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Biomedical subjects

K Tachibana

Publications and source records attributed to K Tachibana.

At least 19 recordsLinked to original sources
PubMed1995

Direct association of pp125FAK with paxillin, the focal adhesion-targeting mechanism of pp125FAK.

Focal adhesion kinase (pp125FAK) is localized to focal adhesions and tyrosine phosphorylated by the engagement of beta 1 integrins. However, it is unclear how pp125FAK is linked to integrin molecules. We demonstrate that pp125FAK is directly associated with paxillin, a 68-kD cytoskeleton protein. The COOH-terminal domain of pp125FAK spanning FAK residues 919-1042 is sufficient for paxillin binding and has vinculin-homologous amino acids, which are essential for paxillin binding. Microinjection and subsequent immunohistochemical analysis reveal that glutathione S-transferase-FAK fusion proteins, which bind to paxillin, localize to focal adhesions, whereas fusion proteins with no paxillin-binding activity do not localize to focal adhesions. These findings strongly suggest that pp125FAK is localized to focal adhesions by the direct association with paxillin.

Amino Acid Sequence↗
PubMed1995

Role of the VLA-4 molecule in T cell costimulation. Identification of the tyrosine phosphorylation pattern induced by the ligation of VLA-4.

The very late activated Ag (VLA) molecules not only mediate T cell adhesions, but also provide costimulation in a TCR/CD3-dependent manner. However, little is known about the signals mediated by the ligation of VLA molecules. Previous work from our laboratory identified a 105-kDa protein that is predominantly phosphorylated on tyrosine residue upon engagement of VLA-4 in a human T lymphoblastic cell line, H9, and in peripheral T cells. In the present study, we have shown that the A and B epitope of VLA-4 plays a key role in VLA-4-mediated T cell costimulation. Moreover, we have demonstrated that the solid phase cross-linking of VLA-4 using Ab (against A and B) or the CS-1 region of fibronectin, stimulated tyrosine phosphorylation of 140-, 120-, 80- to 70-, 60- to 55-, 50-, and 45-kDa proteins in addition to the 105-kDa protein. In contrast, Ab ligation of the C epitope of VLA-4 mainly induced tyrosine phosphorylation of pp105, weakly induced other protein tyrosine phosphorylation, and additionally induced only minimal T cell costimulation. Using immunoblotting, we have identified some of the tyrosine-phosphorylated proteins to be phospholipase C gamma (pp140), pp125 focal adhesion kinase (pp120), paxillin (pp70 and pp50), p59fyn/p56lck (pp60-55), and mitogen-activated protein kinase (pp45). Since solid phase cross-linking of VLA-4 by B2 epitope-specific Ab induced T cell costimulation most strongly via the CD3 pathway, our results suggested that the above tyrosine-phosphorylated proteins may play an important role in VLA-4-mediated T cell costimulatory signaling events.

Antibodies, Monoclonal↗
PubMed1995

Albumin microbubble echo-contrast material as an enhancer for ultrasound accelerated thrombolysis.

BACKGROUND: Recent findings suggest that acoustic cavitation is responsible for acceleration of thrombolysis by ultrasound (US) energy. It is known that albumin microbubbles lower the threshold of acoustic cavitation production. METHODS AND RESULTS: The present study was designed to determine whether the presence of albumin microbubbles used for echo-contrast material (Albunex) can further accelerate fibrinolysis of US. Artificial thrombus was produced by Chandler's loop method with blood extracted from a healthy subject. Urokinase (UK, 1200 IU/mL) was added to the artificial thrombi placed in test tubes. Each thrombus was exposed to US (170 kHz) at a distance of 1.2 cm for a total of 60 seconds at an intensity of 0.5 W/cm2 at intervals of 2 seconds on and 4 seconds off. Echo-contrast material (0.6 x 10(6) microspheres per mL) or 5% albumin (for control) was circulated near the thrombus at a rate of 1 mL/min during the US exposure. Fibrinolysis was later determined by percentage of weight loss of thrombus after 60 minutes of incubation (n = 15). Fibrinolysis with UK alone was 26.6 +/- 4.8%. Fibrinolysis with UK+US treatment was 33.3 +/- 5.8%. Further increase of fibrinolysis to 51.3 +/- 7.7% occurred in the presence of Albunex (UK+US+Albunex). Statistical differences were obtained between all these groups (ANOVA). CONCLUSIONS: The presence of the echo-contrast agent induced further acceleration of thrombolysis by US energy. It is suggested that this diagnostic echo-contrast material can be used as an alternative therapeutic US drug enhancer for thrombolysis.

