PubMed Health⌕ Search

Biomedical subjects

J Hosoi

Publications and source records attributed to J Hosoi.

At least 37 records · Page 2Linked to original sources
PubMed1995

Supernatants from UVB radiation-exposed keratinocytes inhibit Langerhans cell presentation of tumor-associated antigens via IL-10 content.

Exposure of mice to midrange UV radiation (UVB) (280-320 mm) in vivo leads to suppression of the ability to induce delayed-type hypersensitivity (DTH). Systemic administration of supernatants from UVB-exposed keratinocytes (KC) similarly inhibits the ability to induce DTH and the presence of interleukin-10 (IL-10) in the supernatants has been shown to be responsible for this effect. It has been hypothesized that release of IL-10 by KC after exposure to UVB radiation in vivo may be responsible for UVB-induced inhibition of DTH and also for the inability of chronically UVB-irradiated mice to immunologically reject immunogenic UVB-induced skin tumors. To test directly whether supernatants from UVB-irradiated KC can inhibit presentation of tumor-associated antigens (TAA) by epidermal Langerhans cells (LC), cultures of the transformed murine KC line PAM 212 were exposed to 200 J/m2 of UVB radiation and 24 h supernatants obtained. CAF1 (H-2a/d) epidermal cells (EC) enriched for LC content were exposed to supernatants from irradiated (UV-SN) or mock-irradiated (MI-SN) PAM 212 cells for 3 h followed by culture for 16 h in granulocyte-macrophage colony-stimulating factor and then were pulsed with soluble TAA derived from the murine spindle cell tumor S1509a (H-2a). ECs were then washed and injected subcutaneously into naive CAF1 mice three times at weekly intervals for priming. One week after the final immunization these mice were challenged subcutaneously with live S1509a cells and tumor growth scored over time. Pretreatment of EC with UV-SN but not MI-SN inhibited the induction of effective immunity by this immunization scheme. ECs were also treated with UV-SN or MI-SN for 3 h then pulsed with TAA and injected into a hind footpad of previously immunized mice for elicitation of a DTH response. Pretreatment of EC with UV-SN but not MI-SN inhibited the ability of EC to elicit DTH. Neutralization studies with specific neutralizing antibodies to IL-10 demonstrated that the presence of IL-10 in UV-SN was responsible for the inhibition of antigen presentation both for induction and elicitation of immunity. UV-SN inhibits tumor antigen presentation by epidermal LC through the action of IL-10.

Animals↗
PubMed1995

Modulation of Langerhans cell function by epidermal nerves.

Many if not most epidermal Langerhans cells appeared to be closely associated anatomically with calcitonin gene-related peptide (CGRP)-containing nerves as determined by confocal laser scanning microscopy. Furthermore, a small proportion of Langerhans cells had immunoreactive CGRP at or near their cell surfaces, suggesting that nerves are capable of depositing CGRP at or near Langerhans cells. CGRP inhibited Langerhans cell antigen-presenting capability for elicitation of delayed-type hypersensitivity in immunized mice to present alloantigens in the mixed epidermal cell-lymphocyte reaction and to present a protein antigen to a responsive hybridoma. As a whole, these data suggest the possibility that products of nerves within the epidermis might serve to regulate Langerhans cell function. The apparent apposition of epidermal nerves with Langerhans cells suggests a possible locus of interaction between the nervous system and the immune system within the skin.

Animals↗
PubMed1995

Structure-function relations in the inhibition of murine contact hypersensitivity by amiloride.

Topical application of amiloride, a potent inhibitor of the Na+/H+ antiport, inhibits cutaneous inflammation induced by ultraviolet radiation or contact hypersensitivity in mice. Amiloride analogues with greater and lesser inhibition of the Na+/H+ exchange were tested to determine whether anti-inflammatory effects correlate with this activity. Structural analogues of amiloride without significant activity at the Na+/H+ antiport (pyrazine, pyrazinamide, and chloropyrazine) failed to inhibit contact hypersensitivity. N-amidino-3-amino-5-dimethyl amino-6-chloropyrazinecarboxamide (DMA) has a 23-fold greater affinity for the Na+/H+ antiport compared to amiloride, but failed to inhibit contact hypersensitivity in this assay. 3,5-diamino-6-chloropyrazine-amido-guanidine (DCG), which has only 7% of the affinity of amiloride for the antiport, suppressed contact hypersensitivity as well as amiloride. Experiments examining the ability of these agents to diffuse through mouse skin revealed amiloride to be superior to both DCG and DMA, which were approximately equal. DMA, with greater inhibition of the Na+/H+ antiport but lesser ability to inhibit contact hypersensitivity, inhibited protein synthesis and induced cell death more than amiloride or DCG. Amiloride and DCG hold promise as topical anti-inflammatory agents. Their anti-inflammatory properties do not correlate with affinity for the Na+/H+ antiport, ability to penetrate murine skin, or inhibition of protein synthesis.

