Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Retinoids”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMed1983

The development of retinoids in experimental and clinical oncology and dermatology.

The retinoids are a class of compounds consisting of vitamin A and its natural and synthetic analogues. Vitamin A has a marked influence on the differentiation of epithelial tissues, such as skin and mucous membranes. Vitamin A deficiency leads to hyperkeratosis of the skin and squamous metaplasia of mucous membranes, histologic features common to various dermatologic and precancerous diseases. The beneficial effect of vitamin A in these diseases was, however, unsatisfactory. Therefore, a retinoid program was set up in order to find new synthetic retinoids with the highest possible therapeutic activity and the least possible side effects. It was discovered that the chemically induced skin papilloma of the mouse responded to retinoids with a marked regression. This therapeutic activity in combination with the determination of a therapeutic index (relation between therapeutic action and hypervitaminosis A syndrome) served as criteria in choosing retinoids for clinical trials in dermatologic and oncologic diseases. Until now three particular compounds have achieved remarkable usefulness in dermatology: 13-cis-retinoic acid (isotretinoin; Accutane) in the treatment of cystic acne, the aromatic retinoid etretinate in the therapy of severe forms of psoriasis, and an arotinoid. Much less spectacular success has been achieved with these compounds in the prevention and therapy of premalignant and malignant diseases. It is hoped that newer retinoids with a still better therapeutic index or a more selective therapeutic activity will further enrich our therapeutic armamentarium in the fields of dermatology, oncology, and other disciplines of medicine.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Lipid and teratogenic effects of retinoids.

Teratogenicity and the effect on blood lipids are among the most significant side effects produced by oral retinoids. The effects on blood lipids are limited primarily to an increase in plasma triglyceride levels and a decrease in high-density lipoprotein cholesterol. These can be modified by dietary manipulation or dosage reduction. Although elevated serum triglyceride levels and decreased high-density lipoprotein cholesterol have been linked to coronary artery disease, this has not been the case in patients receiving retinoids for acne. Greater caution must be exercised in patients receiving long-term dosing of retinoids. Teratogenic effects of retinoids include those affecting the central nervous system, heart, and craniofacial structures. Therefore female patients taking oral retinoids must not be pregnant, and precautions should be taken so that they do not become pregnant while under treatment. The time at which patients may become pregnant after retinoid treatment varies with the different retinoids.

Abnormalities, Drug-Induced↗
PubMed2000

Cloning and characterization of a novel retinoid-inducible gene 1(RIG1) deriving from human gastric cancer cells.

Retinoids exert wide-spectrum anti-tumor activities, which are mediated via the induction of growth arrest, differentiation or apoptosis. To determine whether the effects of retinoids are mediated by specific gene activation or repression, SC-M1 CL23 gastric cancer cells, pretreated with either vehicle alone or all-trans retinoic acid (10 microM) for 1 day, were analyzed using the technique of differential display. A novel retinoid-inducible gene 1 (RIG1) was isolated. The full-length RIG1 cDNA contained 768 base pairs and encoded a protein of 164 amino acids with a molecular weight of 18 kDa. The RIG1 gene was ubiquitously expressed in normal tissue, and its expression was positively associated with cellular density. Nucleotide sequence analysis demonstrated that the RIG1 gene was similar to a recently-isolated TIG3 gene, and displayed 54% nucleotide sequence homology with a type II tumor suppressor gene H-REV-107-1. RIG1 cDNA, however, contained an extra 32 base pairs located at its 5' end and revealed three base pair differences for the remaining sequences leading to two amino acids substitution between the two encoded proteins. All-trans retinoic acid increased the level of RIG1 mRNA in a time- and concentration-dependent manner in SC-M1 CL23 gastric cancer cells. This was not observed for the H-REV-107-1 gene. The RIG1 regulation was related to cellular retinoid sensitivity. Both retinoic acid receptor alpha- and retinoic acid receptor gamma-selective agonists increased RIG1 mRNA level, and the retinoid x receptor-selective agonist potentiated this regulation. In conclusion, the cDNA of a novel retinoid-inducible gene RIG1 has been cloned. This gene is regulated by retinoic acid through the heterodimer of retinoic acid receptor and retinoid x receptor.

