Biomedical subjects

H Hamano

Publications and source records attributed to H Hamano.

At least 37 records · Page 2Linked to original sources

PubMed1998

[Long-term gadolinium-enhancement of cauda equina on MRI in a case of spinal cord infarction after epidural anesthesia].

A 49-year-old woman developed paraplegia 26 hours after appendectomy under epidural and general anesthesia. Systolic blood pressure fell to 85 mmHg for 25 minutes after epidural anesthesia, which was performed at the level of the L1/2 intravertebral space. Neurological examination revealed paraplegia and superficial sensory impairment below the level of the L 1 spinal cord. The bladder was atonic by cystometry. MRI showed gadolinium enhancement of the cauda equina extending over a long period (3 months) and spinal cord infarction. The infarction was at the level of 10th thoracic spinal vertebra to conus and was limited to the gray matter of the spinal cord. We consider that the reason for spinal cord infarction was prolonged hypotension of the patient, who was diabetic, hypertensive and hypercoagulopathic. The blood supply to the gray matter is mainly from the central artery which is derived from the anterior spinal artery, and the gray matter is particularly vulnerable to hypotension. Our hypotheses concerning gadolinium enhancement of the cauda equina are the following: 1) enhancement of the cauda equina was seen due to collateral formation after spinal cord infarction, and 2) long-term enhancement of the cauda equina was observed due to an ischemic lesion involving a large area.

Anesthesia, Epidural↗

PubMed1997

Mechanism of reduction of cortical blood flow in striatocapsular infarction: studies using [123I]iomazenil SPECT.

Single photon emission computed tomography (SPECT) using [123I]iomazenil (radioligand of central-type benzodiazepine receptors) was employed to examine two patients with striatocapsular infarction. Patient 1 was a 61-year-old female with motor aphasia and hemiplegia on the right side. Magnetic resonance imaging (MRI) showed a lesion in the anterior limb of internal capsule and putamen on the left side. SPECT using 99mTc-HMPAO revealed a reduction of cerebral blood flow (CBF) in the frontoparietal region on the left side, but the delayed images in SPECT using [123I]iomazenil showed only a mild decrease of accumulation in the frontal lobe. Patient 2 was a 55-year-old male with hemiplegia on the left side. MRI showed a lesion localized in the basal ganglia and posterior limb of the internal capsule on the right side. SPECT using 99mTc-HMPAO revealed a reduction of CBF in the frontoparietal region on the right side and in the cerebellar hemisphere on the left side, but the delayed images in SPECT using [123I]iomazenil showed little decrease of accumulation in parietal lobe. The discrepancy between CBF and receptor images suggested that cortical hypoperfusion on striatocapsular infarction might reflect hypometabolism due to disconnection of the neuronal network between subcortical structure and cortex.

Aphasia↗

PubMed1997

Accelerated onset of age-related autoimmune lesions in MRL/+ mice by ovariectomy.

MRL/Mp +/+ (MRL/+) mice, not bearing the lpr gene, are known to have age-related autoimmune lesions in several organs such as pancreas, salivary and lacrimal glands at 30-weeks-old or more. In this study, MRL/+ mice were ovariectomized at 4-weeks-old, and their natural histories were analysed. Ovariectomy (Ovx) of MRL/+ mice led to marked acceleration of organ-specific autoimmune lesions exclusively in the salivary and lacrimal glands at 8-weeks-old or more, whereas no significant inflammatory change was observed in the pancreas. In the vast majority of inflammatory infiltrates, CD3+ CD4+ T cells were predominant in both the salivary and lacrimal glands of Ovx-MRL/+ mice. Up-regulated expression of cytokine genes including IL-1 beta, TNF-alpha, IL-2, interferon (IFN)-gamma, and IL-6 was detected in the salivary gland of Ovx-MRL/+ mice by reverse transcriptase (RT)-PCR analysis. FACS analysis of spleen cells of Ovx-mice revealed increase in I-Ak expression on B220+ cells, and autoantibody production against the salivary gland-specific antigen in sera from Ovx-MRL/+ mice, but not in control mice. These results suggest that age-related autoimmunity in the salivary and lacrimal glands were accelerated in Ovx-MRL/+ mice, and that autoreactive Th1 cells were activated associated with organ-specific autoantibody production.

Aging↗

PubMed1997

The typical pattern of superficial punctate keratopathy in wearers of extended wear disposable contact lenses.

