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PubMed1987

A quantitative analysis of antigen-triggered lymphokine production by activated T cells.

We have developed a theoretical model to describe the triggering of lymphokine release from antigen-specific, activated T (T') cells, and we have used this model to define parameters that regulate this interaction. Under assay conditions of T' cell excess, the efficiency of triggering is a function of the target cell type. When various H-2k-bearing target cells were used to trigger B10.AQR T' cells activated against B10.A cells (anti-Kk), a hierarchy of triggering efficiency was observed with B10.A Con A blasts greater than R1.1 tumor cells greater than B10.A spleen cells greater than B10.A lymph node cells. There was a 10-fold difference in triggering efficiency between Con A blasts and lymph node cells. A similar pattern of reactivity was observed for various H-2d-bearing target cells used to trigger CBA T' cells specific for BALB/c antigens (anti-H-2d). Under assay conditions of T' cell excess, the order of reaction, i.e., the number of target cells per T' cell required to trigger lymphokine release, remained constant for the different target cell types. However, the order of reaction can vary with conditions of T cell activation. CBA T' cells activated against BALB/c spleen cells exhibited pseudo-first-order reactivity when triggered for lymphokine release with P815 target cells, whereas CBA T' cells activated against UV-irradiated P815 cells exhibited pseudo-second-order reactivity when triggered by the same tumor cells. Thus, T cells with the same apparent specificity can be qualitatively different in their reactivity with antigen. Under assay conditions of target cell excess, our analysis indicated that no T-T interaction was involved in the triggering reaction. Finally, our analysis was applied to study the nature of cross-reactivity. The results indicated that the triggering of lymphokine elicited by a cross-reactive antigen was due to the reactivity of a discrete subset of T' cells.

Animals↗
PubMed2001

Does the developmental neurotoxicity of chlorpyrifos involve glial targets? Macromolecule synthesis, adenylyl cyclase signaling, nuclear transcription factors, and formation of reactive oxygen in C6 glioma cells.

The widespread use of chlorpyrifos (CPF) has raised major concerns about its potential to cause fetal or neonatal neurobehavioral damage, even at doses that do not evoke acute toxicity. CPF has been shown to inhibit replication of brain cells, to elicit alterations in neurotrophic signaling governing cell differentiation and apoptosis, and to evoke oxidative stress. However, the specific cell types targeted by CPF have not been clarified, an issue of vital importance in establishing the boundaries of the critical period in which the developing brain is vulnerable. In the current study, we evaluated the effects of CPF on C6 glioma cells, a well-established glial model. In undifferentiated C6 cells, CPF inhibited DNA synthesis in a concentration-dependent manner, with greater potency than had been seen previously with neuronal cell lines. Just as found after in vivo CPF treatment or with neuronal cell lines, the effects on cell replication were independent of cholinergic stimulation, as cholinergic antagonists did not block CPF-induced inhibition. CPF interfered with cell signaling mediated through adenylyl cyclase at the level of G-protein function; the effects again were greater in undifferentiated C6 cells but were still detectable in differentiating cells. In contrast, differentiation enhanced the ability of CPF to elicit the formation of reactive oxygen species and to evoke deficits in Sp1, a nuclear transcription factor essential for differentiation. These results indicate that glial-type cells are targeted by CPF through the same multiple mechanisms that have been demonstrated for the effects of CPF on brain development in vivo. Because glial development continues long after the conclusion of neurogenesis, and given that CPF targets events in both glial cell replication and the later stages of differentiation, the vulnerable period for developmental neurotoxicity of CPF is likely to extend well into childhood.

Adenylyl Cyclases↗
PubMed1982

Dynamics of in situ estrogen uptake by nuclei of individual pituitary and uterine cell types.

This investigation was carried out to examine the temporal aspects of nuclear retention of 3H-estrogen by individual target cell types of the rat uterus and pituitary. A quantitative dry autoradiographic-immunocytochemical method was used to measure relative 3H-estrogen uptake by nuclei of seven different target cell types 15 m, 1 h, 3 h and 7 h after injection of 3H-estradiol-17 beta. All five target cell types in anterior pituitary showed maximal nuclear retention at 15 m. Possible cell-type differences were noted in the rate of release of the isotope from nuclei. In the uterus maximal uptake, occurred between 1 h and 3 h after injection with stromal cells consistently concentrating more 3H-estrogen than luminal epithelial cells. These findings indicate possible differences between the mechanisms controlling nuclear retention of estrogen by the uterus and the pituitary.