Amino Acid Sequence↗
PubMed2002

Retinoid composition and retinal localization in the eggs of teleost fishes.

Retinoids in the eggs of four teleosts, chum salmon (Oncorhynchus keta), black porgy (Acanthopagrus schlegeli), marbled flounder (Pleuronectes yokohamae), and stingfish (Inimicus japonicus), were analyzed by high performance liquid chromatography. Retinal (RAL1) or both RAL1 and 3,4-didehydroretinal (RAL2) were major or exclusive retinoids in the eggs of every species examined. In O. keta eggs, both RAL1 and RAL2 were present at the ratio of approximately 3:4, whereas RAL1 was the only retinal in the eggs of the other three marine species. RAL1 was the exclusive retinoid in the eggs of P. yokohamae and I. japonicus, whose eggs lack lipid bodies. In the eggs of O. keta and A. schlegeli, which have lipid bodies, retinylesters were also detected, and retinals composed 69% and 93%, respectively, of total retinoids. In O. keta eggs, retinals were present mostly in the aqueous part and were bound to a protein homologous to lipovitellin 1, an amphibian yolk protein, and retinylesters were located in lipids. These results indicate that retinals are the essential mode of retinoid storage in eggs of teleosts and they are the precursors of functional retinoids, such as retinoic acid and visual pigment chromophores. Retinylesters are additional retinoids that accompany lipid accumulation.

Animals↗
PubMed2003

Effects of retinoids on proliferation and plasminogen activator expression in a bovine mammary epithelial cell line.

Effects of two natural (retinol and retinoic acid, RA) and one synthetic N-(4-hydroxyphenyl) retinamide (4-HPR) retinoids on proliferation and expression of urokinase-plasminogen activator (u-PA) by bovine mammary epithelial cells were examined. The BME-UV1 established bovine mammary epithelial cell line was used as a model system. All retinoids tested (retinol, RA and 4-HPR) were effective inhibitors of cell proliferation. When cells were cultured in the absence of fetal bovine calf serum (FBCS), inhibition occurred at concentrations as low as 1 nM for all retinoids tested. The effect of retinoids on cell proliferation was not dose-related when cells were cultured in the absence of FBCS. All retinoids (retinol, RA, 4-HPR), when used in the range 1 nM-10 microM (noncytotoxic concentrations), were equally effective and had identical inhibition patterns. Inhibition of cell proliferation by RA was apparent by 6 h and was higher after 24 h in culture. In contrast, when cells were cultured in the presence of FBCS, the effect of RA and retinol on cell proliferation was dose-related. RA and retinol inhibited cell proliferation (P<0.01) when added to the culture medium in concentrations as low as 10 nM and 100 nM, respectively. 4-HPR was inhibitory (P<0.01) in concentrations as low as 1 nM. Higher concentrations of 4-HPR in the range 1 nM-1 microM had no further effect on cell proliferation. None of the retinoids tested, when added to cultures in the presence or absence of FBCS, could completely arrest cell proliferation at noncytotoxic concentrations. RA at 1 microM inhibited (P<0.05) insulin or IGF-I-induced cell proliferation but had no effect (P>0.05) on u-PA mRNA levels or u-PA activity. Furthermore, RA inhibited cell proliferation in the presence of FBCS but had no effect (P>0.05) on u-PA mRNA levels. Thus, retinoids are effective inhibitors of bovine mammary epithelial cell proliferation and this growth inhibition does not seem to correlate with any changes in u-PA mRNA or u-PA activity.

Animals↗
PubMed1993

The retinoid ligand 4-oxo-retinoic acid is a highly active modulator of positional specification.