Amiloride↗
PubMed1994

Epidermal cell presentation of tumor-associated antigens for induction of tolerance.

Intravenous administration of hapten-coupled epidermal cells (EC) induces tolerance in mice. To assess the relevance of this observation to cutaneous tumors, the ability of EC to induce tolerance to the S1509a spindle cell tumor (H-2a) was examined. ECs were prepared from CAF1 (H-2a/d) mice and the supernatant from a freeze-thaw lysate of S1509a cells was used as a source of soluble tumor-associated Ag (TAA). ECs were incubated in TAA or medium alone followed by washing. Two hundred thousand TAA-pulsed ECs, non-TAA-pulsed ECs, or TAA-pulsed ECs killed by freeze-thawing were injected i.v. into groups of CAF1 mice. To determine whether this regimen induced tolerance, a tumor-specific delayed-type hypersensitivity (DTH) response was measured in mice subsequently immunized to the S1509a tumor. To assess the degree of immunity induced in these animals, ECs were prepared and deleted of Thy-1-bearing cells by Ab and complement-mediated lysis. These cells were then pulsed with TAA and 5 x 10(5) were injected into the right hind footpad of each mouse. Footpad swelling was assessed at 24 to 48 h as a measure of the DTH. Mice primed i.v. with viable TAA-pulsed EC but not killed TAA-pulsed EC demonstrated a greatly suppressed DTH response. Other experiments demonstrated that exposure of EC to a dose of ultraviolet radiation (200 J/m2), which inhibits the ability of these cells to induce immunity by subcutaneous injection either before or after TAA pulsing, did not prevent induction of tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The presence of biologically significant concentrations of glucocorticoids but little or no cortisol binding globulin within aqueous humor: relevance to immune privilege in the anterior chamber of the eye.

PURPOSE: Immunosuppressive factors in aqueous humor (AH) contribute to the immune-privileged status of the anterior chamber of the eye. One such factor is transforming growth factor-beta (TGF-beta); other relevant inhibitors have not been fully identified. The authors examined AH to search for other putative inhibitors and to determine their effect on TGF-beta inhibitory activity. METHODS: Radioimmunoassays (RIA) were used to detect the presence of hydrocortisone, corticosterone, cortisol binding globulin (CBG), and alpha-melanocyte stimulating hormone (alpha-MSH) in AH. The ability of these factors to inhibit murine thymocyte proliferation stimulated by phytohemagglutinin-interleukin 1 (PHA/IL-1) and proliferation of a TGF-beta-sensitive cell line (CCL64) in vitro was examined. The ability of hydrocortisone to inhibit a one-way mixed lymphocyte reaction (MLR) and the ability of epidermal cells to present soluble tumor-associated antigens (TAA) for elicitation of immunity in mice in the concentration range present in AH was also examined. RESULTS: Hydrocortisone was detected in mouse, rat, and human AH (10.8 +/- 1.1 ng/ml, 9.3 +/- 2.1 ng/ml, and 18.0 +/- 1.0 ng/ml, respectively; mean +/- SEM), as was corticosterone (2.7 +/- 0.9 ng/ml, 2.2 +/- 0.3 ng/ml, and 0.7 +/- 0.1 ng/ml, respectively). Whereas normal plasma contains a binding protein for corticosteroids (i.e., CBG), the concentration in mouse, rat, and human AH was less than the level detectable by an RIA. Hydrocortisone inhibited PHA/IL-1-stimulated murine thymocyte proliferation and CCL64 cell proliferation in the concentration range present in AH. When hydrocortisone was combined with TGF-beta 2 (125 pg/ml), the degree of inhibition observed was greater than with either alone. Corticosterone inhibited thymocyte costimulation only slightly at concentrations present in AH but was inhibitory for CCL64 cells. alpha-MSH was also detected in AH. The concentration present had only slight inhibitory effects for CCL64 cell proliferation and did not enhance TGF-beta 2-mediated (62 pg/ml to 250 pg/ml) inhibition of CCL64 or thymocyte proliferation. Hydrocortisone inhibited the one-way MLR in the concentration range present in AH and, at 10 ng/ml, inhibited the ability of epidermal cells to present TAA for elicitation of delayed-type hypersensitivity in tumor-immune mice. CONCLUSIONS: These results show that AH contains biologically relevant concentrations of glucocorticoids and that CBG is relatively absent so that glucocorticoids present are largely free, and they suggest that regional sites take advantage of the activities of multiple factors to maintain an immune-privileged status.