Adult↗
PubMed1995

Integrin-mediated cell adhesion promotes tyrosine phosphorylation of p130Cas, a Src homology 3-containing molecule having multiple Src homology 2-binding motifs.

p130Cas (Cas) has been recently identified as a 130-kDa protein that is highly phosphorylated on tyrosine residues and is stably associated with p47v-crk (v-Crk) and p60v-src (v-Src) oncogene products in cells transformed by the respective genes. Cas is a novel signaling molecule having a single Src homology (SH) 3 domain and a cluster of multiple SH2-binding motifs. While the tight association of Cas with v-Crk and v-Src is strongly suggestive of a significant role in regulating cellular transformation, the function of Cas in normal untransformed cells is totally unknown. We report here that cell adhesion to fibronectin rapidly promotes tyrosine phosphorylation of Cas in human and rat fibroblast cell lines. The response was equally induced by cell adhesion to plates coated with vitronectin, laminin, and collagen but not by cell attachment to nonspecific substrate poly-L-lysine. The kinetic profile of Cas phosphorylation was almost identical with that of tyrosine phosphorylation of focal adhesion kinase pp125FAK (Fak), which is well known to be activated subsequent to integrin-mediated cell adhesion. Adhesion-dependent Cas phosphorylation was completely inhibited by treating cells with cytochalasin D, an agent that disrupts polymerization of actin stress fibers. These results suggest that tyrosine phosphorylation of Cas is stimulated by normal cell adhesion in close association with Fak phosphorylation and the formation of actin stress fibers. In v-Src- or v-Crk-transformed cells, however, the tyrosine phosphorylation of Cas is markedly increased in an adhesion-independent manner that is insensitive to treatment with cytochalasin D. Thus, Cas plays a role in signaling pathways mediated by cell adhesion as well as by transformation. We propose that Cas may amplify and propagate integrin-mediated signals by interacting with SH2-containing molecule(s).

Animals↗
PubMed1995

The levels of granulocyte colony-stimulating factor in the plasma of the bone marrow aspirate in various hematological disorders.

We developed a sensitive method of measurement of granulocyte colony-stimulating factor (G-CSF) by an enzyme-linked immunosorbent assay, which we applied in the plasma of the bone marrow aspirate in 70 patients with various hematological disorders. The lowest limit of detection by this method is 2 pg/ml. G-CSF was detected in all but two of the patients. Compared to the G-CSF level in normal healthy controls, those in non-Hodgkin's malignant lymphoma, aplastic anemia, agranulocytosis and multiple myeloma were significantly higher, while the level in refractory anemia was not different. The G-CSF level in acute myelogenous leukemia patients was either elevated or decreased regardless of the French-American-British subgroup. The level in acute lymphoblastic leukemia was not different from the normal value, as was that in refractory anemia with an excess of blasts, and that in chronic lymphocytic leukemia. A patient with chronic myelomonocytic leukemia showed initial elevation of G-CSF with normalization after entering complete remission. The G-CSF level in chronic myelogenous leukemia was significantly decreased, although one patient in hematological remission who was under alpha-interferon therapy showed normal levels. The level in polycythemia vera was not significantly different from the normal value. The G-CSF level for the entire group showed an inverse, although not statistically significant, correlation with the percentages of myeloid cells of the bone marrow (r = -0.174, p = 0.1703, n = 80). These results are thought to reflect the regulatory mechanism of granulopoiesis in the bone marrow in various hematological disorders, and it is concluded that this method may be of clinical use in the treatment of patients with these disorders and in the selection of candidates likely to benefit from G-CSF administration.

