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PubMed2006

Measurement of protection afforded by ultraviolet-absorbing window film using an in vitro model of photodamage.

BACKGROUND AND OBJECTIVES: The effects of chronic sun damage including telangiectasias, solar lentigos, rhytides, enlarged pores, sagging skin, and pre-cancerous and cancerous growths are among the most common presenting complaints in a dermatologist's office. These changes are often worse on the driver's side of the face, emphasizing the role of UVA exposure received while driving in producing these changes. This study was undertaken to measure the ability of car window glass alone and in combination with ultraviolet (UV)-absorbing film to reduce UV-damage as measured using an established in vitro model of photoprotection. STUDY DESIGN MATERIALS AND METHODS: Using the 3T3 neutral red uptake photoprotection assay with solar simulating radiation (SSR) administered by a xenon arc solar simulator, we measured the photoprotection ability of auto glass, window film that filters UV radiation, and the combination of window film and auto glass. RESULTS: As measured by the 3T3 neutral red uptake photoprotection assay, auto glass reduced cell death from SSR by 29%, while window film reduced it 90%, and the combination of auto glass and film reduced cell death by 93%, when compared to unfiltered SSR. CONCLUSIONS: Window film that filters UV radiation results in dramatic reductions in cytotoxicity when measured by the neutral red uptake photoprotection assay. Widespread use of window film provides an ever-present barrier to ultraviolet A (UVA) exposure and could potentially reduce the detrimental effects of UVA, including photoaging, skin cancer, and ocular damage, such as cataracts. In addition, such film is essential for patients suffering from conditions sensitive to UV radiation, such as lupus erythematosis.

Animals↗
PubMed1993

HepG2 cells: an in vitro model for P450-dependent metabolism of acetaminophen.

The human hepatoma cell line, HepG2, retains many cellular functions often lost by cells in culture. This research examined the constitutive bioactivation of acetaminophen and P450-dependent activity in microsomes from HepG2 cells and the effect of 0.1% acetone pretreatment on these activities. Low levels of acetaminophen bioactivation, P450 IIE1 activity, and P450 IA1-IA2 activity were demonstrated in non-induced HepG2 microsomes. Acetone increased acetaminophen bioactivation and IIE1-dependent metabolism but not P450 IA1-IA2-dependent activity. Thus, HepG2 cells may provide an in vitro model for assessing human xenobiotic metabolism of acetaminophen and other drugs.

Acetaminophen↗
PubMed2004

Contribution of glial cells and pericytes to the mRNA profiles of P-glycoprotein and multidrug resistance-associated proteins in an in vitro model of the blood-brain barrier.

P-glycoprotein (P-gp) and the multidrug resistance-associated proteins (MRP), whose expression is associated with multidrug resistance, have been recently located in the brain capillary endothelial cells (BCEC) forming the blood-brain barrier (BBB), without taking into account a possible influence or contribution of glial cells and pericytes. Using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), the present study analysed the transcriptional expression of P-gp and the seven homologues of MRP transporters in BCECs in solo culture or in an in vitro model of the BBB consisting of a co-culture of BCECs and glial cells. Pericytes, glial cells, isolated brain capillaries and bovine grey matter extracts were also tested. P-gp mRNA, absent in glial cells, was found in brain capillaries and in co-cultured BCECs with an increased signal compared to the in solo culture. No amplification was observed in pericytes or grey matter. While MRP2, MRP3 and MRP7 remained undetected, MRP1, absent in capillaries or grey matter, was amplified in BCECs, glial cells and pericytes. MRP4 gave a low signal in most cultures. MRP5 was ubiquitously expressed, displaying a potent signal in all conditions. In spite of its presence in cultured glial cells, MRP6 mRNA expression appeared to be restricted to BCECs, with the same upregulation in the co-cultured condition as observed with P-gp. Moreover, MRP6 was the only transporter whose endothelial mRNA expression was influenced by the presence of pericytes. The tissue distribution of the expression of these transporters and the contribution of the different cell populations are discussed.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Presence of nerve growth factor and its receptors in an in vitro model of islet cell development: implication in normal islet morphogenesis.