11-Hydroxycorticosteroids↗
PubMed1993

Regulation of Langerhans cell function by nerves containing calcitonin gene-related peptide.

Several observations suggest interactions between the immune and nervous systems. Psoriasis and atopic dermatitis may worsen with anxiety and have been associated with anomalous neuropeptide regulation. Neurotransmitters affect lymphocyte function and lymphoid organs are innervated. Calcitonin gene-related peptide (CGRP) is a neuropeptide and vasodilator that modulates some macrophage functions, including antigen presentation in vitro. CGRP is associated with Langerhans cells (LC) in oesophageal mucosa, particularly during inflammation, is present in epidermal nerves and is associated with Merkel cells. We examined the ability of CGRP to modulate LC antigen-presenting function and asked if CGRP-containing nerves impinge on LC. We report here that CGRP-containing nerve fibres are intimately associated with LC in human epidermis and CGRP is found at the surface of some LC. In three functional assays CGRP inhibited LC antigen presentation. These findings indicate that CGRP may have immunomodulatory effects in vivo and suggest a locus of interaction between the nervous system and immunological function.

Adult↗
PubMed1993

Coordinate regulation of collagen II(alpha 1) and H19 expression in immortalized hamster cells.

Loss of tumor suppressor gene function is essential in the multistep progression of cells to neoplasia. Immortalized cells were established by carcinogen treatment of Syrian hamster embryo cells. At early passages, these nontumorigenic cells retained the ability to suppress tumorigenicity in cell hybrids with malignant cells. Upon passage and subcloning of these suppressor-positive (supB+) cells, variant clones that had lost tumor suppressor activity were isolated. These suppressor-negative (supB-) clones remained nontumorigenic. The mRNAs encoding collagen II(alpha 1a), a chondrocyte differentiation marker, and H19, a developmentally controlled gene, were more abundant in supB+ cells than in supB- cells. Nuclear run-on analysis indicated that the transcription of these genes is differentially regulated. Transient transfection experiments revealed that a cis-acting element in the rat collagen II 5' flanking sequences directs differentially regulated transcription. Gel retention analysis demonstrated the presence of a nuclear DNA-binding factor(s) that specifically recognizes a DNA sequence common to both the rat collagen II sequences and the mouse H19 enhancer. In one set of clones, transcriptional regulation could account for differential collagen II and H19 expression in supB+ and supB- cells. In another set of clones, posttranscriptional controls are responsible for the decreased expression of these genes in supB- cells. The emergence of two independent mechanisms that cause differential expression of collagen II and H19 related to tumor suppressor loss suggests that coordinate regulation of these genes, or others regulated by common mechanisms, may be important in tumor suppression.

Animals↗
PubMed1992

Tumor antigen presentation by epidermal antigen-presenting cells in the mouse: modulation by granulocyte-macrophage colony-stimulating factor, tumor necrosis factor alpha, and ultraviolet radiation.

