Biomedical subjects

R Guerrini

Publications and source records attributed to R Guerrini.

At least 163 records · Page 9Linked to original sources

PubMed1997

Address and message sequences for the nociceptin receptor: a structure-activity study of nociceptin-(1-13)-peptide amide.

Nociceptin (NC) and some of its fragments as well as nociceptin-(1-13)-peptide amide [NC- (1-13)-NH2] and a series of its analogues were prepared and tested in the mouse vas deferens in an attempt to identify the sequences involved in the activation (message) and in the binding (address) of nociceptin to its receptor. The NC receptor that inhibits the electrically evoked twitches of the mouse vas deferens was demonstrated to be distinct from the delta opioid receptor, since naloxone and Dmt-Tic-OH (a selective delta opioid receptor antagonist) block the delta opioid receptor but have no effect on the nociceptin receptor. Results from structure-activity experiments suggest that (a) the entire sequence of NC may not be required for full biological activities, since NC(1-13)-NH2 is as active as NC; (b) fragments of NC have however to be amidated as in NC(1-13)-NH2 in order to be protected from degradation by proteases; (c) cationic residues (as Arg8,12, Lys9,13) appear to play a functional role, since their replacement with Ala in the sequence of NC(1-13)-NH2 leads to inactivity; (d) the N-terminal tetrapeptide Phe-Gly-Gly-Phe is essential for activity: its full length and flexibility appear to be required for NC receptor activation and/or occupation; (e) Phe4 and not Phe1 appears to be the residue involved in receptor activation, since the replacement of Phe1 with Leu has no effect, while that of Phe4 leads to inactivity. Results summarized in this paper indicate that the structural requirements of NC for occupation and activation of its receptor are different from that of opioids, particularly delta agonists.

Amino Acid Sequence↗

PubMed1997

Solution conformation of nociceptin.

Nociceptin, a novel heptadecapeptide, interacts with ORL1 a G protein-coupled receptor whose sequence is closely related to that of the kappa opioid receptor but has no opioid activity. We have investigated the conformational preferences of Nociceptin also in comparison to Dynorphin A. The N-terminal part of Nociceptin has the same conformational preferences of the message of endogenous opioids but the C-terminal part of the sequence is more flexible than the corresponding address of Dynorphin A. [Tyr1]-Nociceptin, while retaining nociceptive activity, has also an opioid activity comparable to that of enkephalins.

Amino Acid Sequence↗

PubMed1997

Bilateral parasagittal parietooccipital polymicrogyria and epilepsy.

We describe 9 patients with a bilateral malformation of cortical development, centered around the parasagittal and mesial aspects of the parietooccipital cortex, with magnetic resonance imaging findings suggestive of polymicrogyria. No familial distribution or etiologic factors were identified. Location in a watershed area between anterior and posterior cerebral arteries suggests postmigratory perfusion failure as the underlying cause. In most patients the malformation was detected by magnetic resonance imaging after computed tomography scans with 10-mm-thick sections were considered normal. Seizures, present in all, had started between the ages of 20 months and 15 years (mean, 9 years) and were intractable in 7. Complex partial seizures with or without minor automatisms were the most frequent ictal pattern. In only 4 patients these were preceded by symptoms indicating posterior onset. Interictal electroencephalograms showed both diffuse and bilateral parietooccipital or temporal abnormalities. The range of IQ scores indicated average intelligence to mild retardation. Several patients presented deficits on neuropsychological tasks requiring performance under time constraints, suggesting that the malformation may result in cognitive slowing. Early diagnosis of this malformation may be difficult because of the lack of neurological signs, relatively late seizure onset, difficulty in localizing seizure onset, and inability to recognize the cortical abnormality on computed tomography scans.

Adolescent↗

PubMed1997

Delayed appearance of interictal EEG abnormalities in early onset childhood epilepsy with occipital paroxysms.

Childhood epilepsy with occipital paroxysms is an age-related idiopathic focal epilepsy. Occipital EEG paroxysms are considered necessary for diagnosis. We carried out a close clinical and EEG follow-up (range, 2-12 years; mean, 6 years 7 months; median, 7 years) in 24 patients (age range, 4-19 years; mean, 11 years 8 months; median, 11 years). In five children with early seizure onset and particularly benign prognosis without any treatment, EEG abnormalities appeared 3-10 months after the first seizure. Four of them exhibited the ictal pattern of versive seizures with vomiting. Our findings confirm that in the early idiopathic focal seizure disorders, interictal EEG abnormalities may be lacking at the beginning of the disorder.