In vivo, the differentiation of pancreatic islet stem cells depends on unknown soluble factors produced by the mesenchyme surrounding these cells. We have previously demonstrated that, like some neuronal cells, different beta-cell lines express functional nerve growth factor (NGF) receptors and can respond to NGF by extending neurite-like processes. NGF receptors are also expressed in vivo in mature rat islets and early during development in pancreatic ductular cells, which represent putative beta-stem cells. In this study, we have further characterized an in vitro model of islet development and studied the expression of NGF receptors and its ligand in this model. We have demonstrated the expression of Trk-A messenger RNA coding for the high affinity NGF receptor in islet cells and the localization of Trk protein in both alpha- and beta-islet cells. Moreover, the cells, from which islet cells "bud," also express Trk-A. Furthermore, NGF is produced and secreted by the nonendocrine cells surrounding the islets, suggesting a possible paracrine mode of action of NGF on the adjacent islet cells. Finally, islet morphogenesis is significantly retarded in the presence of K252a, an inhibitor of the tyrosine kinase activity of the family of Trk receptors, suggesting an implication of the neurotrophin-neurotrophin receptor axis in islet development.

Animals↗
PubMed1985

Appearance of Ia antigens on T lymphocytes stimulated by streptococcal mitogen as an in vitro model of autoimmunity.

Streptococcal mitogen (SM) is an extracellular product of group A streptococci, which is nonspecifically mitogenic for both B and T lymphocytes. The mitogenic activity of SM is resistant to digestion with trypsin, to heating at 100 degrees C for 5 min and to treatment with dithiothreitol. The proliferative response of lymphocytes from patients with a history of rheumatic fever is similar to that of lymphocytes from healthy donors when stimulated with optimal concentrations of SM, but is significantly reduced when low doses of SM are used. T lymphocytes stimulated with SM acquire la antigens and the ability to stimulate allogeneic and autologous lymphocytes in mixed lymphocyte reactions. An involvement of la antigens in these reactions is indicated by the specific block by monoclonal antibodies. T lymphocytes may acquire la antigens following exposure to an appropriate antigen. If this occurs following a streptococcal infection, these in vitro findings suggest that la bearing T cells may play a role in the immunopathological events which can follow a streptococcal infection. The system described may be a useful in vitro model to analyse the immunopathological events which can follow a streptococcal infection and to develop therapeutic approaches to autoimmune conditions.

Autoimmune Diseases↗
PubMed2005

T cells support osteoclastogenesis in an in vitro model derived from human periodontitis patients.

BACKGROUND: Periodontitis is characterized by alveolar bone destruction; however, the mechanisms responsible for bone damage are poorly understood. It has been reported that T cells are implicated in the pathogenesis of periodontitis. It has been also demonstrated that activated T lymphocytes secrete receptor activator of nuclear factor-kappa B ligand (RANKL) and can support the differentiation of monocytes into resorbing osteoclasts (OCs). Therefore, the purpose of this study was to examine the OC formation in periodontitis patients (PP) and the role of T cells in osteoclastogenesis. METHODS: To study OC formation, we used an in vitro model consisting of unstimulated and unfractionated peripheral blood mononuclear cells (PBMCs) from PP and controls. In parallel, T-cell-depleted PBMCs from the same patients were also established. The expression of RANKL and tumor necrosis factor-alpha (TNF-alpha) was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot in fresh T cells isolated from PP and controls. Functional antibodies, anti-RANKL and anti-TNF-alpha, were utilized to study osteoclastogenesis in PBMC cultures from PP. RESULTS: We showed that, in unfractionated PBMCs from PP, the OCs spontaneously developed in a T-cell-dependent way. The addition of macrophage colony stimulating factor (MCSF) and RANKL was necessary to promote the osteoclastogenesis in T-cell-depleted PBMC cultures from PP and in unfractionated PBMCs from periodontally healthy controls. Moreover, freshly isolated T cells from PBMCs of PP overexpressed RANKL and TNF-alpha. Finally, functional anti-RANKL and anti-TNF-alpha antibodies significantly inhibited osteoclastogenesis. CONCLUSION: Our data suggest that T cells support spontaneous osteoclastogenesis in PP via RANKL and TNF-alpha overexpression.

Adult↗
PubMed1998

Invasion of human cartilage by cultured multicellular spheroids of rheumatoid synovial cells--a novel in vitro model system for rheumatoid arthritis.