I-A+ epidermal antigen-presenting cells (APCs, Langerhans cells) have been shown to present tumor-associated antigens (TAAs) and to induce tumor immunity in vivo. This study examined the effects of ultraviolet radiation (UVR) and the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor alpha (TNF-alpha) on the ability of epidermal cells (ECs) to induce or to elicit immunity against the murine spindle cell tumor S1509a. Naive syngeneic mice were immunized three times at weekly intervals with ECs that had been cultured in GM-CSF for 18 h and then pulsed with TAA derived from S1509a. This resulted in protective immunity against subsequent tumor challenge, providing a model to study the conditions required for sensitization against TAAs by epidermal APCs. Culture of ECs in GM-CSF was required for induction of significant protective tumor immunity, and UV irradiation or incubation in TNF-alpha for 2 h after GM-CSF incubation abrogated the immunostimulatory effect of GM-CSF. However, unlike UVR, TNF-alpha did not significantly inhibit the induction of immunity when ECs were exposed to TNF-alpha before overnight incubation in GM-CSF, together with GM-CSF, or after pulsing with TAA, and anti-TNF-alpha antibody treatment did not abrogate the effects of UVR on this system. Furthermore, TNF-alpha incubation of ECs augmented their ability to elicit delayed-type hypersensitivity (DTH) and also enhanced elicitation of DTH by GM-CSF-cultured ECs, whereas UV-irradiation reduced it in a dose-dependent fashion. Taken together, these results demonstrate that GM-CSF, TNF-alpha, and UVR are significant regulators of tumor antigen presentation by epidermal APCs and that the effects of the cytokines examined differ with regard to induction or elicitation of immunity.

Animals↗
PubMed1991

Loss of a tumor suppressor gene function is correlated with downregulation of chondrocyte-specific collagen expression in Syrian hamster embryo cells.

We previously described the isolation of closely related, preneoplastic Syrian hamster cell lines that have retained (supB+) or lost (supB-) the ability to suppress the anchorage-independent growth and tumorigenicity of a sarcoma cell line (BP6T) in cell hybrids. In this report, we have used differential cDNA screening to clone several genes that are expressed in supB+ cells and downregulated in supB- cells. The nontumorigenic supB+ and supB- variants are advantageous for differential cDNA cloning because multiple independent cell lines differing in their tumor suppressor activity have been isolated. Differentially expressed cDNAs were isolated and placed into one of four groups based on DNA cross-hybridization. Representative cDNAs from Groups I and II, which were expressed at relatively high levels in two independently derived supB+ cell lines (DES4 and 10W) and downregulated in the supB- and tumor cell lines, were sequenced. The DNA and predicted amino acid sequences of these genes were found to be highly homologous to the chondrocyte-specific collagens type II and type IX. In contrast to the chondrocyte-specific collagens, another collagen isoform, collagen type I, was expressed at similar levels in both supB+ and supB- cells. These results suggest that carcinogen-induced immortalization selected for chondrocyte-like cell lines from the mixed embryo cell population. As these cells progressed toward tumorigenicity, the ability to express the chondrocyte differentiation markers was lost concomitantly with the ability to suppress the tumorigenicity of the BP6T sarcoma cell line. These results are consistent with the hypothesis that the supB+ tumor suppressor gene is involved in the regulation of differentiation. The identification of genes regulated by this suppressor gene may aid in its isolation.

Animals↗
PubMed1991

Identification of genes associated with tumor suppression in Syrian hamster embryo cells.

Loss of a tumor-suppressor gene function appears to play a critical role in the multistep process of neoplastic transformation of Syrian hamster embryo (SHE) cells in vitro. Clonal variants of two independent, preneoplastic cell lines have been isolated that have either retained (termed supB+) or lost (termed supB-) the ability to suppress the tumorigenicity of a highly malignant benzo[alpha]pyrene-transformed SHE cell line (BP6T) in cell hybrids. We have pursued several approaches in an attempt to identify genes that are responsible for tumor suppression in these cells. The only consistent differences detected in two-dimensional gel analyses of supB+ and supB- cellular proteins were decreases in the levels of two high molecular weight isoforms of tropomyosin in supB- cells. Differential screening of a supB+ cDNA library for genes that are preferentially expressed in supB+ cells yielded cDNA clones for four genes, i.e., collagen type II, collagen type IX, H19, and a previously unidentified gene (clone 5). Nuclear run-on assays suggested that higher transcription rates were responsible for the increased steady-state levels of some of these transcripts in supB+ cells. DNA sequence comparisons showed that two copies of a 9 bp element, previously identified in each of the mouse H19 enhancers, were also present in the 5' flanking region of the rat type II collagen gene. A transcription factor that controls expression of the collagen and H19 genes through binding to this conserved motif would be an attractive candidate for the supB+ gene or at least a mediator of the supB+ phenotype.

