[A case of inflammatory granuloma secondary to a foreign body (Cryptomeria) mimicking a bronchial tumor].

This report documents a case of inflammatory granuloma overcoming secondary to a foreign body (Cryptomeria) mimicking a bronchial tumor. A 45-year-old man was referred to the hospital because of hemoptysis and a chronic cough. He had had a chronic cough before visiting the hospital, but had left it untreated for months. A computed tomography (CT) scan showed bronchiectasis in the right lower lobe with evidence of mediastinal lymphadenopathy. Fiberoptic bronchoscopic examinations revealed a tumor with an uneven surface at the orifice of the right B10(b+c), bronchus. The cytological findings of the bronchial tumor showed no malignancy but a predominance of neutrophils. Antibiotics were administered intravenously because of a suspected respiratory infection. After treatment, the abnormal shadows on the chest CT improved. Fiberoptic bronchoscopic examinations showed the bronchial tumor to have disappeared, and a bronchial foreign body was found lodged in the right. B10(b+c) bronchus and it was removed. Pathological examinations and a detailed history revealed that the patient had aspirated a foreign body (Cryptomeria). The tumor was thought to be an inflammatory granuloma secondary to the aspiration of the foreign body. This case highlights the need to search aggressively for foreign bodies in case of clinical symptoms, such as chronic cough, hemoptysis, or findings such as respiratory infection, and bronchial occlusion.

Evidence for shared recognition of a peptide ligand by a diverse panel of non-obese diabetic mice-derived, islet-specific, diabetogenic T cell clones.

MHC class II-restricted autoreactive T cells play a major role in the development of autoimmune diabetes mellitus in both human and mouse. Two of our groups previously established panels of islet-reactive CD4+ T cell clones from prediabetic non-obese diabetic (NOD) mice. These clones express distinct sets of TCR V alpha , V beta , J alpha and J beta , and also differ in the structure of the junctional region of TCR. All of the T cell clones have been shown to cause insulitis and several induce diabetes when transferred to various recipients. The antigen specificities of these T cell clones have not been determined, but they do not react with defined islet cell antigens such as glutamic acid decarboxylase. To identify the peptide ligands recognized by these clones, we examined the reactivity of the T cell clones to peptide mixtures in which anchor residues for H2-A g7 were fixed. Most of the clones showed similar reactivity to the peptide mixtures. To further determine the peptide ligands of the T cell clones, we synthesized several peptides based on the favored amino acid motifs and examined clone reactivity to the synthetic peptides. Some of the peptides, e.g. HLAI-RM and HIPI-RM, could stimulate most of the T cell clones tested, even though the clones expressed different TCR. The results suggest that our islet-reactive T cell clones recognize in islet beta cells a natural ligand that is similar to these peptides.