OBJECTIVE: A new 3-dimensional cell culture system was established to examine the invasion of rheumatoid synovial cells into cartilage. METHODS: Synovial cells from 20 patients with rheumatoid arthritis (RA) and 15 patients with osteoarthritis (OA) were co-cultured as multicellular spheroids with cartilage fragments. RESULTS: After 4 weeks the rheumatoid spheroids eroded the cartilage. The destruction of cartilage was supported by a high expression level of cathepsin D and matrix metalloproteinases. In contrast, the OA tissue showed attachment to the cartilage only. CONCLUSION: Our results indicate that spheroid/cartilage co-cultures seem to be a suitable in vitro model for the study of destructive cellular mechanisms that occur in RA.

Arthritis, Rheumatoid↗
PubMed1995

In vitro model of human umbilical venous perfusion to study the effects of meconium staining of the umbilical cord.

Because meconium diffuses into placental and umbilical cord tissue, its bioactive components are potentially capable of entering the fetal circulation. Meconium diluted in Krebs solution produces vasoconstriction in human umbilical vein segments that are suspended in a milieu similar to that of the amniotic cavity. Based on published observations, we wanted to determine if very diluted meconium could induce vasospasm in intact umbilical cords. Human umbilical cords were obtained from full-term deliveries, cut into 2 equal segments, cannulated, and perfused continuously as test and control cords. The study included four parts: (1) intraluminal meconium (n = 6; 0.01-1% solution); (2) 4-hour exposure to 10% meconium-stained amniotic fluid of intact umbilical cords (n = 8); (3) 4-hour exposure to a 10% meconium-stained amniotic fluid of umbilical cords denuded of their epithelial layer (n = 5); (4) 24-hour exposure to a 10% meconium-stained amniotic fluid of intact umbilical cords (n = 9). Significant vasoconstriction of the umbilical vein occurred only with the intraluminal meconium solution exposure (p = 0.034). In this in vitro model meconium staining of the umbilical cord was not associated with vasoconstriction of the umbilical vein.

Humans↗
PubMed2003

Double-edged effect of Vgamma9/Vdelta2 T lymphocytes on viral expression in an in vitro model of HIV-1/mycobacteria co-infection.

A reciprocal influence exists between mycobacteria and HIV: HIV-infected individuals are more susceptible to mycobacterial infections and, on the other hand, mycobacterial infection results inacceleration of HIV disease progression. Vgamma9/Vdelta2 T lymphocytes are known to participate in the defense against intracellular pathogens, including Mycobacterium tuberculosis. Indeed, they kill mycobacteria-infected macrophages and, upon recognition of mycobacterial Ag, release TNF-alpha and IFN-gamma, which are also up-regulators of HIV expression. To assess whether mycobacteria-activated gamma delta T lymphocytes contribute to the enhancement of HIV replication, we established an in vitro model mimicking HIV and mycobacteria co-infection with the latently HIV-infected promonocytic U1 cell line and Vgamma9/Vdelta2 peripheral lymphocytes stimulated with mycobacterial Ag. gamma delta T cell activation determined two distinct, but connected effects, namely U1cell death and HIV expression. Both effects were mainly mediated by release of TNF-alpha and IFN-gamma from activated gamma delta lymphocytes, although Fas-FasL interaction also contributed to U1 apoptosis. The final outcome on U1 survival, and thus, on HIV expression, highly depended on mycobacterial Ag concentration coupled to the differential secretory potency of gamma delta cells. In particular, the induction of viral expression prevailed at low Ag concentration and with lower cytokine production by mycobacteria-activated gamma delta cells. Notably, during the course of HIV infection, Vgamma9/Vdelta2 lymphocytes are reported to be functionally impaired and may thus indirectly influence the progression of HIV disease. In addition, a predominant inhibition of viral replication was encountered when mycobacteria-activated gamma delta T cells were co-cultured with primary HIV-infected macrophages. Thus, we suggest that specific recognition of mycobacterial Ag by gamma delta T lymphocytes in co-infected individuals may modulate viral replication through the complex array of soluble factors released.

Apoptosis↗
PubMed1997

In vitro models for prediction of antimicrobial activity: a pharmacokinetic and pharmacodynamic perspective.