Retinoids (vitamin A and its metabolites) are suspected of regulating diverse aspects of growth, differentiation, and patterning during embryogenesis, but many questions remain about the identities and functions of the endogenous active retinoids involved. The pleiotropic effects of retinoids may be explained by the existence of complex signal transduction pathways involving diverse nuclear receptors of the retinoic acid receptor (RAR) and retinoid X receptor (RXR) families, and at least two types of cellular retinoic acid binding proteins (CRABP-I and -II). The different RARs, RXRs, and CRABPs have different expression patterns during vertebrate embryogenesis, suggesting that they each have particular functions. Another level at which fine tuning of retinoid action could occur is the metabolism of vitamin A to active metabolites, which may include all-trans-retinoic acid, all-trans-3,4-didehydroretinoic acid, 9-cis-retinoic acid, and 14-hydroxy-4,14-retroretinol. Formation of the metabolite all-trans-4-oxo-retinoic acid from retinoic acid was considered to be an inactivation pathway during growth and differentiation. We report here that, in contrast, 4-oxo-retinoic acid is a highly active metabolite which can modulate positional specification in early embryos. We also show that this retinoid binds avidly to and activates RAR beta, and that it is available in early embryos. The different activities of 4-oxo-retinoic acid and retinoic acid in modulating positional specification on the one hand, and growth and differentiation on the other, interest us in the possibility that specific retinoid ligands regulate different physiological processes in vivo.

Animals↗
PubMed1997

Retinoid metabolism and all-trans retinoic acid-induced growth inhibition in head and neck squamous cell carcinoma cell lines.

Retinoids can reverse potentially premalignant lesions and prevent second primary tumours in patients with head and neck squamous cell carcinoma (HNSCC). Furthermore, it has been reported that acquired resistance to all-trans retinoic acid (RA) in leukaemia is associated with decreased plasma peak levels, probably the result of enhanced retinoid metabolism. The aim of this study was to investigate the metabolism of retinoids and relate this to growth inhibition in HNSCC. Three HNSCC cell lines were selected on the basis of a large variation in the all-trans RA-induced growth inhibition. Cells were exposed to 9.5 nM (radioactive) for 4 and 24 h, and to 1 and 10 microM (nonradioactive) all-trans RA for 4, 24, 48 and 72 h, and medium and cells were analysed for retinoid metabolites. At all concentrations studied, the amount of growth inhibition was proportional to the extent at which all-trans-, 13- and 9-cis RA disappeared from the medium as well as from the cells. This turnover process coincided with the formation of a group of as yet unidentified polar retinoid metabolites. The level of mRNA of cellular RA-binding protein II (CRABP-II), involved in retinoid homeostasis, was inversely proportional to growth inhibition. These findings indicate that for HNSCC retinoid metabolism may be associated with growth inhibition.

Antineoplastic Agents↗
PubMed2002

Classical and novel retinoids: their targets in cancer therapy.

Retinoids are important mediators of cellular growth and differentiation. Retinoids modulate the growth of both normal and malignant cells through their binding to retinoid nuclear receptors and their subsequent activation. While retinoids have demonstrated therapeutic efficacy in the treatment of acute promyelocytic leukemia, their spectrum of activity remains limited. Other agents such as histone deacetylase inhibitors may significantly increase retinoid activity in a number of malignant cell types. The novel retinoids N-(4-hydroxyphenyl) retinamide (4-HPR) and 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437; AHPN) induce apoptosis in a wide variety of malignant cells. Their mechanism(s) of action remain unclear, although a number of potential targets have been identified. Whether the retinoid receptors are involved in 4-HPR and CD473/AHPN mediated apoptosis remains unclear. Both 4-HPR and CD437/AHPN display significant potential as therapeutic agents in the treatment of a number of premalignant and malignant conditions.

Animals↗
PubMed2001

Differential effects of chromosome 3p deletion on the expression of the putative tumor suppressor RAR beta and on retinoid resistance in human squamous carcinoma cells.

Retinoids' effects on cell growth and differentiation are mediated by nuclear retinoid receptors, which are ligand-activated transcription enhancing factors. Because the expression of the retinoic acid receptor beta (RARbeta) gene, which is located on chromosome 3p24, is diminished in premalignant and malignant tissues it has been proposed that it acts as a tumor suppressor. To test the hypothesis that RARbeta loss leads to retinoid resistance, we studied several karyotyped head and neck squamous carcinoma (HNSCC) cell lines (UMSCC-17A, -17B, -22A, -22B, and -38) with deletion of one chromosome 3p arm. RARbeta mRNA was neither detected nor induced by retinoic acid in these cells, whereas it was expressed and induced by retinoic acid in two other HNSCC cell lines (1483 and 183) without 3p deletion. Methylation of the RARbeta gene promoter was detected in the 17B and 22B cells that failed to express RARbeta but no methylation was found in 183A cells that did express RARbeta mRNA. Responsiveness of HNSCC cells to several retinoids in assays of growth inhibition and colony formation, was rank ordered as: 22B>1483>38>183>17B. Additionally, retinoid response elements were transactivated in 22B more efficiently than in 17B cells. These results indicate that loss of RARbeta expression does not necessarily lead to loss of growth inhibition by retinoids or to a block of retinoid signaling.