Animals↗
PubMed1990

1,24(R)-dihydroxyvitamin D3, a novel active form of vitamin D3 with high activity for inducing epidermal differentiation but decreased hypercalcemic activity.

1 alpha,25-Dihydroxyvitamin D3 (1,25(OH)2D3) is known to be a hormonally active form of vitamin D3 in the regulation of intracellular and extracellular calcium levels and of differentiation of myeloid cells and epidermal keratinocytes. We found that 1 alpha,24(R)-dihydroxyvitamin D3 (1,24(OH)2D3), a novel synthetic derivative of vitamin D3, is also active in regulating the differentiation of epidermal keratinocytes. 1,24(OH)2D3 had the same affinity as 1,25(OH)2D3 for a receptor isolated from the epidermis of newborn mice. The incubation of mouse epidermal keratinocytes with 1,24(OH)2D3 induced their differentiation in a time- and dose-dependent manner, as determined by the formation of a cornified envelope and an increase in the activity of transglutaminase. 1,24(OH)2D3 inhibited DNA synthesis of epidermal keratinocytes and also increased their cytosolic calcium level. These effects of 1,24(OH)2D3 were similar to, or rather more than, those of physiologically active 1,25(OH)2D3. However, 1,24(OH)2D3 was found to cause less hypercalcemia than 1,25(OH)2D3 when administrated intravenously to rats, suggesting its possible therapeutic value in psoriasis.

Animals↗
PubMed1989

Induction of metallothionein mRNA by tumor promoters in mouse skin and its constitutive expression in papillomas.

A single topical application of 12-O-tetradecanoylphorbol-13-acetate (TPA) was found to induce mRNA of a metallothionein (MT) gene or genes in the skin of Sencar mice, and papillomas produced by repeated applications of TPA were shown to have elevated levels of MT mRNA. Induction of MT mRNA was maximal 4-8 h after application of TPA and returned to the control level 24 h later. A dose-dependent increase of MT mRNA was observed with doses of TPA of 1-5 micrograms. Of the other promoters tested, phorbol-12, 13-didecanoate, mezerein, and the ionophore A23187 also induced MT mRNA, but 4-O-methyl-TPA and benzoyl peroxide did not. Phorbol and 4 alpha-phorbol-12,13-didecanoate, which are not promoters, also did not induce MT mRNA. Retinoic acid and 1 alpha, 25-dihydroxyvitamin D3, inhibitors of tumor promotion, did not induce MT mRNA themselves or inhibit the induction of MT mRNA by TPA. In C57BL/6 promotion-resistant mice, TPA caused only slight induction of MT mRNA. These data suggest a correlation between induction of MT mRNA and epidermal hyperplasia. The constitutive elevation of MT mRNA levels in papillomas may be due to the loss, during the process of tumor promotion, of some mechanism regulating MT gene expression.

Administration, Topical↗
PubMed1987

Regulation of metallothionein gene expression by 1 alpha,25-dihydroxyvitamin D3 in cultured cells and in mice.

1 alpha,25-Dihydroxyvitamin D3 [1 alpha,25(OH)2D3], a hormonally active form of vitamin D3, has been shown to modulate cell differentiation and tumor promotion. This report demonstrates that mRNA of the metallothionein (MT) gene was induced by 1 alpha,25(OH)2D3 in cultured epidermal keratinocytes and also in liver, kidney, and skin tissues when 1 alpha-hydroxyvitamin D3, a synthetic precursor of 1 alpha,25(OH)2D3, was applied in vivo. Exposure of FRSK cells, a cell line derived from fetal rat skin keratinocytes, to 1 alpha,25(OH)2D3 at 5 ng/ml (12 nM) increased MT mRNA to almost the same extent as that induced by 10 microM dexamethasone or 1 microM CdCl2. This increase in the level of MT mRNA was evident within 2 hr and was maximal 12-24 hr after the addition of 1 alpha,25(OH)2D3. The induction was dose-dependent with concentrations of 1 alpha,25(OH)2D3 from 0.05 to 5.0 ng/ml. Amounts of MT increased with the increase of MT mRNA induced by 1 alpha,25(OH)2D3. Of the derivatives of vitamin D3 tested, only 1 alpha,25(OH)2D3 caused marked induction. Treatment with cycloheximide did not inhibit MT mRNA induction by 1 alpha,25(OH)2D3. 1 alpha,25(OH)2D3 induced MT mRNA in primary cultures of mouse epidermal keratinocytes but not in IAR-20, a liver cell line. 1 alpha,25(OH)2D3 had a similar effect in vivo: oral administration of 1 alpha-hydroxyvitamin D3 to mice resulted in increased levels of MT mRNA in the liver, kidney, and skin 24 hr later. Increase in the level of MT mRNA may be relevant to some biological actions of 1 alpha,25(OH)2D3.