The endpoints associated with conventional susceptibility testing, e.g., the minimum inhibitory concentration or minimum bactericidal concentration (MIC or MBC), are discrete in nature. These endpoint measurements do not provide any information, regarding the pharmacodynamic changes exhibited by the bacteria in reaction to the antibiotic activity during the incubation period. Another limitation of these susceptibility tests is the maintenance of constant antibiotic concentrations; this condition contrasts sharply to the continuously changing concentrations observed in vivo. To tackle these problems, various in vitro pharmacokinetic/pharmacodynamic models have been developed. Taking into consideration various pharmacokinetic determinants, such models allow more comprehensive study of the pharmacodynamic effects demonstrated by antibiotics. In this paper, the implications and usefulness of these in vitro models to the characterization of antimicrobial activity are discussed. Limitations associated with their use are also addressed.

Anti-Bacterial Agents↗
PubMed1997

Acid modulation of HT29 cell growth and differentiation. An in vitro model for Barrett's esophagus.

Cell proliferation and differentiation are influenced by environmental factors, including the extracellular pH. We recently showed, using an ex vivo organ culture system of human mucosal Barrett's esophageal biopsies, that acid has a highly variable effect on cell proliferation and differentiation depending on the pattern of acid exposure. Study of the mechanisms underlying these dynamic effects of acid on this premalignant intestinal-like epithelium is hampered by lack of an immortalized cell line. We therefore investigated the effect of acid exposure on the human colonic carcinoma cell line HT29, chosen because of its intestinal cell derivation and its ability to differentiate in vitro. HT29 cells exposed to pH 5 medium either continuously (up to 3 weeks), or as a short (1 hour) pulse, were compared with cells cultured at pH 7.4. Villin expression was induced only by long term acid exposure, and correlated with the development of differentiated polarized cells that contain a brush border and microvillus inclusions. Chronic acid exposure arrested cell proliferation, whereas a 1 hour acid-pulse enhanced cell proliferation, as determined by [3H]thymidine incorporation assays and proliferating cell nuclear antigen expression. Serum starvation attenuated the hyperproliferative effect of an acid-pulse. In addition, the doubling time of at least the first cell cycle after an acid-pulse was shortened. The Na/H exchanger is likely to play a role since the hyperproliferative acid-induced response was blocked by amiloride; and the activity of the exchanger was increased at acidic pH as determined by 22Na uptake. These results support a role for extracellular pH on cell proliferation and differentiation of HT29 cells. Furthermore, these findings parallel the dynamic effects of acid on Barrett's esophagus, and suggest that HT29 cells could serve as an in vitro model for studying the mechanism of acid modulation in Barrett's esophagus.

Barrett Esophagus↗
PubMed2004

Enhanced repair of the anterior cruciate ligament by in situ gene transfer: evaluation in an in vitro model.

The inability of the ruptured anterior cruciate ligament (ACL) of the knee joint to heal spontaneously presents numerous clinical problems. Here we describe a novel, gene-based approach to augment ACL healing. It is based upon the migration of cells from the ruptured ends of the ligament into a collagen hydrogel laden with recombinant adenovirus. Cells entering the gel become transduced by the vector, which provides a basis for the local synthesis of gene products that aid repair. Monolayers of bovine ACL cells were readily transduced by first-generation, recombinant adenovirus, and transgene expression remained high after the cells were incorporated into collagen hydrogels. Using an in vitro model of ligament repair, cells migrated from the cut ends of the ACL into the hydrogel and were readily transduced by recombinant adenovirus contained within it. The results of experiments in which GFP was used as the transgene suggest highly efficient transduction of ACL cells in this manner. Moreover, during a 21-day period GFP+ cells were observed more than 6 mm from the severed ligament. This distance is ample for the projected clinical application of this technology. In response to TGF-beta1 as the transgene, greater numbers of ACL cells accumulated in the hydrogels, where they deposited larger amounts of type III collagen. These data confirm that it is possible to transduce ACL cells efficiently in situ as they migrate from the ruptured ACL, that transduction does not interfere with the cells' ability to migrate distances necessary for successful repair, and that ACL cells will respond in a suitable manner to the products of the transgenes they express. This permits optimism over a possible clinical use for this technology.

Adenoviridae↗
PubMed1999

Application of an in vitro model to evaluate bioadhesion of fibroblasts and epithelial cells to two different dressings.

