Atopic dermatitis (AD) is a chronic inflammation of the skin characterized by marked infiltration of lymphocytes, suggesting an important role for cellular immune responses in the pathogenesis of AD. It is still unclear, however, whether accumulation of lymphocytes results from antigen-driven mechanisms or by nonspecific inflammatory processes. We applied a novel method of T cell clonotypic analysis, using a combination of reverse transcriptase-PCR with multiple T cell receptor (TCR) primers and subsequent single-strand conformation polymorphism (SSCP). Using this method, we were able to detect oligoclonal accumulation of T cells in inflamed skin areas of patients with AD, but not in normal skin. Identical T cell clones with the same antigen specificities were present in samples obtained from separate skin regions. Our results indicate that antigen(s) that exist in large areas of the skin stimulate and expand a relatively restricted number of antigen-specific T cells, leading to oligoclonal accumulation of T cells. We suggest that a marked antigen-driven infiltration of T cells is present in AD.

Adolescent↗

PubMedDate not supplied

Patient survival and microsatellite instability in gliomas by high-resolution fluorescent analysis.

Deficient repair of nucleotide mismatches in the genome is considered a major factor in tumorigenesis. Such deficiency is evidenced by alterations in dinucleotide repeats of microsatellite sequences, specifically microsatellite instability (MSI) or replication errors. We investigated the frequency of MSI in human gliomas in terms of patient outcome. Frequency of MSI was estimated by examining five loci on chromosomes 2, 5, 10, 11, and 13 in 31 gliomas using high-resolution fluorescent microsatellite analysis. MSI was found at all loci in only 2 malignant gliomas (6.5%). MSI was detected at the D10S197 locus in 3 of 11 glioblastomas (27.2%) and 4 of 8 anaplastic astrocytomas (50%), while no MSI was detected in low-grade gliomas. Among patients with anaplastic astrocytoma, the 4 with MSI at D10S197 died from local recurrence less than 18 months after surgery, while 3 of the patients without MSI survived for more than 20 months. MSI at D10S197 may be a prognostic marker for patients with anaplastic astrocytomas.

Adolescent↗

PubMedDate not supplied

Abnormal cytoarchitecture of cortical dysplasia verified by immunohistochemistry.

Cortical dysplasia is a broad category for an abnormal structure of the cerebrum due to a disorder of the normal developmental process for neocortex. We investigated the cortical dysplastic lesions which were surgically resected from 4 patients with intractable epilepsy. All cases showed a derangement of the cortical laminar structure and dysplastic changes in the neurons. In addition, 3 of them showed large round cells (balloon cells) in the deep cortex and subcortical white matter. Since each lesion showed slightly different features, we further examined the lesions immunohistochemically by using a panel of antibodies against cytoskeletal proteins to recognize and classify the cortical dysplastic lesions. An immunohistochemical study revealed marked abnormalities of the cytoskeletal structures of dysplastic neurons, bizarre glial cells and balloon cells. These cells showed an accumulation of either phosphorylated NF, MAP2 or GFAP in a distinct fashion. Ubiquitin immunoreactivity highlighted the extent of cortical dysplastic lesions. In a young patient, we also found the neuronal cytoplasmic lipofuscin deposition. It is thus considered that these diverse immunohistochemical appearances of cortical dysplasia may thus imply a different pathogenesis and they should therefore be classified based on the extent of histological abnormalities.

Adult↗