Adolescent↗

PubMed1997

Identification of a duplication of Xq28 associated with bilateral periventricular nodular heterotopia.

Bilateral periventricular nodular heterotopia (BPNH) is a malformation of neuronal migration and is characterized by nodules of heterotopic gray matter lining the lateral ventricles of the brain. The majority of BPNH patients are female and have epilepsy as a sole clinical manifestation of their disease. Familial BPNH has been mapped to Xq28 by linkage analysis. A multiple congenital anomaly-mental retardation syndrome (BPNH/MR) was recently delineated in three unrelated boys with BPNH, cerebellar hypoplasia, severe mental retardation, epilepsy, and syndactyly. High-resolution chromosome analysis revealed a subtle abnormality of Xq28 in one of the boys with BPNH/MR syndrome. FISH with cosmids and YACs from Xq28 further characterized this abnormality as a 2.25-3.25-Mb inverted duplication. No abnormality of Xq28 was detected by G-banding or FISH in the other two boys. These data support the linkage assignment of BPNH to band Xq28 and narrow the critical region to the distal 2.25-3.25 Mb of Xq28.

Brain Diseases↗

PubMed1997

Linkage and physical mapping of X-linked lissencephaly/SBH (XLIS): a gene causing neuronal migration defects in human brain.

While disorders of neuronal migration are associated with as much as 25% of recurrent childhood seizures, few of the genes required to establish neuronal position in cerebral cortex are known. Subcortical band heterotopia (SBH) and lissencephaly (LIS), two distinct neuronal migration disorders producing epilepsy and variable cognitive impairment, can be inherited alone or together in a single pedigree. Here we report a new genetic locus, XLIS, mapped by linkage analysis of five families and physical mapping of a balanced X;2 translocation in a girl with LIS. Linkage places the critical region in Xq21-q24, containing the breakpoint that maps to Xq22.3-q23 by high-resolution chromosome analysis. Markers used for somatic cell hybrid and fluorescence in situ hybridization analyses place the XLIS region within a 1 cM interval. These data suggest that SBH and X-linked lissencephaly are caused by mutation of a single gene, XLIS, that the milder SBH phenotype in females results from random X-inactivation (Lyonization), and that cloning of genes from the breakpoint region on X will yield XLIS.

Cerebral Cortex↗

PubMed1997

The influence of dosage, age, and comedication on steady state plasma lamotrigine concentrations in epileptic children: a prospective study with preliminary assessment of correlations with clinical response.

The effects of age, dosage, and type of comedication on plasma lamotrigine (LTG) concentrations and the relationship between plasma drug levels and clinical response were evaluated in a prospective study of 45 patients, aged 3 to 38 years, with epilepsy uncontrolled by conventional anticonvulsant therapy. Six of the 45 patients were on single-drug therapy, and 39 were on two to five concurrently administered antiepileptic drugs when LTG was added. Thirteen patients were assessed at three or more LTG dosage levels. Within individuals, steady state plasma LTG concentrations increased linearly with increasing daily dosage over the examined dose range (25 to 575 mg/day or 0.75 to 21 mg/kg.day). Among patients also receiving enzyme-inducing agents, such as carbamazepine, barbiturates, or phenytoin, plasma LTG concentrations normalized to a 1 mg/kg daily dose were lower in children aged 3 to 6 years (0.30 +/- 0.17 microgram/ml; n = 6) than in the older children (0.43 +/-0.18 microgram/ml; n = 12) and adolescents/adults (0.68 +/- 0.26 microgram/ml; n = 10). In patients treated with valproate, the age dependency of plasma LTG was less evident, possibly because of a smaller sample size and the confounding effect of comedication. Within any given age group, dose-normalized LTG concentrations were about five-fold higher in patients comedicated with valproic acid than in those comedicated with enzyme inducers. Twenty patients showed a favorable response (with a > or = 40% reduction in seizure frequency compared with the pre-LTG period) and continued on long-term treatment. Plasma drug concentrations in these apparent responders were highly variable and did not differ significantly from those observed in nonresponders (6.6 +/- 5.2 versus 4.8 +/- 3.3 microgram/ml). These findings show that plasma LTG concentrations exhibit a wide interindividual variability under the influence of age and type of comedication, but they are predictably related to dosage within individual patients. Although there was no apparent relationship between drug levels and clinical response in this difficult-to-treat population, further studies on the potential value of monitoring plasma LTG concentrations are indicated.