Animals↗
PubMed2003

Biomimetic design in microparticulate vaccines.

Current efforts to improve the effectiveness of microparticle vaccines include incorporating biomimetic features into the particles. Many pathogens use surface molecules to target specific cell types in the gut for host invasion. This observation has inspired efforts to chemically conjugate cell-type targeting ligands to the surfaces of microparticles in order to increase the efficiency of uptake, and therefore the effectiveness, of orally administered microparticles. Bio-mimicry is not limited to the exterior surface of the microparticles. Anti-idiotypic antibodies, cytokines or other biological modifiers can be encapsulated for delivery to sites of interest as vaccines or other therapeutics. Direct mucosal delivery of microparticle vaccines or immunomodulatory agents may profoundly enhance mucosal and systemic immune responses compared to other delivery routes.

Animals↗
PubMedDate not supplied

A whole blood method for measurement of intracellular TNF-alpha, IFN-gamma and IL-2 expression in stimulated CD3+ lymphocytes: differences between young and elderly subjects.

Cytokines, the central regulators of leucocyte growth and differentiation, are produced by a wide variety of cell types, target various cell subsets and exhibit numerous biological activities. Cytokine dysregulation is believed to play a role in the remodelling of the immune system in old age, however, previous reports of cytokine levels in elderly subjects have been conflicting, possibly due to methodologies employed. We used the relatively new technique of intracellular cytokine detection by flow cytometry to measure cytokine production in CD3+ lymphocytes from young and elderly subjects, but applied it to whole blood, thereby eliminating the need for laborious cell separation techniques and maintaining cells in their normal physiological environment. We found the assay to be very reproducible with acceptable intra- (2.9%) and inter- (6.3%) assay CVs. The percentages of CD3+ cells producing TNF-alpha and IFN-gamma were significantly higher in elderly compared to young people (p=0.0049; p=0.0026, respectively) after stimulation with PMA and ionomycin. Absolute counts of CD3+IFN-gamma+ and CD3+TNF-alpha+ cells were also significantly higher in the elderly group (p=0.039; p=0.051) respectively. There was no significant difference between the age groups for the percentage or numbers of IL-2-producing CD3+ cells on stimulation. CD3+ cells expressing TNF-alpha were highly associated with CD3+ cells expressing IFN-gamma in both elderly and young people. In contrast, IL-2 secreting CD3+ cells were associated with TNF-alpha and IFN-gamma producing CD3+ cells in young but not elderly subjects providing further evidence for the remodelling of the cytokine network associated with old age.

Adult↗
PubMed1993

The mechanism for the activation of latent TGF-beta during co-culture of endothelial cells and smooth muscle cells: cell-type specific targeting of latent TGF-beta to smooth muscle cells.

Transforming growth factor-beta (TGF-beta) is secreted in a latent form and activated during co-culture of endothelial cells and smooth muscle cells. Plasmin located on the surface of endothelial cells is required for the activation of latent TGF-beta (LTGF-beta) during co-culture, and the targeting of LTGF-beta to the cellular surface is requisite for its activation. In the present study, the cellular targeting of LTGF-beta was examined. We detected the specific binding of 125I-large LTGF-beta 1 isolated from human platelets to smooth muscle cells but not to endothelial cells. A mAb against the latency-associated peptide (LAP) of large LTGF-beta 1 complex, which blocked the binding of 125I-large LTGF-beta 1 to smooth muscle cells, inhibited the activation of LTGF-beta during co-culture. The binding of 125I-large LTGF-beta 1 could not be competed either by mannose-6-phosphate (300 microM) or by the synthetic peptide Arg-Gly-Asp-Ser (300 micrograms/ml). These results indicate that the targeting of LTGF-beta to smooth muscle cells is required for the activation of LTGF-beta during co-culture of endothelial cells and smooth muscle cells. The targeting of LTGF-beta to smooth muscle cells is mediated by LAP, and the domain of LAP responsible for the targeting to smooth muscle cells may not be related to mannose-6-phosphate or an Arg-Gly-Asp sequence, both of which have been previously proposed as candidates for the cellular binding domains within LAP.

Amino Acid Sequence↗
PubMed1982

NK cell-target interactions: approaches towards definition of recognition structures.

