glycoprotein complex inhibited partially their capacity to bind to untreated psoriatic plaques. These observations suggest that the emigration of human CD4+ T cell and the CDw29+ helper-inducer subset is promoted by selective adherence to psoriatic dermal endothelia, with LFA-1 molecules playing an accessory role in the binding process.

Administration, Topical↗
PubMed1989

Lymphocyte recognition of psoriatic endothelium: evidence for a tissue-specific receptor/ligand interaction.

Epidermotropic lymphocytes are an essential cellular component of the skin-associated lymphoid tissues (SALT). Dermal lymphocytic infiltrates are also characteristics of inflammatory dermatoses, such as psoriasis, and may be involved in the pathogenesis of the disease, although the mechanisms by which lymphocytes are recruited into these sites are not known. We have used an in vitro lymphocyte adherence assay to test the hypothesis that specialized endothelial cells are present in inflamed skin, and are capable of supporting lymphocyte adherence and promoting lymphocyte emigration. In this assay, we assessed the binding of lymphocytes overlaid onto frozen sections of normal and psoriatic skin. Peripheral blood mononuclear cells (PBMC) from patients, from healthy volunteers, and from rat thoracic duct bound specifically to dermal endothelia in psoriatic plaques, in steroid-resistant areas of plaques, but not in uninvolved skin or skin from healthy individuals. Analysis of the binding properties of lymphocyte subsets revealed preferential adherence by CD4+ T cells as compared with CD8+ T cells and to B cells. Interestingly, PBMC from patients undergoing ultraviolet light therapy failed to adhere to autologous skin or to lesion-containing skin sections from untreated patients. Additional studies indicate that the lymphocyte-endothelial interaction is an energy- and calcium-dependent process and involves surface glycoprotein and carbohydrate moieties, requirements similar to those found in specific lymphocyte interactions with high endothelial venules in lymph nodes during the homing process. Pretreatment of lymphocytes with antibodies directed against homing receptors mediating migration into lymph nodes and into gut-associated lymphoid tissues, however, did not interfere with lymphocyte adherence to psoriatic endothelium. In contrast, anti-lymphocyte function associated antigen (LFA)-1 antibody partially inhibited lymphocyte binding to chronic plaques. We conclude that a tissue-specific receptor/ligand interaction independent of LFA-1 directs lymphocyte emigration from the dermal microvasculature into the psoriatic dermis and that LFA-1 plays only an accessory role in the adhesion process.

Animals↗
PubMed1988

Lymphocyte adhesion to psoriatic dermal endothelium is mediated by a tissue-specific receptor/ligand interaction.

Dermal lymphocytic infiltrates are characteristic of psoriasis and may be involved in the pathogenesis of the disease. We have utilized an in vitro lymphocyte adherence assay to examine the mechanism(s) mediating lymphocyte migration into psoriatic skin. In this assay, we assessed the binding of lymphocytes overlaid onto frozen biopsy sections of normal and psoriatic skin. Lymphocytes isolated from human blood and rat thoracic duct bound specifically to dermal endothelia in psoriatic plaques but not to those of uninvolved skin from psoriatic patients or skin from normal individuals; analysis of the binding properties of B cells and T lymphocyte subsets revealed a preferential binding of CD4+ T cells compared with CD8+ T cells or B cells. This lymphocyte-endothelial interaction is an energy- and calcium-dependent process and involves surface protein and carbohydrate moieties, requirements similar to those found in lymphocyte interaction with post-capillary high endothelial venules (HEV) in lymphoid tissues. However, preincubation of lymphocytes with antibodies directed against surface molecules mediating adhesion to HEV of peripheral lymph node and gut-associated lymphoid tissue did not interfere with the capacity of lymphophocytes to bind to the skin. The results of this study support the hypothesis that emigration of lymphocytes from vasculature into psoriatic skin is promoted by the presence of specialized endothelia in psoriatic dermis capable of mediating specific lymphocyte-endothelial interactions.

Adult↗
PubMed1986

A monoclonal anti-HEBFPP antibody with specificity for lymphocyte surface molecules mediating adhesion to Peyer's patch high endothelium of the rat.