Agranulocytosis↗
PubMed1995

Focal adhesion kinase (pp125FAK) is tyrosine phosphorylated after engagement of alpha 4 beta 1 and alpha 5 beta 1 integrins on human T-lymphoblastic cells.

pp125FAK is a novel protein tyrosine kinase associated with focal adhesions. It has been shown that ligation of VLA beta 1 integrins on a number of cell types enhanced tyrosine phosphorylation and kinase activity of pp125FAK. Cellular transformation by retroviral oncogene products or mitogenic neuropeptides also result in the activation of this kinase. On the basis of these observations, pp125FAK has been proposed to be a key regulatory molecule connecting cell adhesion, transformation, and growth. We have previously shown that ligation of VLA beta 1 integrins induced CD3-dependent T cell proliferation and stimulated tyrosine phosphorylation of a molecular mass with a 105-kDa protein (pp105). Here we report that engagement of alpha 4 beta 1 and alpha 5 beta 1 integrins by adherence to their respective ligands stimulated tyrosine phosphorylation of 105- to 120-kDa proteins (pp105 and pp120, respectively) in human H9 T-lymphoblastic cells. At least one component of the 105- to 120-kDa proteins was found to be tyrosine-phosphorylated pp125FAK. While kinetics of adherence-dependent tyrosine phosphorylation of pp120/pp125FAK and pp105 are closely similar, pp105 appeared to be distinct from pp125FAK. Given T cell costimulation induced by VLA beta 1 integrins and the putative functional role of pp125FAK in cell growth, tyrosine phosphorylation of these two distinct proteins may be involved in T cell activation and proliferation.

Cell Adhesion↗
PubMed1995

Contribution of brain injury to hypertension following intravenously-administered pancuronium in rats.

Abnormal hypertension sometimes occurs following intravenous administration (i.v.) of pancuronium in patients with brain injury. The present experiment was designed to determine whether brain injury contributes to the hypertensive response of i.v. pancuronium. Forty-six Wister strain rats were studied, of which 39 had induced brain injury at (a) upper pons (b) midbrain (c) thalamus region (excluding hypothalamus) and (d) cerebellum or a combination of these sites. The injury was made by single insertion of a 22 Gauge needle through the skull surface. The quantity of pancuronium solution administered i.v. in each case was 1.0 ml containing either 0.8 mg/kg or 8 mg/kg of pancuronium. Group A (n = 7) had no brain injury and the mean arterial pressure (MAP) did not change following i.v. administration of pancuronium. In Group B (n = 9) (a+b+c, 8.0 mg/kg) MAP rose from 90.9 +/- 15.4 to 102 +/- 22.0 mmHg and in Group C (n = 7) (a+b+c, 0.8 mg/kg) MAP rose from 148.4 +/- 13.3 to 160 +/- 14.4 mmHg. In Group D (n = 5) (b+c, 8.0 mg/kg) MAP remained unchanged. In Group E (n = 5) (a, 8.0 mg/kg) MAP rose from 130.3 +/- 18.7 to 146 +/- 27.6 mmHg and in Group F (n = 6) (a, 0.8 mg/kg) MAP rose from 129.7 +/- 15.6 to 135.8 +/- 13.8 mmHg. In Group G (n = 7) (d, 8.0 mg/kg) MAP remained unchanged. Since the MAP was elevated in only those groups that received injury in the upper pons, we concluded that injury in the upper pons can lead to hypertension following i.v. administration of pancuronium.

Animals↗
PubMed1995

Cyclin B interaction with microtubule-associated protein 4 (MAP4) targets p34cdc2 kinase to microtubules and is a potential regulator of M-phase microtubule dynamics.

We previously demonstrated (Ookata et al., 1992, 1993) that the p34cdc2/cyclin B complex associates with microtubules in the mitotic spindle and premeiotic aster in starfish oocytes, and that microtubule-associated proteins (MAPs) might be responsible for this interaction. In this study, we have investigated the mechanism by which p34cdc2 kinase associates with the microtubule cytoskeleton in primate tissue culture cells whose major MAP is known to be MAP4. Double staining of primate cells with anti-cyclin B and anti-MAP4 antibodies demonstrated these two antigens were colocalized on microtubules and copartitioned following two treatments that altered MAP4 distribution. Detergent extraction before fixation removed cyclin B as well as MAP4 from the microtubules. Depolymerization of some of the cellular microtubules with nocodazole preferentially retained the microtubule localization of both cyclin B and MAP4. The association of p34cdc2/cyclin B kinase with microtubules was also shown biochemically to be mediated by MAP4. Cosedimentation of purified p34cdc2/cyclin B with purified microtubule proteins containing MAP4, but not with MAP-free microtubules, as well as binding of MAP4 to GST-cyclin B fusion proteins, demonstrated an interaction between cyclin B and MAP4. Using recombinant MAP4 fragments, we demonstrated that the Pro-rich C-terminal region of MAP4 is sufficient to mediate the cyclin B-MAP4 interaction. Since p34cdc2/cyclin B physically associated with MAP4, we examined the ability of the kinase complex to phosphorylate MAP4. Incubation of a ternary complex of p34cdc2, cyclin B, and the COOH-terminal domain of MAP4, PA4, with ATP resulted in intracomplex phosphorylation of PA4. Finally, we tested the effects of MAP4 phosphorylation on microtubule dynamics. Phosphorylation of MAP4 by p34cdc2 kinase did not prevent its binding to microtubules, but abolished its microtubule stabilizing activity. Thus, the cyclin B/MAP4 interaction we have described may be important in targeting the mitotic kinase to appropriate cytoskeletal substrates, for the regulation of spindle assembly and dynamics.