NK cells lyse an uncommonly wide range of cell types, implying either that they (the NK cells) have clonally distributed receptors each of which is capable of interacting with a very limited number of cell types or, alternatively, that susceptible target cells share a common characteristic. A number of experimental approaches have suggested that the cytotoxic 'specificity' of NK cells is not clonally distributed. Thus, clones of NK cells, established from mouse spleen cell suspensions, showed no greater restriction in the spectrum of target cells which they could lyse, than did the parent spleen cell populations from which they were derived. It seems likely therefore that the wide range of target cell types that can be lysed by NK cells share common cell surface characteristics which render them susceptible. As lysis results from membrane-membrane interactions, it seemed logical that a search for 'hallmarks' of NK susceptibility should begin with a detailed examination of the plasma membrane of susceptible cells. Analysis of one pair of lymphoma cell variants, selected on account of their markedly different susceptibility to NK cells, suggests that cell surface glycoconjugates may be of significance in determining those effector cell-target cell interactions that lead to lysis. This review outlines attempts to characterize such glycoconjugates.

Animals↗
PubMed2006

Rat testicular germ cell type(s) targeted by anti-spermatogenic agents in vivo and their recovery on withdrawal of treatment--a flow cytometric study.

Spermatogenesis goes through very critically and precisely balanced ratios of germ cells with diverse DNA ploidies (1C, 2C and 4C). Antispermatogenic agents that reversibly interrupt spermatogenesis may have a contraceptive relevance. With a view to study the precise mechanism of action of antispermatogenic agents and identify the germ cell type(s) targeted by various agents in vivo, spermatogenic cells with diverse DNA ploidies were measured in rat testis during treatment and recovery with compounds CDRI-84/35, gossypol and estradiol, using Flow Cytometry. Rats were treated with either CDRI-84/35 (100mg/(kg day) for 15 days followed by 25mg/(kg day) for 55 days) or gossypol (20mg/(kg day) for 70 days) or estradiol benzoate (2.5microg/(rat day) for 70 days) and 3 rats from each group were sacrificed after 22, 41, 53 and 70 days of treatment to monitor the changes in population of 1C, 2C, S-phase and 4C germ cell types. Treatment with CDRI-84/35 resulted in a significant and rapid drop in 1C population with a concomitant and parallel rise in 2C population. In gossypol-treated animals 1C peak disappeared gradually and the arrest was seen predominantly at 2C stage and partially at 4C stage. At the end of the treatment most of the germ cells were arrested at 2C stage. Estradiol affected spermatogenesis differently with 1C population falling in complement to rise in both 2C and 4C peaks. Germ cells were mainly arrested at the 4C stage after the treatment. The data suggest that germ cells fail to enter meiosis in CDRI-84/35-treated rats. Few cells entering meiosis do not complete the cell division and remain arrested at 4C stage. However in case of estradiol and gossypol the meiotic 4C cells become incapable of further differentiation into haploid cells. After receiving 70 days of treatment a few rats were allowed to recover for 60, 90 and 120 days. The population of various germ cell types in the testis of recovery-group animals indicated that spermatogenesis resumes substantially in case of estradiol treatment and partially in case of treatment with the other two agents.

Animals↗
PubMed1998

Two types of anti-TL (thymus leukemia) CTL clones with distinct target specificities: differences in cytotoxic mechanisms and accessory molecule requirements.

TCRalphabeta CTL clones recognizing mouse thymus leukemia (TL) Ags were established and categorized into two groups: those killing any TL+ target cells (type I) and those killing only TL+ Con A blasts (type II). Cold target inhibition assays showed that the antigenic determinant(s) recognized by type II clones are expressed not only on TL+ Con A blasts but also on other TL+ target cells. The relation of the target specificity to the killing machinery and the accessory molecules involved in cytotoxicity were therefore analyzed using four representative clones selected from each type. Of the target cells tested, Fas was only expressed on Con A blasts, indicating that Fas ligand (FasL)-dependent cytotoxicity is limited to such cells. All four type II and one of four type I clones expressed FasL on the surface, while both types contained perforin in the cytoplasm. Blocking studies using neutralizing anti-FasL mAbs and concanamycin A (CMA), a selective inhibitor of the perforin pathway, suggested that type I clones kill target cells by way of perforin, while type II clones kill TL+ Con A blasts through FasL together with perforin. For their cytotoxicity, type I CTLs require a signal through CD8, while type II require LFA-1/ICAM-1 interactions. Type II clones also need a co-stimulatory signal through an unknown molecule for perforin-dependent cytotoxicity. These results taken together suggest that the difference in the target specificity of anti-TL CTL clones is due to variation in the killing machineries and the dependence on accessory molecules.