PURPOSE: We investigated both the incidence and types of corneal epithelial complications associated with extended wear of the Acuvue disposable soft contact lens, in particular with respect to risk factors for the typical pattern of superficial punctate keratopathy (SPK). METHODS: We conducted a retrospective study of 5,478 eyes. Clinical characteristics of the corneal epithelial complications, tear volumes, and patient compliance were analyzed. RESULTS: A total of 3.6% (197 eyes/5,478 eyes) were observed to have a corneal epithelial complication on at least one examination during the entire follow-up period. Among the 197 eyes, 112 eyes were observed to have a complication during the initial 2 weeks of trial lens use. This included nine eyes that developed SPK with only daily wear use of the lenses. Sixty-eight eyes were beginners with no previous contact lens experience. SPK was observed in 193 eyes and corneal infiltrates in four eyes, although there were no cases of corneal epithelial erosion or corneal ulcer. With respect to type of SPK, a "smile mark" pattern confined to the area below the pupil was observed in 179 eyes (3.3%). CONCLUSIONS: The typical pattern of SPK was observed in 3.3% of users of extended wear disposable soft contact lenses, although the condition usually improved with the use of artificial tears.

Adolescent↗

PubMed1997

[An adult case of purulent meningitis secondary to retropharyngeal and deep neck abscess after treatment of odontogenic infection].

Retropharyngeal and deep neck abscess, which may follow odontogenic infection, is uncommon in adults, but can be fatal. Furthermore, bacterial meningitis secondary to this disorder is extremely rare. A 67-year-old man was brought to our hospital because he had developed neck pain, trismus, and disturbance of consciousness over several days. A few days prior to the appearance of neck pain, he had the periodontitis treated. Based on CSF, cervical X-ray and CT findings, he was diagnosed as having bacterial meningitis secondary to deep neck abscess. Culture of the CSF yielded gram-positive cocci, later identified as Gemella species, that is a rare organism for bacterial meningitis. Although the administration of antibiotics and drainage of the abscess resulted in gradual improvement of the infectious process, neurologically he remained with apallic syndrome. We would like to stress the importance of odontogenic and pharyngolaryngogenic sources as potential foci of purulent meningitis.

Abscess↗

PubMed1997

[Mitochondrial neurogastrointestinal encephalomyopathy presenting with protein-losing gastroenteropathy and serum copper deficiency: a case report].

We report a 56-year old female with mitochondrial neurogastrointestinal encephalomyopathy (MNGIE), presenting with protein-losing gastroenteropathy and serum copper deficiency. There was no neuromuscular disease in her family members. Three years prior to admission, she developed severe gastrointestinal symptoms including diarrhea, nausea, vomiting and ascites, and was diagnosed as having protein-losing gastroenteropathy based on alpha(1)-antitrypsin clearance and other tests. She was referred to our department when neurological symptoms were apparent. Neurological examinations revealed bilateral ptosis, ophthalmoplegia, hearing loss, facial and limb muscle weakness, mild sensory deficit of vibration on her feet and hypoactive deep tendon reflexes. Pigmentary retinopathy, cerebellar ataxia and heart block were not seen. Serum copper level was decreased to 45 micrograms/dl (normal: 83-155). Chronic intestinal pseudo-obstruction was proven by X-ray studies, and diffuse leukoencephalopathy demonstrated on brain MRI. On EMG, motor nerve conduction velocities were prolonged with temporal dispersion. Her muscle biopsy from biceps brachii muscle showed both neuropathic and myopathic changes, scattered ragged-red fibers and focal cytochrome c oxidase deficiency. Southern blot and polymerase chain reaction analysis on mitochondrial DNA showed no deletions nor point mutations. The clinical and pathologic findings of the present patient fulfilled the diagnostic criteria of mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) proposed by Hirano et al. There are few reported patients with MNGIE in Japan, but none presented with protein-losing gastroenteropathy and serum copper deficiency. Since the copper is a cofactor of cytochrome c oxidase, decreased serum copper level may aggravate the respiratory chain enzyme metabolism in mitochondria. Therefore, treatment for gastrointestinal tract disturbance and copper administration may be necessary to prevent disease progression.

Brain↗

PubMed1997

[Inflammatory sensory ataxic neuropathy presenting with alternating skew deviation on lateral gaze: a case report].