The cellular component of a healing wound consists of many cell types and the environment in which these cells grow is important to the rate and quality of healing which can be influenced by the type of dressing used. The most commonly used dressings are traditional gauze-type dressings. In many cases these dressings may adhere to the wound surface, and subsequent removal is often traumatic, causing pain and tissue reinjury. Some modern gelling dressings have been developed to overcome this adherence problem. In order to evaluate in more detail cell-dressing interactions, an in vitro model has been developed utilising wound fibroblasts and epithelial cells. Quantitative evaluation of adherence of cells cultured with a traditional gauze or a new gelling dressing has been undertaken using radiolabel and manual counting techniques. Scanning electron microscopy has been used to visualise the cells adherent to dressings allowing evaluation of their adhesion-morphology. The results show differential attachment of cells to viscose and gelling fibres of the dressings; considerably reduced cell adhesion to the gelling fibre was evident, and it was apparent that cells adhered predominantly to the viscose component of the dressing. This model can be used to investigate and compare the adhesion of cells to different dressings and their components.

Animals↗
PubMed1991

A novel hemidesmosomal plaque component: tissue distribution and incorporation into assembling hemidesmosomes in an in vitro model.

The hemidesmosome and its associated structures, such as anchoring fibrils, form a complex structure, the polypeptide composition of which has only recently begun to be elucidated. We describe the characterization of a monoclonal antibody, mAb6A5, directed against a 200-kDa polypeptide found in the cytoplasmic-most area of the hemidesmosomal plaque. This 200-kDa polypeptide is immunologically distinct from the 180- and 230-kDa hemidesmosomal plaque components recognized by bullous pemphigoid (BP) autoantibodies. mAb6A5 recognizes hemidesmosomes of stratified squamous epithelia in a number of species, including human tissue. mAb6A5 also recognizes pseudo-stratified epithelium, but not simple or transitional epithelia. During de novo hemidesmosome assembly in an in vitro model of epithelial wound healing, the 200-kDa polypeptide is in most instances deposited at the epithelial-stromal interface after plaque components recognized by BP autoantibodies, but before the collagen type VII component of anchoring fibrils. We discuss possible mechanisms of hemidesmosomal plaque assembly.

Animals↗
PubMed1996

In-vitro model of uterine leiomyomas: formation of ball-like aggregates.

To clarify the biological characteristics of uterine leiomyomas, cells explanted and cultured from uterine leiomyomas and from normal myometrial tissue were observed by time-lapse cinemicrography and phase-contrast microscopy. The histological characteristics were evaluated by electron microscopy and immunofluorescence microscopy, and these observations revealed significant differences. By time-lapse cinemicrography, the cells cultured from leiomyomas and myometrium differed in their behaviour. Cells from the myometrium started to grow in parallel with the cell's major axis and formed topographically uniform hills and valleys by day 21 of culture. In contrast, the cells from leiomyomas started to grow irregularly, as if having no contact inhibition, and formed ball-like aggregates of cells by day 21 of culture. The aggregates resembled the nodules of leiomyoma in vivo. Ultrastructurally, cells from both leiomyomas and myometrium had typical features of smooth muscle. Immunofluorescently, a different distribution of alpha-smooth muscle actin-positive filaments and different staining of cellular fibronectin and N-cadherin between the cells from leiomyomas and myometrium were observed, which may contribute in part of the different behaviour of the cells. Given that the explant cell culture system resembles the features of uterine leiomyomas in vivo, this suggests that it can be used as an in-vitro model.

Antibodies↗
PubMed2007

An in vitro model of the leukocyte interactions associated with granuloma formation in Mycobacterium tuberculosis infection.