Amino Acid Sequence↗
PubMed1995

Orotracheal intubation through the laryngeal mask airway in paediatric patients with Treacher-Collins syndrome.

The laryngeal mask airway (LMA) is useful as an airway intubator (conduit) for an intubating tracheal bougie or fibreoptic bronchoscope, over which a tracheal tube is passed. However, in our paediatric patients with Treacher-Collins syndrome, only the latter technique was successful. This was attributed to the fact that a posteriorly protruded tongue displaced the LMA, made the glottis move considerably anterior and interfered with the attempts to enter the trachea with a bougie. Downward displacement of the epiglottis, which can sometimes impair the intubation technique through the LMA, was not observed in our patients. Partial obstruction of a tracheal tube within the LMA occurred in one of the patients.

Airway Obstruction↗
PubMed1995

A highly sensitive enzyme immunoassay for G-CSF in human plasma.

We have developed a sensitive sandwich enzyme-linked immunosorbent assay (ELISA) to measure granulocyte colony-stimulating factor (G-CSF) in human plasma. This ELISA employs a combination of a mouse monoclonal antibody (MAb) as the first antibody and an affinity-purified sheep polyclonal antibody conjugated with beta-D-galactosidase as the second antibody. The coefficients of intra- and interassay variations were 2.2 to 3.6% and 8.3 to 10.2%, respectively. The assay had no cross-reactivity with four other human cytokines. Plasma G-CSF levels in healthy volunteers could easily be measured because the detection limit was 0.5 pg/mL. The mean plasma G-CSF concentration in 57 healthy volunteers (aged 19 to 47; 27 males and 30 females) was 10.5 +/- 4.5 pg/mL standard deviation [SD]). There was no statistically significant relationship between plasma G-CSF concentration and absolute neutrophil counts in those healthy volunteers (r = 0.259; p = 0.052).

Adult↗
PubMed1995

Lesions of the lumbar posterior end plate in children and adolescents. An MRI study.

We have reviewed 37 patients under the age of 18 years with lesions of the lumbar posterior end plate. All but one were active in sport, and most were seen because of low back pain. An abnormality was commonly found at the inferior rim of the body of L4 and at the superior rim of the sacrum. All adjacent intervertebral discs showed a decrease of signal intensity on the T2-weighted MRI. In 12 patients there was no interposed tissue at the posterior end-plate lesions. When disc material had migrated posteriorly none protruded beyond the posterior margin of the end plate, the dissociated portion of which was the main element compressing neural tissue. The posterior end-plate lesion should be regarded as a vertebral non-articular osteochondrosis.

Adolescent↗
PubMed1994

[Serum levels of intact molecular osteocalcin in children with growth hormone (GH) deficiency during GH therapy: an early predictor of GH therapy].