Adolescent↗

PubMed1997

Early-onset benign occipital seizure susceptibility syndrome.

PURPOSE: Childhood epilepsy with occipital paroxysms (CEOP) is characterised by ictal visual hallucinations and occipital epileptiform activity on interictal EEG. A variant has been described with nonvisual symptoms including tonic head and eye deviation, vomiting, and episodes of partial status epilepticus. We fully documented the electroclinical features of such patients to determine whether classification separate from CEOP is justified. METHODS: This was a multicentre study with participating investigators submitting details of patients with idiopathic occipital seizures characterised by ictal head or eye deviation and vomiting. RESULTS: One hundred thirteen patients were recruited. Seizures began in early childhood (mean, 4.6 years) and occurred infrequently (mean total seizures, 3); 30% of patients had only a single seizure. Two thirds of seizures were nocturnal. Ictal eye deviation occurred in 79%, vomiting in 70%, and head deviation in 35%. Seizures were predominantly complex partial in type. Partial status epilepticus occurred in 44% of patients. Seventy-four percent of patients had occipital interictal EEG epileptiform activity, predominantly right sided, with fixation-off sensitivity. Extraoccipital EEG abnormalities occurred in 35% of patients. Prognosis was excellent: the mean duration of active seizures was 1 year. CONCLUSIONS: Although the two groups shared identical EEG features, the distinct clinical symptoms probably justify separate classification. Early-onset benign occipital seizure syndrome (EBOSS) is suggested as an appropriate name for the variant group.

Adolescent↗

PubMed1997

Adolescent onset of idiopathic photosensitive occipital epilepsy after remission of benign rolandic epilepsy.

PURPOSE: We describe 2 girls, aged 19 years, who experienced a rolandic seizure at ages 4 and 5, respectively, together with the interictal EEG features of benign rolandic epilepsy (BRE). In adolescence both patients developed photosensitive occipital seizures accompanied by spontaneous and photic-induced occipital EEG paroxysms. METHODS: We have been following 33 patients with a history of BRE, between ages 12 and 28 years (mean 17 years). Twenty-one of these patients had experienced their last rolandic seizure before the age of 10 years and 9 of them had been without treatment since age 11 or earlier. In 2 of these 9 patients, other types of seizures recurred after remission of BRE. Clinical, EEG, and evoked potential findings on these 2 patients are presented. RESULTS: After having experienced BRE, both patients suffered partial seizures from age 12, with elementary visual hallucinations, visual blurring, slow head turning, cephalic pain, epigastric discomfort, unresponsiveness, and vomiting. Seizure onset was related to watching TV or exposure to bright light. EEG showed interictal occipital spikes, and a photoparoxysmal response limited to the occipital lobes. Visual evoked potentials were greatly increased in amplitude. One patient had two visual attacks only and remained seizure free after 4 years of follow-up, while the other had seizures controlled by an association of valproate and carbamazepine. CONCLUSIONS: Clinical and neurophysiological characteristics suggest that these two patients may have presented different age-related expressions within the spectrum of a benign seizure susceptibility syndrome rather than sharply distinct epilepsy syndromes.

Adolescent↗

PubMed1997

Bilateral periventricular nodular heterotopia with mental retardation and syndactyly in boys: a new X-linked mental retardation syndrome.

Bilateral periventricular nodular heterotopia (BPNH) is a recently recognized malformation of neuronal migration, and perhaps proliferation, in which nodular masses of gray matter line the walls of the lateral ventricles. Most affected individuals have epilepsy and normal intelligence with no other congenital anomalies. A striking skew of the sex ratio has been observed because 31 of 38 probands have been female, and one gene associated with BPNH was recently mapped to chromosome Xq28. We report three unrelated boys with a new multiple congenital anomaly-mental retardation syndrome that consists of BPNH, cerebellar hypoplasia, severe mental retardation, epilepsy, and syndactyly. Variable abnormalities included focal or regional cortical dysplasia, cataracts, and hypospadius. We hypothesize that this syndrome involves the same Xq28 locus as isolated BPNH, and we review the expanding number of syndromes associated with BPNH.