Antineoplastic Agents↗
PubMed2004

Effect of organochlorine contaminants and individual biological traits on blubber retinoid concentrations in bottlenose dolphins (Tursiops truncatus).

Here we assessed retinoids as biomarkers of contaminant exposure by studying whether the sex, age, lipid content and organochlorine concentrations of bottlenose dolphins induced variation in retinoid status and its deposition in blubber. Blubber samples were collected from 47 individuals of known age and gender from Sarasota Bay in June 2000 and 2001. The sample included a representative cross-section of the resident dolphin community, with ages ranging from 2 to 50 years. Organochlorine levels showed the age- and sex-related variation commonly observed in other species, with concentrations increasing in youngsters of both sexes and in adult males, and decreasing in adult females after the onset of maturity. Blubber lipid content was low in the overall population and significantly decreased with age in adult males. Retinoid blubber concentrations were comparable to other odontocete species previously studied, and were strongly determined by lipid content. As a consequence of the latter, retinoid concentration was observed to decrease with age in adult males. This effect could not be statistically dissociated from the negative correlation observed between levels of organochlorines and retinoid blubber concentration. Consequently, we could not clarify whether high organochlorine loads in this population lowered retinoid concentrations or, conversely, whether depleted lipid reserves were indeed responsible for the high organochlorine concentrations and the low retinoid levels detected in blubber. With the current knowledge, both options should be considered and investigated, with initial focus on male dolphins.

Adipose Tissue↗
PubMed2000

Retinoids induce apoptosis in cultured keratinocytes.

BACKGROUND: Apoptosis is a genetically controlled process linked to growth and differentiation, involving specific molecular and cellular events activated as a result of a variety of internal and external stimuli. OBJECTIVES: To examine the ability of physiological and synthetic retinoids to induce apoptosis in the BALB/MK mouse keratinocyte cell line. METHODS: Cell viability was assessed by flow cytometry, various staining techniques and the TUNEL method. RESULTS: When keratinocytes were simultaneously exposed to retinoids and stimulated to differentiate at a high (1.5 mmol L(-1))extracellular Ca(2+) concentration over 48 h, apoptosis was induced. Of the retinoids tested, 3,4-didehydroretinoic acid and 3-methyl-tetrahydro-tetramethyl-naphthylenyl-propenyl benzoic acid were more potent than the others. In this system, the apoptosis induced by retinoids could not be correlated to the expression of tissue transglutaminase or epidermal transglutaminase. Furthermore, expression of antiapoptotic bcl-2 or proapoptotic Bax did not change significantly under the experimental conditions used, indicating that the regulation of apoptosis is complex and may be influenced by different factors. CONCLUSIONS: The results suggest that retinoids activating either retinoic acid receptors or retinoid X receptors can induce apoptosis in cultured keratinocytes. Moreover, the well-established inhibitory effect of retinoids on keratinocyte differentiation implies that the apoptotic programme represents a distinct biological process.

Animals↗
PubMed2000

The expression of nuclear retinoid receptors in human implantation.

Vitamin A and retinoids play an important role during development. They affect morphogenesis, cell growth and differentiation by interacting with two types of receptor, the RARs and the RXRs. Despite the well known established teratogenic effects of retinoids during human pregnancy, little is known about the effect of retinoids on human placental development. We studied the possible involvement of retinoids during the implantation process by investigating the spatial distribution of retinoid receptors in the human implantation site by in situ hybridization and immunohistochemistry. For in situ hybridization, we used digoxigenin-labelled antisense riboprobes. Immunochemical staining was performed with specific antibodies against the various retinoid receptors and a streptavidin-alkaline phosphatase immunostaining kit. We found that only two types of receptors were expressed at the implantation site: RARalpha and RXRalpha. Both types of receptors were present in the proliferative intermediate trophoblast, the invasive extravillous trophoblast and decidual cells. Both receptors were also present in the villous cytotrophoblasts. The presence of this retinoid receptor in the cytotrophoblasts suggests a key role for all-trans retinoic acid and/or 9-cis retinoic acid in the development of human placenta.