Animals↗
PubMed2000

Cell-type specific targeting of the alpha 2c-adrenoceptor. Evidence for the organization of receptor microdomains during neuronal differentiation of PC12 cells.

We have previously shown differences in the intracellular targeting of alpha2a (alpha(2A))- and alpha2c (alpha(2C))-adrenoreceptors expressed in the same cell line (von Zastrow, M., Link, R., Daunt, D. , Barsh, G., and Kobilka, B. (1993) J. Biol. Chem. 268, 763-766; Daunt, D. A., Hurt, C., Hein, L., Kallio, J., Feng, F., and Kobilka, B. K. (1997) Mol. Pharmacol. 51, 711-720). alpha(2A)-Adrenoreceptors reside primarily in the plasma membrane in HEK 293 cells, while co-expressed alpha(2C)-adrenoreceptors are found mainly in an intracellular compartment. Since alpha(2c)-adrenoreceptors are expressed primarily in the brain, we compared the intracellular targeting of alpha(2C)-adrenoreceptors in two neuroendocrine cell lines with the targeting in three epithelial cell lines and one fibroblast cell line. In transiently transfected COS7 cells, and in stably transfected normal rat kidney cells, Madin-Darby canine kidney cells, and Rat1 fibroblasts, a significant proportion of alpha(2C)-adrenoreceptor detected by immunocytochemistry co-localized with markers for both the endoplasmic reticulum and the cis/medial Golgi compartments. In contrast, both PC12 cells and AtT20 cells efficiently targeted alpha(2C)-adrenoreceptors to the plasma membrane. Ligand binding and Western blot analyses indicate that intracellular receptor in normal rat kidney cells is functional and undergoes normal post-translational processing. In PC12 cells the expressed alpha(2C)-adrenoreceptors become concentrated in neurite outgrowths in discrete regions of the plasma membrane having a high density of F-actin following treatment with nerve growth factor. These findings provide evidence for cell-type specific factors that facilitate the targeting of the G protein-coupled receptors to the plasma membrane.

Animals↗
PubMed2005

Cell type-specific targeting with sindbis pseudotyped lentiviral vectors displaying anti-CCR5 single-chain antibodies.

Lentiviral vectors are among the most efficient tools for gene delivery into mammalian cells. A major goal of lentiviral gene delivery systems is to develop vectors that can efficiently target specific cell types. In the present work, we attempt to generate viral particles for targeting gene delivery. We have used CCR5-positive cells as the target for our strategy. Therefore, we developed a novel Sindbis pseudotyped lentiviral vector where the Sindbis receptor binding envelope protein was modified to directly encode a single-chain antibody fragment (scFv) against the CCR5 chemokine receptor. We have generated two chimeric scFv-Sindbis envelopes, varying the length of the peptide linker that connects the heavy chain and light chain of anti-CCR5 scFv. The two chimeric scFv-Sindbis envelopes were successfully incorporated into lentiviral-derived vectors, and the resulting pseudotyped viral particles showed specific targeting to CCR5-expressing cells. However, our data demonstrate that the length of the peptide linker significantly affects the efficiency of infection. Pseudotyped viral particles, which display single-chain antibody fragments with longer peptide linkers, allowed higher titers of infection. The present study can be a model strategy for specific gene delivery mediated by lentiviral vectors pseudotyped with Sindbis envelope displaying scFv that recognizes specific cellular surface proteins. Furthermore, this strategy has the potential to become a powerful approach for targeting gene delivery in anti- HIV gene therapy due to the important role of CCR5 expression in disease progression.

Antibodies, Anti-Idiotypic↗
PubMed2003

Cell-type specific targeting and gene expression using a variant of polyoma VP1 virus-like particles.