Adolescent↗

PubMed1997

Opioid diketopiperazines: synthesis and activity of a prototypic class of opioid antagonists.

Discovery of high affinity and ultraselective delta opioid dipeptide antagonists composed of 2',6'-dimethyl-L-tyrosyl (Dmt) and 1,2,3,4-tetrahydroisoquinoline-3-carboxylic (Tic) served as the basis for the conformationally restricted diketopiperazine cyclo(Dmt-Tic) and related open chain analogues. These peptides primarily bind to delta opioid receptors: c(Dmt-Tic) displayed 30- to 50-fold higher delta affinity (Ki delta) than its diastereo-isomeric analogues and more than 4000-fold greater than its Tyr cognate; all of the c(Tyr-Tic) analogues were essentially inactive; c[(N-methyl)Dmt-Tic] lost 5-fold in Ki delta, while Ki mu increased 10-fold to yield a nonselective peptide; and the c(Dmt-Phe) series exhibited considerably reduced binding which indicated a synergism between Dmt and Tic in the binding mechanism. Whereas acetyl-Dmt-Tic linear peptides weakly interacted with opioid receptors, Ac-Dmt-Tic-NH2, exhibited better delta antagonist activity than c(Dmt-Tic) and greater delta receptor selectivity (Ki mu/Ki delta = 570). A three point attachment hypothesis for the interaction between c(Dmt-Tic) and the delta receptor was proposed: hydrophobicity imparted by the aromatic rings and the methyl groups of Dmt, hydrogen bonding through the tyramine hydroxyl group, and cation-pi interactions were suggested as contributing factors in binding the diketopiperazine in the receptor pocket. Although c(Dmt-Tic) exhibited a weak antagonist activity with mouse vas deferens, this diketopiperazine may provide a scaffolding for the formation of more potent antagonists for potential therapeutic applications.

Animals↗

PubMed1997

Opioid diketopiperazines: refinement of the delta opioid antagonist pharmacophore.

Bioactive models for a delta opioid receptor antagonist are proposed based on the structurally rigid, diketopiperazine containing cyclo 2',6'-dimethyl-L-tyrosyl (Dmt)-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid (Tic). Monte Carlo conformational analysis of c(Dmt-Tic) generated three low energy clusters (I-III) of conformers. The lowest energy conformer representing cluster I superimposed best with the X-ray crystal structures of c(Tyr-Tic), an inactive diketopiperazine with similar framework as c(Dmt-Tic), with H-Tyr-Tic-NH2, a dipeptide of moderate delta opioid affinity and lacking bioactivity, and with H-Tyr-Tic-Phe-Phe-OH (TIPP), a selective and potent delta opioid receptor antagonist. Clusters I and II superimposed best with three different overlays of naltrindole, a potent delta opiate antagonist, and with two other H-Tyr-Tic-NH delta opioid antagonist pharmacophores proposed by Temussi et al. (1994) and Wilkes and Schiller (1995). The 3-dimensional topography of these two clusters of c(Dmt-Tic) conformations may represent bioactive models for interaction of an antagonist at delta opioid receptors. Cluster I conformers exhibited gauche- (- 64 degrees) and gauche+ (53 degrees) orientations of the side chains Dmt and Tic, respectively, while cluster II contained trans (179 degrees) and gauche+ (62 degrees) orientations of those side-chains. Aromatic ring distances were 5.4 A for cluster I conformations and 8.2 A for cluster II structures. Orientation about the peptide bond N-C' was cis (- 5 degrees and 3 degrees) for both clusters, respectively. These structural features may provide optimal alignment of the physicochemical moieties important for delta opioid receptor interaction, such as the hydrophobic methyl groups of Dmt, hydrogen bonding of the dimethyltyrosine hydroxyl group within the receptor pocket and cation-pi interactions involving the aromatic rings of Dmt and Tic, as profiled by the three point attachment hypothesis.

Diketopiperazines↗

PubMed1997

Pharmacological characterization of nociceptin receptor: an in vitro study.