We report a 56-year-old female with chronic progressive sensory ataxic neuropathy presenting with alternating skew deviation on lateral gaze in the clinical course. She initially developed dysesthesias in the hands and feet asymmetrically, then gait disturbance developed over several months, and she was admitted to our hospital. Neurological examinations revealed profound deep sensory loss and mild superficial sensory disturbance with the absence of deep tendon reflexes, but muscular strength was completely preserved. EMG showed no evoked response of sensory nerve velocities and normal motor nerves. Sural nerve biopsy showed moderate demyelination with mild infiltration of inflammatory cells, and no vasculitis or onion bulb formation. CSF examination revealed elevation of cell counts and protein with marked intrathecal IgG synthesis and myelin basic protein, but finding of neurosyphillis. Serological examinations did not show any evidence of collagen disease, paraproteinemia, retrovirus infections or Lyme disease. Serum antiganglioside antibodies and anti-Hu antibody were negative. No evidence of malignancy was seen by radiological examinations and assays of tumor markers. In the weeks after admission, gait ataxia progressively worsened, and then she developed alternating skew deviation on lateral gaze, suggesting that the CNS was involved. No responsible lesion was detected on MRI. Corticosteroid administration improved not only the CSF findings, but also the neurologic symptoms, including the alternating skew deviation on lateral gaze. Although the disease entity was not identified, inflammatory demyelinating processes and immune-mediated mechanisms were considered to play important roles.

Anti-Inflammatory Agents↗

PubMed1996

Effector mechanism of experimental autoimmune sialadenitis in the mouse model for primary Sjögren's syndrome.

We have recently established a new animal model for primary Sjögren's syndrome in NFS/sld mutant mice thymectomized 3 days after birth (3dTX) bearing an autosomal recessive gene with sublingual gland differentiation arrest. In this study, we analyze developing mechanisms of experimental autoimmune sialadenitis (EAS) in the mouse model, focusing on local expressions of cytokine and cell adhesion molecule genes by reverse transcriptase-polymeric chain reaction (RT-PCR) and immunohistochemistry, kinetic analysis of splenic lymphocytes expressing activation markers, and I-Aq class-II molecules by flow cytometry (FACS). We found up-regulation of local cytokine genes (IL-1 beta, TNF-alpha, IL-2, IFN-gamma, IL-6, IL-10, IL-12p40) and cell adhesion molecule genes (ICAM-1, LFA-1, CD44, Mel-14) in the salivary glands from mice with EAS by RT-PCR, which were supported by immunohistochemistry. FACS analysis demonstrated that a significant proportion of splenic CD4+ T cells express activation markers (CD44, LFA-1, Mel-14low, CD45RB(low)) at a high level and an increase in expression of B220+ B cells bearing I-Aq class-II molecules. These data suggest that spontaneous EAS in 3dTX NFS/sld mutant mice may be triggered by an in situ activation of autoreactive CD4+ T cells comprising unique cytokine profile (high levels of IL-2, IFN-gamma, IL-10, and IL-12p40 mRNA) in the salivary glands.

Animals↗

PubMed1996

Mechanism of the development of autoimmune dacryodenitis in the mouse model for primary Sjögren's syndrome.

To elucidate the mechanism of development in autoimmune lacrimal gland disease, we analyzed different aspects of autoimmune dacryoadenitis in a newly established mouse model for primary Sjögren's syndrome, focusing on the local expressions of cytokine genes, and the repertoire of T cell receptor (TCR) V beta genes transcribed within the inflammatory infiltration in the lacrimal glands. We found that the vast majority of inflammatory infiltration into the lacrimal glands were CD4+ V beta 8+ T cells. We detected the up-regulation of local cytokine genes (IL-1 beta, TNF-alpha, IL-2, IFN-gamma, IL-10, IL-12p40) in the lacrimal glands with very early inflammatory lesions by reverse transcriptase (RT)-PCR analysis. The predominant expression of the V beta 8 gene segment was detected from a very early stage, while extensive age-related diversity of TCR V beta gene usage was observed. Single-strand conformation polymorphism (SSCP) analysis demonstrated a distinct and a common binding pattern in the PCR product of the V beta 8 gene on the infiltrating cells during the course of the disease. These data suggest that in autoimmune dacryoadenitis of the mouse model for primary Sjögren's syndrome there may be a restricted usage of TCR V beta elements on a very early stage of the autoimmune lesion to recognize unknown self-antigen, and the autoreactive CD4+ T cells constitute a unique cytokine profile in the autoimmune lacrimal gland disease.