Recently we developed a sandwich enzyme immunoassay (EIA) specific for intact molecular osteocalcin (I-OC), produced only by osteoblast cell and partially released into blood circulation, to establish a specific biochemical marker of bone formation. In order to confirm whether serum I-OC levels constitute a specific marker for bone formation and to assess the relationship between serum I-OC levels and growth response to growth hormone (GH) therapy, we measured the serum I-OC in serial serum samples using this EIA from 61 children with GH deficiency who showed significant bone growth during GH therapy. The serum I-OC levels in children with GH deficiency before GH therapy were slightly lower than those in normal children (Kanzaki S. et al., J. Clin Endocrinol Metab. 1992;75:1104-9), and had a wide distribution overlapped with the normal range. These levels were apparently increased during GH treatment; that is, in contrast to the levels of 22.9 +/- 1.5 ng/ml (mean +/- SE) before GH treatment, the levels after 1 and 2 months of GH treatment were 29.1 +/- 1.6 ng/ml and 32.5 +/- 1.8 ng/ml, respectively. However, they decreased slightly at 3 months and then they gradually rose to 37.5 +/- 2.8 ng/ml after 12 months, I-OC ratios, represented by the I-OC level at each month of GH therapy in relation to pretreatment level, correlated well with the growth response (growth velocity, growth velocity SD score and delta growth velocity SD score) after 12 months of GH treatment. Correlation coefficients of the growth velocity versus I-OC ratio at 1 and 6 months of GH treatment were 0.677 (p < 0.001, N = 58) and 0.752 (p < 0.001, N = 55), respectively. However, both IGF-I and ALP ratios represented in the same way as the I-OC ratio, correlated poorly as compared with the I-OC ratio. These results demonstrate that the change of serum I-OC levels indicates a direct and sensitive reflection of bone formation, because serum I-OC levels significantly increased with the growth response to GH therapy. The measurement of serum I-OC levels after 1 month of GH treatment may be a useful tool in predicting improved growth velocity during long-term GH therapy.

Body Height↗
PubMed1994

Differential regulation of CD27 expression on subsets of CD4 T cells.

Our earlier studies showed that although CD27 was stably expressed on the CD45RA(+)-CD45RO-CD29low subset of CD4 T cells, its expression on the CD45RA-CD45RO+CD29high subset of CD4 T cells was gradually lost within 3 weeks after PHA activation. In the present study, we further determined the mechanisms by which the CD27 expression was differentially regulated on the subsets of CD4 T cells. We showed that disappearance of CD27 from the surface of the CD45RA-CD45RO+ subset of CD4 T cells was not solely due to the shedding of the CD27 molecule from the cell surface since the release of a soluble form of the CD27 molecule from the CD45RO+ CD4 T cells was consistently less than that from CD45RA+ CD4 T cells. Although the surface CD27 expression was undetectable on long-term cultured T cell lines originally derived from CD45RO+ CD4 T cells, some of these cells still expressed intracellular CD27 and CD27 mRNA. Moreover, restimulation could not induce CD27 expression on such cells. Further analysis of CD27 protein and mRNA expression at a clonal level showed that cloned cells derived from CD45RO+ CD4 T cells having lost cell surface expression of CD27 were of two types: one expressed intracellular CD27 mRNA and protein whereas the second lacked both intracellular CD27 mRNA and protein.

Blotting, Northern↗
PubMed1994

Liver tissue damage by ultrasound in combination with the photosensitizing drug, Photofrin II.

We have investigated whether ablation of normal rat liver by ultrasound can be enhanced after administration of a photosensitizing agent (Photofrin II). After laparotomy and administration of Photofrin II (30 mg/kg), ultrasound (210 kHz, 1.3 W/cm2) was directed directly to the surface of the liver for a total duration of 3 min by a plane type unfocused transducer (6 mm x 6 mm). The depth of tissue damage was histologically compared to rats exposed to ultrasound alone. The mean maximum lesion depth on rats applied with ultrasound and Photofrin II was 5.7 +/- 0.9 mm (mean +/- SD) whereas in rats treated with ultrasound alone this was 3.0 +/- 0.4 mm. There was a significant difference between the two groups (P < 0.05). The present study suggests the possible use of a photosensitizing agent as an enhancer for the treatment of liver tumors by ultrasound.

Animals↗
PubMed1994

Sequence analysis of the thyrotropin (TSH) receptor gene in congenital primary hypothyroidism associated with TSH unresponsiveness.

Congenital primary hypothyroidism due to thyrotropin (TSH) unresponsiveness is a very rare disorder and only a few cases have been documented previously. To elucidate whether structural abnormalities in the TSH receptor (TSHR) could be a primary underlying mechanism of this disorder, we analyzed nucleotide sequence of the entire coding region of the TSHR gene in three patients diagnosed with congenital primary hypothyroidism associated with TSH unresponsiveness. Diagnosis of TSH unresponsiveness was largely made based on the following criteria: (a) congenital primary hypothyroidism with autosomal recessive inheritance, (b) a nongoitrous thyroid gland in a normal position with low thyroidal radioactive iodine uptake, (c) normal in vitro TSH bioactivity or absent in vivo response to exogenous TSH, and (d) absence of thyroid autoantibodies. The TSHR cDNA was successfully obtained from RNA of peripheral mononuclear leukocytes with reverse transcription and polymerase chain reaction, and was sequenced directly. Comparison of these nucleotide sequences with the normal TSHR sequence revealed no difference in the predicted amino acid sequence with a heterozygous polymorphism in codon 601 in one patient, indicating absence of TSHR structural abnormalities in these patients. Our results indicate that congenital primary hypothyroidism associated with TSH unresponsiveness is unlikely to be due to mutations in the TSHR-structure gene.