Cell Nucleus↗
PubMed1979

Retinoid prevents mammary gland transformation by carcinogenic hydrocarbon in whole-organ culture.

The mouse mammary gland in whole-organ culture, an in vitro system that is capable of alveolar development, differentiation, involution, and oncogenic transformation, has been used to examine the effects of the retinoid 2-retinylidene-5,5-dimethyl-1,3-cyclohexanedione (retinylidene dimedone) on epithelial transformation by a low concentration (10 nM) of the carcinogen 7,12-dimethylbenz[a]anthracene. The retinoid significantly prevented mammary gland transformation only when administered after the carcinogen. In addition, the phenotypes of the early transformed state of the mammary gland were suppressed for 20 days after removal of the retinoid. The retinoid was effective during both mammary alveolar development and regression in culture at concentrations as low as 1 nM, and itself had no significant transforming or cytotoxic activity. Mammary glands treated with both the carcinogen and the retinoid resembled, at the microscopic level, those given the solvent (dimethyl sulfoxide) only. The mouse mammary gland in whole-organ culture provides a promising model system in which to study the actions by which retinoids prevent and suppress the chemical transformation in vitro and oncogenesis in vivo of epithelial cells in general and of mammary gland in particular. The present findings support the suggestion that a search for suitable retinoids as chemopreventive agents against human breast cancer is warranted. This model system may be useful as initial indicator in that search.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1998

Identification and characterization of a retinoid-induced class II tumor suppressor/growth regulatory gene.

Retinoids, synthetic and natural analogs of retinoic acid, exhibit potent growth inhibitory and cell differentiation activities that account for their beneficial effects in treating hyperproliferative diseases such as psoriasis, actinic keratosis, and certain neoplasias. Tazarotene is a synthetic retinoid that is used in the clinic for the treatment of psoriasis. To better understand the mechanism of retinoid action in the treatment of hyperproliferative diseases, we used a long-range differential display-PCR to isolate retinoid-responsive genes from primary human keratinocytes. We have identified a cDNA, tazarotene-induced gene 3 (TIG3; Retinoic Acid Receptor Responder 3) showing significant homology to the class II tumor suppressor gene, H-rev 107. Tazarotene treatment increases TIG3 expression in primary human keratinocytes and in vivo in psoriatic lesions. Increased TIG3 expression is correlated with decreased proliferation. TIG3 is expressed in a number of tissues, and expression is reduced in cancer cell lines and some primary tumors. In breast cancer cell lines, retinoid-dependent TIG3 induction is observed in lines that are growth suppressed by retinoids but not in nonresponsive lines. Transient over-expression of TIG3 in T47D or Chinese hamster ovary cells inhibits colony expansion. Finally, studies in 293 cells expressing TIG3 linked to an inducible promoter demonstrated decreased proliferation with increased TIG3 levels. These studies suggest that TIG3 may be a growth regulator that mediates some of the growth suppressive effects of retinoids.

Amino Acid Sequence↗
PubMed2000

Molecular basis for differential substrate specificity in class IV alcohol dehydrogenases: a conserved function in retinoid metabolism but not in ethanol oxidation.

Mammalian class IV alcohol dehydrogenase enzymes are characteristic of epithelial tissues, exhibit moderate to high K(m) values for ethanol, and are very active in retinol oxidation. The human enzyme shows a K(m) value for ethanol which is 2 orders of magnitude lower than that of rat class IV. The uniquely significant difference in the substrate-binding pocket between the two enzymes appears to be at position 294, Val in the human enzyme and Ala in the rat enzyme. Moreover, a deletion at position 117 (Gly in class I) has been pointed out as probably responsible for class IV specificity toward retinoids. With the aim of establishing the role of these residues, we have studied the kinetics of the recombinant human and rat wild-type enzymes, the human G117ins and V294A mutants, and the rat A294V mutant toward aliphatic alcohols and retinoids. 9-cis-Retinol was the best retinoid substrate for both human and rat class IV, strongly supporting a role of class IV in the generation of 9-cis-retinoic acid. In contrast, 13-cis retinoids were not substrates. The G117ins mutant showed a decreased catalytic efficiency toward retinoids and toward three-carbon and longer primary aliphatic alcohols, a behavior that resembles that of the human class I enzyme, which has Gly(117). The K(m) values for ethanol dramatically changed in the 294 mutants, where the human V294A mutant showed a 280-fold increase, and the rat A294V mutant a 50-fold decrease, compared with those of the respective wild-type enzymes. This demonstrates that the Val/Ala exchange at position 294 is mostly responsible for the kinetic differences with ethanol between the human and rat class IV. In contrast, the kinetics toward retinoids was only slightly affected by the mutations at position 294, compatible with a more conserved function of mammalian class IV alcohol dehydrogenase in retinoid metabolism.