The variant VP1-Z of the polyomavirus coat protein VP1 has been recently described as an engineered fusion protein of VP1 and the antibody binding domain protein Z. This construct is able to specifically bind and functionally present antibodies on the surface of virus-like particles of VP1-Z. Here we demonstrate that with the binding of Herceptin, an antibody directed against the receptor tyrosine kinase ErbB2, a cell type-specific targeting was established. ErbB2-positive cell lines were transduced with different plasmids encoding eGFP or beta-galactosidase. With both reporter systems functional gene expression in transduced cells could be observed. The transduction was strictly dependent on the use of a ternary complex formed of VLPs of VP1-Z, Herceptin, and the reporter plasmid DNA. The use of single components or ErbB2-negative cell lines did not result in functional gene transfer. The transduction was also completely dependent on the use of chloroquine, a lysosomotropic reagent. This indicates that the complex is internalized by ErbB2-mediated endocytosis.

Antibodies, Monoclonal↗
PubMed2004

Cell-type-dependent targeting of human immunodeficiency virus type 1 assembly to the plasma membrane and the multivesicular body.

The human immunodeficiency virus type 1 (HIV-1) assembly-and-release pathway begins with the targeting of the Gag precursor to the site of virus assembly. The molecular mechanism by which Gag is targeted to the appropriate subcellular location remains poorly understood. Based on the analysis of mutant Gag proteins, we and others have previously demonstrated that a highly basic patch in the matrix (MA) domain of Gag is a major determinant of Gag transport to the plasma membrane. In this study, we determined that in HeLa and T cells, the MA mutant Gag proteins that are defective in plasma membrane targeting form virus particles in a CD63-positive compartment, defined as the late endosome or multivesicular body (MVB). Interestingly, we find that in primary human macrophages, both wild-type (WT) and MA mutant Gag proteins are targeted specifically to the MVB. Despite the fact that particle assembly in macrophages occurs at an intracellular site rather than at the plasma membrane, we observe that WT Gag expressed in this cell type is released as extracellular virions with high efficiency. These results demonstrate that Gag targeting to and assembly in the MVB are physiologically important steps in HIV-1 virus particle production in macrophages and that particle release in this cell type may follow an exosomal pathway. To determine whether Gag targeting to the MVB is the result of an interaction between the late domain in p6(Gag) and the MVB sorting machinery (e.g., TSG101), we examined the targeting and assembly of Gag mutants lacking p6. Significantly, the MVB localization of Gag was still observed in the absence of p6, suggesting that an interaction between Gag and TSG101 is not required for Gag targeting to the MVB. These data are consistent with a model for Gag targeting that postulates two different cellular binding partners for Gag, one on the plasma membrane and the other in the MVB.

Antigens, CD↗
PubMed2003

Pegylation of charged polymer-photosensitiser conjugates: effects on photodynamic efficacy.

Conjugates between photosensitisers (PS) and charged polymeric carriers are under investigation for photodynamic therapy of cancer and may allow targeting to certain cell types or compartments in tumours. Covalent attachment of polyethylene glycol to macromolecules (pegylation) may alter their pharmacokinetics, cell type targeting, and photophysical properties. Macrophages may take up large amounts of aggregated PS, thus lessening the selectivity for cancer cells in tumours. We investigated the effect of pegylation on the uptake and phototoxicity of poly-L-lysine chlorin(e6) conjugates with either cationic or anionic charges in two cell lines, human ovarian cancer cells and mouse macrophages. The cationic conjugate after pegylation became less aggregated, consumed less oxygen and had reduced cellular uptake. However, the phototoxicity corrected for cellular uptake increased three- to five-fold. In contrast, the anionic succinylated conjugate on pegylation became more aggregated, consumed similar amounts of oxygen, and had higher cellular uptake. The anionic conjugate showed the highest relative phototoxicity towards both the cell lines (compared to the other three conjugates) and it decreased most towards the macrophages after pegylation. Pegylation reduced the amount of oxygen consumed per chlorin(e6) molecule when photosensitised cells were illuminated. These in vitro studies suggest that pegylation alters the phototoxicity of PS conjugates depending on the effect produced on the aggregation state.

Animals↗
PubMed2006

Nanog transforms NIH3T3 cells and targets cell-type restricted genes.

The transcription factor Nanog is uniquely expressed in embryonic stem (ES) cells and in germ cell tumors and is important for self-renewal. To understand the relation between this and cell transformation, we expressed Nanog in NIH3T3 cells, and these cells showed an increased growth rate and a transformed phenotype as demonstrated by foci formation and colony growth in soft agar. This suggests that Nanog possesses an oncogenic potential that may be related to the role it plays in germ cell tumors and to its function in self renewal of ES cells. We studied the transcription targets of Nanog using microarrays to identify Nanog regulated genes. The list of genes regulated by Nanog was unique for each cell type and more than 10% of the Nanog regulated genes, including transcription factors, are primary Nanog targets since their promoters bind Nanog in ES cells. Some of these target genes can explain the transformation of NIH3T3.