The newly discovered neuropeptide nociceptin (NC) (alias orphanin FQ) was tested for its potential direct effects as well as for its ability to modify the electrically evoked contractions in several isolated organs suspended in vitro. NC was inactive both as stimulant and as inhibitor of smooth muscle in several preparations, whereas it inhibited the contractions induced by electrical field stimulation in the mouse vas deferens and guinea pig ileum. NC showed the same potency (IC50 = 10 nM) in the two preparations. However, it was significantly more effective in the mouse vas deferens (maximal effect -80%) than in the guinea pig ileum (maximal effect -50%). The inhibitory effect exerted by NC in the two preparations was not affected by naloxone or more selective opioid receptor antagonists. Moreover, by truncation of C-terminal sequences, NC fragments were designed. These fragments were subsequently tested in the mouse vas deferens and in the guinea pig ileum: NC(1-13)-NH2 was the smallest peptide maintaining the same efficacy and potency as the natural peptide. Finally, NC-NH2 and its fragments NC(1-13)-NH2 and NC(1-9)-NH2 were modified by substituting the phenylalanine 1 residue with a tyrosine. These peptides were tested in the guinea pig ileum, where they behaved as mixed NC-opioid receptor agonists ([Tyr1]NC-NH2 and [Tyr1]NC(1-13)-NH2) or as pure opioid receptor agonists ([Tyr1]NC(1-9)-NH2. In conclusion, the present paper demonstrated that the electrically stimulated mouse vas deferens and guinea pig ileum can be used as a sensitive bioassay for studying the pharmacology of NC and related compounds.

Amino Acid Sequence↗

PubMed1996

The mouse vas deferens: a pharmacological preparation sensitive to nociceptin.

The newly discovered neuropeptide, nociceptin (alias orphanin FQ), was tested for its potential direct effects, as well as for its ability to modify the electrically evoked contractions in several isolated organs suspended in vitro. The electrically stimulated mouse vas deferens is a sensitive preparation on which nociceptin exerts an inhibitory effect which is not affected by naloxone. The mouse vas deferens is therefore proposed as a bioassay for nociceptin and related compounds.

Amino Acid Sequence↗

PubMed1996

Opioid receptor selectivity alteration by single residue replacement: synthesis and activity profile of [Dmt1]deltorphin B.

The single amino acid replacement of 2',6'-dimethyl-L-tyrosine in deltorphin B (H-Dmt-D-Ala-Phe-Glu-Val-Val-Gly-NH2) yielded high affinity for mu- and delta-binding sites. [Dmt1]Deltorphin B lacks activity at kappa-opioid binding sites. Bioactivity in vitro with guinea-pig ileum confirmed that [Dmt1]deltorphin B interacted with mu-opioid receptors by reducing electrically induced contractions in a naloxone-reversible manner and was 150-fold more potent than morphine and comparable to [D-Ala2,NMePhe4,Gly-ol5]enkephalin (DAGO). The inhibition of spontaneous contractions of rabbit jejunum provided evidence for delta-opioid receptor interaction. Analgesia (hot plate and tail flick tests) revealed that [Dmt1]deltorphin B was 180- to 200-fold more potent than morphine. Pretreatment with naloxone, naltrindole or H-Dmt-Tic-Ala-OH (a highly selective delta-opioid receptor antagonist) prevented [Dmt1]deltorphin B antinociception. Thus, [Dmt1]deltorphin B exhibited remarkably high dual affinity and bioactivity toward delta- and mu-opioid receptors.

Animals↗

PubMed1996

Design and synthesis of 1-aminocycloalkane-1-carboxylic acid-substituted deltorphin analogues: unique delta and mu opioid activity in modified peptides.