Cell surface molecules involved in lymphocyte adhesion to high endothelial cell venules (HEV) of Peyer's patches (PP) have been studied in the rat by using a mouse monoclonal anti-HEBFPP (1B.2) antibody. We previously showed that rat thoracic duct lymph contains a high endothelial cell binding factor termed HEBFPP, which in vitro blocks lymphocyte binding sites of HEVPP but not HEVLN. Monoclonal 1B.2 antibody was produced by fusing P3U1 myeloma cells with spleen cells of a mouse immunized with this material. Immunoprecipitation studies with 125I surface-labeled rat thoracic duct lymphocytes (TDL) showed that the antibody recognized an 80-kilodalton protein. This antigen was present in the majority of TDL, spleen, LN, and PP cells but was found on few (5 to 10%) thymus and bone marrow cells (indirect immunofluorescence). Treatment of TDL with 1B.2 antibody blocked their ability to bind in vitro to HEVPP; antibody treatment did not interfere with TDL adhesion to HEVLN. Analysis of 1B.2 antigen isolated from lymph and detergent lysates of TDL by antibody-affinity chromatography showed that this material had the capacity to block lymphocyte binding sites of HEVPP but not HEVLN. In contrast, material with such blocking activity was not isolated from detergent lysates of thymocyte, a population deficient in HEV-binding cells. The results indicate that the 1B.2 antigen is a component of the lymphocyte surface recognition structure mediating adhesion to HEVPP and provide further evidence that distinct adhesion molecules of rat TDL mediate interaction with high endothelium of LN and PP.

Animals↗
PubMed1985

Lymphocyte recognition of lymph node high endothelium. VII. Cell surface proteins involved in adhesion defined by monoclonal anti-HEBFLN (A.11) antibody.

Lymphocyte entry into lymph nodes (LN) and Peyer's patches (PP) occurs specifically at high endothelial cell venules (HEV). We previously isolated a high endothelial binding factor (HEBFLN) from rat lymph that blocked the lymphocyte binding sites of HEVLN but not HEVPP. In this study, mouse monoclonal anti-HEBFLN antibody (A.11) was used to investigate rat lymphocyte surface structures mediating adhesion to high endothelium. The A.11 antigen was expressed on the majority of thoracic duct lymphocytes (TDL), spleen, LN, PP cells, but was only detected on few (1 to 10%) thymus and bone marrow cells (indirect immunofluorescence). The treatment of TDL with the A.11 IgG blocked their ability to bind to HEVLN. This effect was specific, inasmuch as A.11 antibody did not block lymphocyte binding to HEVPP, and an anti-leukocyte-common antigen monoclonal antibody, OX1, did not block lymphocyte binding to HEVLN. In addition, the A.11 antigen isolated from the lymph and detergent lysates of TDL by antibody affinity chromatography had the capacity to block the lymphocyte binding sites of HEVLN but not HEVPP. Immunoprecipitation studies revealed that the A.11 antibody recognized the radioiodinated surface membrane proteins of TDL and TDL-derived T cells and B cells, which resolved with SDS-PAGE autoradiography into three polypeptides with relative m.w. of approximately 135,000, 63,000, and 40,000. We conclude that the A.11 antigen is a component of the lymphocyte surface recognition structure that mediates adhesion to high endothelial cells of rat peripheral lymph nodes.

Animals↗
PubMed1984

Lymphocyte recognition of lymph node high endothelium. VI. Evidence of distinct structures mediating binding to high endothelial cells of lymph nodes and Peyer's patches.

Lymphocytes migrate from blood into lymph nodes (LN) and Peyer's patches (PP) of rats specifically at segments of venules lined by high endothelium (HEV). We previously identified and isolated a lymphocyte surface component termed high endothelial binding factor (HEBF) that appears to be involved in lymphocyte adhesion to high endothelial cells of LN. HEBF has also been isolated from thoracic duct lymph and is antigenically related to the cell surface component. Soluble HEBF derived from detergent lysates of thoracic duct lymphocytes (TDL) or directly from lymph has affinity for HEVLN in vitro, and is able to block sites where lymphocytes would normally attach. In the present study, lymphocyte binding sites of HEVLN and HEVPP were investigated through the use of lymph-derived HEBF and rabbit antibody to this factor. The results show that treatment of rat TDL with anti-HEBF Fab did not block binding to HEVPP, even though adhesion to HEVLN was reduced by 80% or more. Similarly, HEBF isolated by anti-HEBF F(ab')2 affinity chromatography blocked lymphocyte binding sites of HEVLN but not HEVPP. This material is therefore designated HEBFLN, and antibody to it is designated anti-HEBFLN Ig. Fractionation of thoracic duct lymph revealed that it contained an antigenically distinct component, HEBFPP, which blocked lymphocyte binding to HEVPP but not to HEVLN. Lymph components precipitating between 40 and 60% (NH4)2SO4 saturation contained both factors, which were separated from the bulk of lymph proteins by DEAE-Sepharose chromatography and then from each other by fractionation on the anti-HEBFLN F(ab')2-Sepharose column. The unbound fraction from this column contained HEBFPP, which was then partially purified by CM-Sepharose filtration. HEBFPP appeared to be a glycoprotein because it was destroyed by trypsin, bound to lentil lectin, and was eluted with alpha-methyl-mannoside. Together, the results demonstrate the existence of two antigenically distinct species of HEBF, and imply that lymphocyte binding sites of HEVLN and HEVPP are structurally different. We interpret the results to mean that distinct high endothelial adhesion molecules on lymphocytes mediate their entry into LN and PP.