Administration, Oral↗
PubMed1987

Induction of anchorage-independent growth of mouse JB6 cells by cholera toxin.

Cholera toxin (CT) at concentrations of 0.1-100 ng/ml induced anchorage-independent growth and DNA synthesis of JB6 cells derived from mouse epidermis. This induction was reversible. CT caused marked increase in the level of intracellular cAMP. Forskolin also increased the cAMP level and induced anchorage-independent growth. However, 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] induced irreversibly anchorage-independent growth of JB6 cells but did not increase the cAMP level. TPA-resistant clone-30 cells were also resistant to CT in terms of anchorage-independent growth and cAMP induction. Retinoic acid inhibited the induction of anchorage-independent growth of JB6 cells by CT, TPA and 1 alpha,25(OH)2D3. These results suggest that anchorage-independent growth of JB6 cells is induced by cAMP-dependent and cAMP-independent pathways, both of which may include a retinoic acid-sensitive step.

Animals↗
PubMed1987

Inter-individual variations of arylhydrocarbon-hydroxylase activity in cultured human epidermal and dermal cells.

Arylhydrocarbon hydroxylase (AHH) activity was determined in cultured human epidermal and dermal cells with and without induction by benz[a]anthracene (BA). Large inter-individual variations were found in the basal and induced AHH activities and the induction ratio. The average basal AHH activity of 29 epidermal cultures in primary culture was 3.9 units (SD, 4.2; range, 0-16.3) (one unit was defined as 1 pmol of 3-hydroxybenzo[a]pyrene formed/mg protein/hr). AHH activity was induced time- and dose-dependently by BA. The average AHH activity induced by treatment with 13 microM BA for 24 hr was 97.4 units (SD, 69.4; range, 2.7-216.9). The induction ratio ranged from 0.6 to 262.0, but in the majority of cultures (15 of 27 cultures, 55%) it was less than 30. The mean induction ratio and SD was 51.1 +/- 63.0. The frequency distributions of basal AHH activity and the induction ratio were asymmetrical with a right tail. No correlation was found between the AHH activity or induction ratio and the age or sex of the donors or their residential district. The basal and induced AHH activities of dermal fibroblasts were both lower than those of epidermal cells; the average basal AHH level of 14 cultures was 1.5 units (SD, 1.4; range, 0-5.2), while the average induced AHH activity was 9.6 units (SD, 6.3; range 0-23.5). The induction ratio of dermal fibroblasts was lower than that of epidermal cells, the mean and SD being 7.5 +/- 7.4 (range, 1.9-27.0). There was no correlation between the AHH activities or induction ratios in epidermal and dermal cells isolated from the same donors.

Adolescent↗
PubMed1986

Effects of anti-Tac antibody on the response of large granular lymphocytes to interleukin-2.

Large granular lymphocytes (LGL), which consist of a unique population comprising almost all of the natural killer (NK) cell activity, were separated from peripheral blood mononuclear cells by sequential depletion of monocytes and conventional discontinuous Percoll density gradient sedimentation. The LGL populations thus obtained exhibited significant levels of interferon-gamma (IFN-gamma) production and proliferation, as well as augmentation of NK cell activity in response to interleukin-2 (IL-2). Among these IL-2-driven phenomena, only IFN-gamma production was markedly inhibited by the monoclonal anti-Tac antibody, which presumably recognized the IL-2 receptor, whereas the proliferative response and the augmentation of NK cell activity were only minimally affected by the same antibody, even at the higher concentration. The dissociation of the effects of anti-Tac antibody on these IL-2-driven events gives us some insight on the role of IL-2 receptors involved in these immunologically interesting functions of IL-2.

Antibodies, Monoclonal↗