The principal defense of the human host against a Mycobacterium tuberculosis infection is the formation of granulomas, organized collections of activated macrophages, including epithelioid and multinucleated giant cells, surrounded by lymphocytes. This granuloma can sequester and contain the bacteria preventing active disease, and if the granuloma is maintained, these bacteria may remain latent for a person's lifetime. Secretion of a variety of chemoattractant cytokines following phagocytosis of the bacilli by the macrophage is critical not only to the formation of the granuloma but also to its maintenance. To investigate this process of early granuloma formation, we developed an in vitro model composed entirely of human cells. Combining blood lymphocytes and autologous macrophages from healthy purified protein derivative skin test-negative individuals and mycobacteria resulted in the formation of small, rounded aggregate structures. Microscopic examination found macrophage-specific CD68(+) epithelioid macrophages and small round CD3(+) lymphocytes that in complex resembled small granulomas seen in clinical pathology specimens. Acid-fast staining bacteria were observed between and possibly within the cells composing the granulomas. Supernatants from the infected cells collected at 24 and 48 h and 5 and 9 days after infection were analyzed by a multiplexed cytokine bead-based assay using the Luminex 100 and were found to contain interleukin (IL)-6, IL-8, interferon-gamma and tumor necrosis factor-alpha, cytokines known to be involved in human granuloma formation, in quantities from two-fold to 7000-fold higher than supernatants from uninfected control cells. In addition, chemotaxis assays demonstrated that the same supernatants attracted significantly more human peripheral blood mononuclear cells than those of uninfected cells (P<0.001). This model may provide insight into the earliest stages of granuloma formation in those newly infected.

Adult↗
PubMed1994

Self-renewal and differentiation of stem cells in a biopotential murine leukemia: an in vitro model for differentiation therapy.

PGM-2 is a variant of the transplantable PGM-1 leukemia of strain C3H/HeJ. Freshly explanted cells had lymphoid morphology with a CD5+ CD45R (B220)- IgM- phenotype. They were not viable in unstimulated cultures, but formed IgM+ lymphoid colonies in response to interleukin-2 (IL-2), IL-4, IL-5, IL-6, IL-7, and Steel factor, and macrophage colonies in response to IL-3. IL-3-stimulated colonies had no recloning potential, but colonies from IL-7 cultures gave rise to large numbers of secondary macrophage colonies in IL-3-stimulated cultures and secondary lymphoid colonies in IL-7-stimulated cultures. The latter ones could be serially transferred in vitro for several months, and formed typical PGM-2 tumors in vivo. IL-7-stimulated colonies could therefore be used to measure leukemic stem cells in vitro. Supramaximal IL-3 stimulation (2,500 U/mL) of suspension cultures was followed by an increase in overall cell numbers and a disappearance of leukemic stem cells, compatible with differentiation induction. This could not be counteracted by simultaneous stimulation with IL-7. However, lower IL-3 concentrations (500 U/mL) induced an expansion of the stem cell pool, possibly by facilitating density-dependent autostimulatory mechanisms involving endogenous production of IL-7. The system described is a simple in vitro model for differentiation therapy. It shows that leukemic stem cells can be induced by hematopoietic growth factors to undergo terminal differentiation, but the concentrations required for differentiation induction in stem cells are much higher than those required for other biologic effects. Submaximal stimulation may favor expansion rather than repression of the leukemic cell population.

Animals↗
PubMed1998

An in vitro model of T cell activation by autologous cytomegalovirus (CMV)-infected human adult endothelial cells: contribution of CMV-enhanced endothelial ICAM-1.

Cellular immunity is strongly implicated in control of CMV disease; however, many mechanistic details remain unresolved. We previously demonstrated T cell activation responses to CMV-infected allogeneic endothelial cells (EC), suggesting EC as a mediator of CMV response in the transplant recipient. We now test the hypothesis that CMV-specific T cell responses can be directly stimulated by infected EC in an environment free of potentially confounding allogeneic factors. By isolating splenic T cells and gonadal vein endothelial cells (GVEC) from individual cadaveric organ donors, we have developed an in vitro model of T cell interaction with autologous CMV-infected EC. Proliferation assays demonstrated significantly enhanced responses by CMV-seropositive donor-derived T cells cocultured with CMV-infected GVEC, as compared with those elicited by uninfected cells. Similarly, as determined by limiting dilution analysis of IL-2-producing cells, T cell response frequencies to infected GVEC were significantly greater than to uninfected EC. In contrast, responses of CMV-seronegative donor-derived T cells were minimal, regardless of CMV status of stimulator GVEC. Intriguingly, CD4 responses were observed in spite of the fact that CMV-infected EC express no HLA class II. Finally, attenuation of CMV-stimulated T cell proliferation observed in the presence of blocking Ab specific for ICAM-1 suggests a contributing role for CMV-enhanced endothelial ICAM-1 expression in the activation response. These studies demonstrate that EC can stimulate autologous T cell responses to CMV in the absence of accessory APC and suggest potentially novel mechanisms of immune activation.

Adult↗