Deltorphin analogues were substituted by a series of achiral C alpha,alpha-dialkyl cyclic alpha-amino acids (1-aminocycloalkane-1-carboxylic acids, Ac chi c, where chi = a hexane, pentane, or propane cycloalkane ring) in position 2, 3, 4, or 2 and 3 in deltorphin C, and in position 2 in [Ac6c2,-des-Phe3]deltorphin C hexapeptide. Receptor assays indicated that even though Ac6c2 and Ac6c3 exhibited a diminished Ki delta by ca. 20-fold (2.5-3.3 nM) relative to deltorphin C (Ki delta = 0.15 nM), selectivity was marginally elevated (Ki mu/Ki delta = 1250) or enhanced by about 70%, and both peptides fitted stringent iterative calculations for a two-site binding model (eta = 0.625 and 0.766, respectively, P < 0.0001). The disubstituted [Ac6c2,3]- or [Ac6c2,des-Phe3]deltorphin analogues yielded peptides with decreased Ki delta, such that the latter peptide was essentially inactive. The presence of Ac5c or Ac3c in place of Phe3 further diminished Ki delta (15.4 to 19.0 nM), yet delta selectivity only fell about one-half (Ki mu/Ki delta = 440 and 535, respectively), and only the former peptide fitted a two-site binding model (eta = 0.799). The replacement of Asp4 by Ac6c, Ac5c, or Ac3c produced essentially nonselective analogues through the acquisition of high mu affinities (2.5, 0.58 and 0.27 nM, respectively) while maintaining high delta affinities (Ki delta = 0.045-0.054 nM) which were about 3-fold greater than that of deltorphin C. Using pharmacological assays in vitro (mouse vas deferens and guinea pig ileum), position 3-substituted analogues all indicated substantial losses in bioactivity, whereas substitution by 1-aminocycloalkanes at the fourth position retained high delta activity. In fact, the bioactivity of [Ac3c4]deltorphin C indicated a peptide with relatively weak delta selectivity, which was comparable to the observations with the receptor binding data. In summary, the data confirmed that (i) delta selectivity occurs in the absence of D-chirality at position 2, (ii) the aromaticity of Phe3 is replaceable by an achiral residue with a hydrophobic ring-saturated side chain, and (iii) the acquisition of dual high-affinity analogues occurs through the elimination of the anionic function at position 4 and replacement by an amino acid with a hydrophobic side chain.

Amino Acid Sequence↗

PubMed1996

Cortical myoclonus in Angelman syndrome.

Angelman syndrome (AS) results from lack of genetic contribution from maternal chromosome 15q11-13. This region encompasses three GABAA receptor subunit genes (beta3, alpha5, and gamma3). The characteristic phenotype of AS is severe mental retardation, ataxic gait, tremulousness, and jerky movements. We studied the movement disorder in 11 AS patients, aged 3 to 28 years. Two patients had paternal uniparental disomy for chromosome 15, 8 had a >3 Mb deletion, and 1 had a microdeletion involving loci D15S10, D15S113, and GABRB3. All patients exhibited quasicontinuous rhythmic myoclonus mainly involving hands and face, accompanied by rhythmic 5- to 10-Hz electroencephalographic (EEG) activity. Electromyographic bursts lasted 35 +/- 13 msec and had a frequency of 11 +/- 2.4 Hz. Burst-locked EEG averaging in 5 patients, generated a premyoclonus transient preceding the burst by 19 +/- 5 msec. A cortical spread pattern of myoclonic cortical activity was observed. Seven patients also demonstrated myoclonic seizures. No giant somatosensory evoked potentials or C-reflex were observed. The silent period following motor evoked potentials was shortened by 70%, indicating motor cortex hyperexcitability. Treatment with piracetam in 5 patients significantly improved myoclonus. We conclude that spontaneous, rhythmic, fast-bursting cortical myoclonus is a prominent feature of AS.

Adolescent↗

PubMed1996

Polymorphonuclear neutrophils pulsed with synthetic peptides efficiently activate memory cytotoxic T lymphocytes.

Polymorphonuclear neutrophils (PMNs), traditionally considered effector cells in the inflammatory response, have recently been regarded as potential regulators of the immune response. In the present study we investigate whether PMNs are efficient antigen-presenting cells for reactivation of memory cytotoxic T lymphocytes (CTLs). PMNs were pulsed with synthetic peptides derived from Epstein-Barr virus (EBV) antigens. We have used the IVTDFSVIK (IVT) peptide derived from the Epstein-Barr virus-encoded nuclear antigen 4 protein, corresponding to the immunodominant epitope of HLA-AII-restricted CTL responses, and the CLGGLLTMV (CLG) peptide derived from the latent membrane protein 2 antigen, representing a subdominant epitope of HLA-A2-restricted CTL responses. The data indicate that peptide-pulsed PMNs selectively activate specific CTL responses to both immunodominant and subdominant epitopes. The efficiency of CTL induction by PMNs was comparable to that observed with the conventional method of EBV-specific CTL reactivation with the autologous lymphoblastoid cell line, as well as with peptide-pulsed monocyte-enriched adherent cells. On the contrary, unactivated peptide-pulsed lymphocytes failed to induce an epitope-specific CTL response. These results demonstrate that PMNs efficiently present antigens to memory virus-specific CTLs and suggest that they may have a role as antigen-presenting cells.

Amino Acid Sequence↗