Adult↗
PubMed1994

Testicular juvenile granulosa cell tumor in an infant with X/XY mosaicism clinically diagnosed as true hermaphroditism.

We report a testicular juvenile granulosa cell tumor (T-JGCT) with characteristic clinical and histopathological features. The tumor was present in the left abdominal testis of a 7-month-old infant with a 45,X/46,XY karyotype and ambiguous genitalia. Preoperatively, the infant was diagnosed as having functional testicular and ovarian elements based on elevated levels of serum testosterone and estradiol following human chorionic gonadotropin and human menopausal gonadotropin administration, respectively. Histologically, the left gonad contained a tumorous lesion composed of an admixture of cellular areas and multiple cystic follicles that had some continuity with the adjacent testicular tubules. Some tumor cells showed immunoreactivity for estradiol. The right gonad was a streak gonad containing small irregular nests of sex cord-type cells. No maturing ovarian follicle was present in either gonad. To our knowledge, this is the fifth reported case of T-JGCT with abnormal sex chromosomes, and the first case of T-JGCT confirmed to have not only the morphological but also the functional characteristics of granulosa cells.

Disorders of Sex Development↗
PubMed1994

Prolonged impairment of very late activating antigen-mediated T cell proliferation via the CD3 pathway after T cell-depleted allogeneic bone marrow transplantation.

One of the major obstacles in allogeneic bone marrow transplantation (allo-BMT) is prolonged T cell dysfunction resulting in a variety of infectious complications in the months to years after hematologic engraftment. We previously showed that immobilized extracellular matrix (ECM) proteins such as fibronectin (FN), the CS-1 domain of FN, or collagen (CO) acted synergistically with immobilized anti-CD3 to induce T cell proliferation. In addition, the comitogenic effect of ECMs could be mimicked by immobilized mAb reactive with a common beta 1 chain (CD29) of very late activating (VLA) antigens which include ECM receptors. Since the interaction of T cells with ECMs appears to play an important role in the process of T cell reconstitution following allo-BMT, we examined the expression of VLA antigens (alpha 1-alpha 6, beta 1) and their functional roles in CD3-mediated T cell proliferation at various times after T cell depleted allo-BMT. VLA beta 1 as well as VLA alpha 4, alpha 5, and alpha 6 expression was lower than normal controls during the first 3 mo after allo-BMT and auto-BMT, whereas these expressions returned to normal levels by 4 mo after allo-BMT and auto-BMT. Although alpha 1 and alpha 2 were not expressed on lymphocytes from normal controls, these antigens were expressed on lymphocytes at the detectable levels (5-15%) from patients after allo-BMT and auto-BMT. Both CD29 and CD3 were expressed at normal levels on lymphocytes from patients > 3 mo after allo-BMT, whereas T cell interaction with ECM through VLA proteins or crosslinking of VLA beta 1 expressed by T cells with anti-CD29 mAb results in poor induction of CD3-mediated T cell proliferation for a prolonged period (> 1 yr) after allo-BMT. In contrast, T cell proliferation induced by crosslinking of anti-CD2 or anti-CD26 with anti-CD3 was almost fully recovered by 1 yr post-allo-BMT. After autologous BMT, impaired VLA-mediated T cell proliferation via the CD3 pathway after auto-BMT returned to normal levels within 1 yr despite no significant difference in CD3 and CD29 expression following either allo- or auto-BMT. The adhesion of T cells from post-allo-BMT patients to FN-coated plate was normal or increased compared to that of normal controls. Moreover, the induction of the tyrosine phosphorylation of pp105 protein by the ligation of VLA molecules was not impaired in allo-BMT patients. These results suggest that there are some other defects in the process of VLA-mediated signal transduction in such patients. Our results imply that disturbance of VLA function could explain, at least in part, the persistent immunoincompetent state after allo-BMT and may be involved in susceptibility to opportunistic infections after allo-BMT.

Antigens, CD↗