Animals↗
PubMed1985

Functional clonal deletion versus active suppression in transplantation tolerance induced by total-lymphoid irradiation.

Transplantation tolerance and stable chimerism were established in adult mice conditioned with a short course of total-lymphoid irradiation (TLI) followed by infusion of 30 X 10(6) allogeneic bone marrow cells. Spleen cells of tolerant mice could not exert a proliferative or cytotoxic response against host-type cells in vitro and were unable to induce graft-versus-host reaction in secondary host-type recipients. The degree of suppression assessed by coculturing tolerant splenocytes in vitro in the one-way mixed lymphocyte reaction was quite variable--and, in some cases, was not at all demonstrable, although tolerance was clearly maintained. Suppression, when apparent, could not be ascribed to T lymphocytes. Suppressor cells were found to bind soybean agglutinin and could be separated from the nonsuppressive cells by means of this lectin. Dissociation of the suppressive population (SBA+ cells) from that which is normally alloreactive (SBA- cells) resulted in a suppressor cell-depleted fraction that was still unable to respond to host-type cells but regained reactivity to unrelated cells. Limiting dilution analysis of chimeric splenocytes revealed markedly reduced frequencies of cytotoxic T lymphocyte precursors (CTL-P) directed against host-type cells, as compared with normal splenocytes reacting against the same target cells. This difference was accentuated when these cells were sensitized to host-type target cells prior to plating in limiting dilution cultures. In 1:1 mixing experiments of normal and chimeric splenocytes, there was no evidence of any in vitro suppressive activity to account for hyporeactivity of chimeric cells against host-type cells. Thus, maintenance of TLI-induced tolerance seemed not to be mediated primarily through an active suppressor cell mechanism.

Animals↗
PubMed2002

Positron emission tomography imaging analysis of G2A as a negative modifier of lymphoid leukemogenesis initiated by the BCR-ABL oncogene.

G2A is a lymphocyte-expressed G protein-coupled receptor whose genetic ablation results in the development of autoimmunity. Using HSV-TK reporter gene directed positron emission tomography (PET), we demonstrate that prior to any indication of the onset of illness, mice transplanted with BCR-ABL transduced G2A-deficient bone marrow harbor expanded populations of leukemic cells compared to recipients of wild-type bone marrow. The target cell type and anatomical locations of leukemia development are indistinguishable in animals transplanted with G2A+/+ or G2A-/- cells. Shorter disease latency in the G2A-deficient background is associated with an increased rate of cellular expansion. PET can be successfully applied to the temporal and spatial analysis of Bcr-Abl driven leukemic progression and should have utility for the study of other leukemias and lymphomas.

Animals↗
PubMed1984

Human cytolytic T lymphocyte interactions with vascular endothelium and fibroblasts: role of effector and target cell molecules.

Monoclonal antibodies (mAb) against cell surface structures have been used to identify several molecules involved in the interaction of human cytolytic T lymphocytes (CTL) with lymphoid and other bone marrow-derived targets. In allograft rejection or in graft-vs-host disease, however, major cellular targets are vascular and stromal cells, especially endothelium. Yet little is known about whether the same cell surface molecules are involved in the interactions of CTL with these cell types. We assessed the ability of mAb against effector or target cell structures to inhibit cytolysis of susceptible, cultured human vascular endothelium or dermal fibroblasts by a cloned human CTL line. Using mAb reactive with T3, T4, LFA-1, LFA-2, LFA-3, and HLA-DR, we found a qualitatively similar but quantitatively different pattern of inhibition of cytolysis as previously established for lymphoid targets by using the same CTL clone. These results have two implications: 1) the target cell structures recognized by CTL molecules such as T4, LFA-1 and LFA-2 are present on diverse cell types; and 2) the relative importance of such interactions may vary with target cell type. Furthermore, our studies provide several insights into the mechanisms of the interacting molecules. Our model system, and the use of pathophysiologically important target cells, may be useful for further analysis of CTL-mediated immune injury.

Antibodies, Monoclonal↗