Animals↗

PubMed1996

In vivo role of IL-10 and IL-12 during development of Sjögren's syndrome in MRL/lpr mice.

Expression of local cytokine genes including interleukin 10 (IL-10) and IL-12 was analyzed in the salivary gland tissues of MRL/lpr mice with Sjögren's syndrome. We demonstrate a significant role of IL-10 and IL-12 in vivo during development of Sjögren's syndrome in MRL/lpr mice. IL-10 mRNA expression was detected before the onset of disease and was upregulated during the course of autoimmune sialadenitis by RT-PCR. A predominant level of expression of IL-12 mRNA was also detected earlier in the proinflammatory stage of autoimmune sialadenities. Moreover, MHC class II (I-Ak) mRNA was detected before the onset of inflammatory lesions until older ages in the salivary glands of MRL/lpr mice. These results suggest that endogenous IL-10 and IL-12 may play important roles on immune-mediated destruction of the salivary glands during development of organ-specific autoimmunity in MRL/lpr mice.

Animals↗

PubMed1996

Docosahexaenoic acid reduces GABA response in substantia nigra neuron of rat.

.1. The effects of docosahexaenoic acid (DHA) on gamma-aminobutyric acid (GABA) response (IGABA) were investigated on the neuron acutely dissociated from rat substantia nigra (SN), with the use of patch recordings in a whole cell mode. 2. DHA (5 x 10(-6) M) reduced bicuculline-sensitive GABA (10(-4) M) current by 50.3 +/- 13.1% (mean +/- SE) at a holding potential (Vh) of -40 mV under voltage clamp. 3. The GABA concentrations for the half-maximum and threshold of IGABA were not altered by the presence or absence of 5 x 10(-6) M DHA in the external solution. 4. The decrease of 10(-4) M IGABA, following the peak during GABA application, was more rapid in the presence of 5 x 10(-6) M DHA than in its absence. The time constants for IGABA decay were significantly different between the two conditions. 5. DHA reduced the IGABA and the glycine-induced response (Igly) in a concentration-dependent manner. On the contrary, DHA potentiated the aspartate-induced response (Iasp) in a concentration-dependent manner, suggesting that DHA influences the activity of chloride channels but does not exhibit a nonspecific blocking effect on any ionic channel. 6. The application of thimerosal did not affect the reduction of IGABA by DHA, suggesting it unlikely that DHA reduces the IGABA by binding to phospholipids or triglycerides and altering the lipid environment around the chloride channel. 7. Arachidonic acid (AA) also reduced the IGABA in a manner similar to DHA. Docosapentaenoic acid (DPA) reduced the IGABA less potently than DHA. Other polyunsaturated and saturated fatty acids, such as docosatrienoic acid, docosatetraenoic acid, palmitic acid, and oleic acid, had very little or no effect on the IGABA. 8. DHA, as well as AA, may play an important role in modulating neuronal excitability by reducing the IGABA and Igly, and potentiating N-methyl-D-aspartate receptor-mediated responses in the SN.

Animals↗

PubMed1996

Immunopathological analysis of mucosal melanocyte distribution in the human lower lip of the elderly.

Mucosal melanocyte distribution in the human lower lip was analyzed immunopathologically using a wide selection of 195 surgical specimens. An age-related increase of mucosal melanocyte distribution was observed in the human lower lip by Fontana-Masson argentaffin stain and S-100 protein immunoreactivity. The mean number of mucosal melanocytes increased gradually with advancing age. A large number of them was found at or beyond the seventh decade of life in both sexes, which was statistically significant compared with those in all other decades (p < 0.01 or < 0.05). In addition, the sex difference in mucosal melanocyte density was statistically significant (p < 0.001) in each decade (men > women). These results suggest that physiological changes in mucosal melanocyte distribution are dependent upon aging and sex difference, and may play an important role in development of melanocytic lesions such as senile lentigo, pigmented nevi, and also intraepithelial malignant melanomas.

Adult↗

PubMed1996

Expression of HLA-DR and cytokine genes on interferon-gamma-stimulated human salivary gland cell line.