Animals↗
PubMed1984

Lymphocyte recognition of lymph node high endothelium: adhesive interactions determining entry into lymph nodes.

Our interpretation of these results is that lymphocyte surface HEBF is composed of high endothelial adhesion molecules which mediate cell-cell interactions that result in lymphocyte entry from blood into lymph nodes. The evidence that anti-HEBF antibody does not interfere with lymphocyte entry into PP is intriguing, since migration into this tissue as well as LN, occurs via HEV. This suggests that high endothelial cells differ in LN and PP at least with respect to the specificity of surface molecules involved in lymphocyte adherence. It could be that separate lymphocyte subpopulations express receptors for these two types of high endothelium. If this explanation is correct, then cells negatively selected using this antibody should be capable of binding to HEV of PP but not HEV of LN. However, if receptors for both high endothelial types are present on the same lymphocyte, then it is unlikely that such selection would yield cells exhibiting tissue specificity. Our observations are consistent with previous findings which suggested that high endothelial cells of mouse LN and PP exhibit differences in lymphocyte binding properties. For example, it has been reported that certain murine lymphomas bind to HEV of either peripheral LN or PP and that, to a limited degree, this preference is a property of most B and T cells [Butcher et al, 1980; Stevens et al, 1982]. Thymus and bone marrow cells show only low levels of HEV binding and less than 10% of such cells react with anti-HEBF antibody. During differentiation lymphocytes appear to acquire surface components which mediate high endothelial adhesion and this event is associated with the appearance of surface molecules recognized by anti-HEBF antibody. This suggests that it is the expression of these surface molecules during differentiation which confers high endothelial recognition properties on lymphocytes and that this mechanism plays a role in adhesive interactions leading to entry of both T and B cells into LN.

Animals↗
PubMed1983

Lymphocyte recognition of lymph node high endothelium. V. Isolation of adhesion molecules from lysates of rat lymphocytes.

Lymphocytes migrate from blood into lymph nodes (LN) of rats specifically at segments of venules lined by high endothelium (HEV). Investigation of lymphocyte surface molecules mediating this interaction has been carried out using an in vitro assay in which lymphocytes adhere selectively to HEV when overlaid onto sections of peripheral LN. Using this assay we have previously isolated a thoracic duct lymph component termed High Endothelial Binding Factor (HEBF), which is detected by its ability to block HEV sites where lymphocytes attach. In the current study, we present evidence that anti-HEBF antibody recognizes surface molecules of lymphocytes involved in adhesion to high endothelium. Rabbit antibody was produced against HEBF isolated from lymph by sequential ion exchange [diethylaminoethyl (DEAE)-cellulose and carboxymethyl (CM)-Sepharose] and Sephacryl S-200 gel filtration. Anti-HEBF F(ab')2 bound to 60 to 70% thoracic duct lymphocytes (TDL), spleen, and LN cells but to only 2 to 9% thymus and bone marrow cells (indirect immunofluorescence). In addition, biologically active HEBF was isolated from lymph and detergent lysates of lymphocytes by antibody affinity chromatography. Comparable amounts of the factor were isolated from lysates of TDL, LN, and spleen cells whereas little or no HEBF was detected in lysates of thymus or bone marrow cells or in serum. HEBF obtained from TDL appeared to be a glycoprotein because it was trypsin sensitive, bound to lentil lectin, and was eluted with alpha-methyl-D-mannoside. The finding that HEBF was not recovered from lysates of trypsinized TDL indicates that the activity was mediated by components expressed on cell surface membranes. Immunoprecipitation studies revealed that anti-HEBF antibody recognized radioiodinated surface membrane proteins of TDL and TDL-derived T cells and B cells that resolved on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) autoradiography into three major bands with m.v. of 230,000, 210,000, and 92,000 (nonreduced) and one major band with m.w. of 70,000 and two minor bands with m.w. of 92,000 and 45,000 (reduced). These observations indicate that HEBF is a surface membrane component that is not class-specific. It is suggested that lymphocyte surface HEBF is composed of high endothelial adhesion molecules that mediate cell-cell interactions involved in entry of lymphocytes from blood into peripheral lymph nodes.

Animals↗