Alanine↗
PubMed2003

Physicians underutilize topical retinoids in the management of acne vulgaris: analysis of U.S. National Practice Data.

BACKGROUND: Topical retinoids are effective in the treatment of acne, yet no current guidelines existed in the literature until recently recommending their use as an integral part of mild to moderate acne treatment. OBJECTIVE: To assess whether underutilization of topical retinoids occurs in clinical practice. DESIGN: Weighted data on representative office visits with acne vulgaris diagnoses were analyzed using the National Ambulatory Medical Care Survey (NAMCS), from 1990 to 1999. RESULTS: Of the 54.2 million acne vulgaris visits, retinoids were prescribed at 35.3% visits. Dermatologists prescribed significantly more retinoids than non-dermatologists (39.4%' versus 23%). Dermatology visit was a significant predictor of topical retinoid prescription (RR: 2.27,95% CI: 1.63-3.17). Data suggest that prescribing retinoids for acne has been increasing over the past decade, primarily among dermatologists. CONCLUSION: There is a major difference between suggested treatment guidelines for acne and actual practice in the community. There is distinct under-utilization of topical retinoids for treatment of acne vulgaris by dermatologists and non-dermatologists.

Acne Vulgaris↗
PubMed2003

Hematopoiesis and retinoids: development and disease.

Retinoids function as activating ligands for a class of nuclear receptors that control gene expression programs for a wide range of tissues and organs during embryogenesis and throughout life. Over the years, three sets of observations have spurred interest in the function of retinoids with respect to development and disease of hematopoietic cells. Since the 1920s, epidemiological studies indicated altered hematopoiesis in vitamin A-deficient (VAD) human populations. More recently, the ability of retinoids to affect various aspects of hematopoietic development has been demonstrated in vitro. Finally, it was discovered that the gene encoding a retinoid receptor is a key target for chromosomal translocations that cause acute promyelocytic leukemia (APL). More recent investigations using targeted gene disruptions, VAD animal models, and mouse models of leukemia have continued to shed light on the function of the retinoid pathway in blood cells. It is now clear that retinoids are required for normal hematopoiesis during both yolk sac and fetal liver stages of hematopoiesis, while the pathway has at least modulatory functions for bone marrow derived progenitors. Studies of normal development and APL have provided complementary insight into the molecular control of blood cell differentiation. Here we review the evidence for retinoid requirements in hematopoiesis and also summarize current ideas regarding how this pathway is subverted in leukemia.

Animals↗
PubMed2003

Retinoids regulate survival and antigen presentation by immature dendritic cells.

Maturation of dendritic cells (DCs) is a critical step for the induction of an immune response. We have examined the role of retinoid nuclear receptor pathways in this process. Retinoids induce DC apoptosis, in the absence of inflammatory signals, through retinoic acid receptor (RAR)alpha/retinoic X receptor (RXR) heterodimers. In contrast, via a cross talk with inflammatory cytokines, retinoids increase DNA binding activity of nuclear factor kappaB in DCs, trigger membrane major histocompatibility complex class II and costimulatory molecule expression, induce the differentiation of immature DCs into mature DCs, and enhance antigen-specific T cell response. This maturation of DCs is mediated via a RXR-dependent/RAR-independent pathway and via an RARalpha/RXR pathway distinct from the one responsible for apoptosis. Apoptosis and activation, mediated through distinct nuclear retinoid receptor pathways, can be dissociated from each other with selective synthetic retinoids. We identify a novel cellular function for retinoids and suggest that selective retinoids might be of interest for controlling antigen presentation.

Antigen Presentation↗