Stimulation of a cultured human salivary gland (HSG) cell line by interferon (IFN)-gamma leads to HLA-DR gene expression concomitant with inflammatory cytokine genes such as IL-1 beta, tumor necrosis factor (TNF)-alpha, and IL-6 in vitro. IFN-gamma-induced HLA-DR mRNA expression was clearly detected at 2 h after the stimulation, and thereafter its level of gene expression increased until day 7 on HSG cells by reverse transcriptase (RT)-PCR. Immunofluorescence analysis revealed that cytoplasmic HLA-DR immunoreactivity was detected for the first time at 2 days after the stimulation, and its immunoreactivity increased gradually until day 7, while no immunoreactivity with HLA-DP and HLA-DQ was observed at any of the days. In addition, the expression of IL-1 beta, TNF-alpha, and IL-6 on the IFN-gamma-stimulated HSG cells was detected by immunohistochemistry and RT-PCR analysis. These results indicate that human salivary gland cells can be induced to express HLA-DR mRNA by IFN-gamma concomitant with inflammatory cytokine gene expressions such as IL-1 beta, TNF-alpha, and IL-6.

Cytokines↗

PubMed1996

Cytokine gene expression and autoantibody production in Sjögren's syndrome of MRL/lpr mice.

In an attempt to elucidate the mechanism of development of organ-specific autoimmune lesions resembling human Sjögren's syndrome of MRL/lpr mice, we have analyzed local cytokine gene expressions and organ-specific autoantibody production in vivo. We have demonstrated that a major proportion of T cells bearing CD4 and V(beta)8 molecules are essentially responsible for triggering the autoimmunity in the salivary glands of MRL/lpr mice. The local cytokine gene expressions including interferon(IFN)-gamma, IL-12(p40) mRNAs were observed during the course of murine Sjogren's syndrome in MRL/lpr autoimmune strain. In particular, a high level of local expressions of IL-12 mRNA was detected earlier in the proinflammatory stage of autoimmune lesions. A significant level of local expression of MHC class-II(I-Ak) mRNA was detected before the onset of inflammatory lesions in the salivary glands, and I-Ak-positive epithelial duct cells were frequently observed in the salivary glands of MRL/lpr mice. In addition, we found the salivary gland-specific autoantibody in sera from MRL/lpr mice with early phase of autoimmune lesions by immunoblot analysis. These results suggest that cytokine gene stimulation and autoantibody production are essentially involved in the development of organ-specific autoimmune lesions in Sjögren's syndrome of MRL/lpr mice.

Animals↗

PubMed1996

Transient corneal stromal and endothelial changes following soft contact lens wear: a study with confocal microscopy.

PURPOSE: Previous studies have described transient corneal endothelial changes in non-contact lens wearers after a short period of soft contact lens wear by means of contact and noncontact specular microscopy and modified slit lamp biomicroscopy, which provide magnifications from 60 to 100x. In this investigation, we documented and characterized these contact lens-related corneal changes using the white light, real-time confocal microscope, which is capable of cellular resolution imaging of all layers within the cornea at magnifications of 100 to 500x. METHODS: We used a clinical confocal microscope to study corneal changes in three patients wearing a high water content soft contact lens for the first time. RESULTS: In one patient, endothelial changes consisting of irregularly shaped, round or oval, dark regions were observed within the endothelial mosaic. Scattered hyper-reflective keratocyte nuclei were seen in the posterior stroma. The keratocytic and endothelial changes were most evident 20 minutes after placement of the lens. By 30 minutes, the changes were fewer and less prominent, and the brightness of the highly reflective keratocyte nuclei had decreased. CONCLUSIONS: These studies show, for the first time, that the transient changes associated with contact lens wear occur not only in the endothelium, but also in the corneal stroma. It has been suggested that the changes result from an increase in CO2 and lactic acid, which causes a transient reduction in the corneal pH. We hypothesize that the resulting acidic environment may induce gene expression that causes changes in the involved nuclei, which in the keratocytes become hyper-reflective, and in the endothelium become enlarged, resulting in posterior displacement of the cell membrane and producing the dark "blebs" and irregular lines observed at this level of the posterior cornea.

Contact Lenses, Hydrophilic↗

PubMed1996

[An adult case of homocystinuria probably due to methylenetetrahydrofolate-reductase deficiency--treatment with folic acid and the course of coagulation-fibrinolysis parameters].

We report a rare male case of homocystinuria probably due to methylenetetrahydrofolate-reductase deficiency. The onset of his disorder was at 19 years of age, and he had no family history. He initially developed gait disturbance, and then generalized seizure in several months, which made him admitted to our hospital. Neurological examinations revealed mental dysfunction, spastic paraplegia, cerebellar ataxia, and sensory disturbance in his feet. MRI showed multiple increased intensities on T2-weighted images in the cerebral white matter. EMG revealed neurogenic changes. These symptoms and signs slowly progressed, and he then developed thrombophlebitis in his lower extremities. Thrombin-antithrombin III complex (TAT) and D-dimer remained high continuously, and plasma homocysteine level was more than ten times higher than the normal range. Plasma cystathionine level was high and methionine level was low. The serum folic acid, vitamin B12, and methylmalonic acid in the urine were normal. Megaloblastic anemia was not seen. Based on these data, he was diagnosed to have homocystinuria probably due to methylenetetrahydrofolate-reductase deficiency. Treatment with high doses of folic acid, pyridoxine and cobalamin normalized plasma cystathionine and methionine levels, and markedly decreased plasma homocysteine, although it remained about three times higher than the normal range. Thereafter, both TAT and D-dimer levels also markedly decreased. The administration of folic acid reduced elevated plasma homocysteine as well as the coagulation--fibrinolysis factors. This implies that they may serve as useful markers for effective treatment of this disease.

Adult↗

PubMed1995

Biased T cell receptor V beta gene usage during specific stages of the development of autoimmune sialadenitis in the MRL/lpr mouse model of Sjögren's syndrome.

OBJECTIVE: To analyze the repertoire of T cell receptor (TCR) V beta gene transcribed and expressed within the autoimmune lesions of the salivary gland in the MRL/lpr mouse model of Sjögren's syndrome. METHODS: Monoclonal antibodies (MAb) were used to determine the prevalence of selected V gene elements on T cell infiltrates from salivary glands of MRL/lpr mice. To analyze TCR V beta gene usage, we used reverse-transcriptase polymerase chain reaction (RT-PCR) and single-strand conformational polymorphism (SSCP) analyses. RESULTS: A predominance of V beta 8+ T cells was detected within the inflammatory lesions during development of autoimmune disease (confirmed by flow cytometry). RT-PCR analysis revealed that in autoimmune sialadenitis, the predominant expression of the V beta 8 gene segment began in the early stages of disease (2-month-old mice) and increased over time. Extensive age-related diversity of TCR V beta gene usage was also observed. SSCP analysis demonstrated a distinct and common binding pattern of the V beta 8 gene PCR product from the cell infiltrates during the course of the disease. CONCLUSION: Our data suggest that in the MRL/lpr mouse model of Sjögren's syndrome, there is restricted usage of TCR V beta elements according to the stage of the disease, and that V beta 8 are probably used preferentially in the recognition of a single unknown self antigen in the salivary gland.

Age Factors↗

PubMed1995

Prevention of adoptive transfer of murine Sjögren's syndrome into severe combined immunodeficient (SCID) mice by antibodies against intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1).

We have analysed the role of ICAM-1 and LFA-1 during development of autoimmune sialadenitis in MRL/lpr mice by direct analysis of RNA obtained from the salivary gland tissues, and the therapeutic effects with antibody administration on adoptive transfer system into SCID mice. The expression of cell adhesion molecules was assessed by using reverse transcriptase polymerase chain reaction (RT-PCR) and Southern blot analysis, and immunohistochemical analysis. Up-regulated expression of ICAM-1 mRNA was observed before the onset of inflammatory lesions in the salivary glands at 1 month and 2 months old, and thereafter LFA-1 mRNA was expressed within the typical inflammatory lesions, resembling human Sjögren's syndrome in MRL/lpr mice. Immunohistochemically, ICAM-1 was localized exclusively in the endothelial cells of varying sized blood vessels before the onset of disease, and LFA-1 expressing inflammatory cells were found within these lesions. When the therapeutic effects in vivo were examined, antibodies to ICAM-1 in combination with anti-LFA-1 prevented adoptive transfer of Sjögren's syndrome in MRL/lpr mice into SCID mice, while no significant effect was found when treated with either antibody. These findings indicate that in Sjögren's syndrome-like autoimmune lesions in MRL/lpr mice the ICAM-1/LFA-1 pathway may play a crucial role in the initiation and subsequent progression of T cell-mediated autoimmunity in the salivary and lacrimal glands of MRL/lpr mice.

Animals↗