Cytochrome P450 1A2 is a hepatic autoantigen in autoimmune polyglandular syndrome type 1.

Autoantibodies directed against proteins of the adrenal cortex and the liver were studied in 88 subjects of Sardinian descent, namely six patients with autoimmune polyendocrine syndrome type 1 (APS1), 22 relatives of APS1 patients, 40 controls with other autoimmune diseases, and 20 healthy controls. Indirect immunofluorescence, using tissue sections of the adrenal cortex, revealed a cytoplasmatic staining pattern in 4 of 6 patients with APS1. Western blotting with adrenal mitochondria identified autoantigens of 54 kDa and 57 kDa, Western blotting with placental mitochondria revealed a 54-kDa autoantigen.

Membrane-bound and soluble IL-2 receptors (p55 and p75 chains) on peripheral blood mononuclear cells from patients with solid malignancies.

The aim of the investigation was to study directly the IL-2 receptor (IL-2R) and its subunits, p55 and p75 chains, either membrane-bound or soluble, on PBMC of patients with solid malignancies and, indirectly, the same patients' PBMC ability to produce IL-2. Fifty-eight cancer patients, 29 men and 29 women, were studied: their mean age was 57.3 yr, range 35-79.

Immunologic assessment determined by response to IL-2 and immunophenotyping of tumor-infiltrating lymphocytes, of invaded and non invaded lymph nodes and of peripheral blood lymphocytes from twenty-one patients with primary laryngeal cancer.

The aim of the study was to identify the lymphocyte sets and/or subsets possibly involved in the response to malignant cells. For this purpose we have investigated both the cells at the tumor site, i.e.

Hodgkin's disease presenting in 1 of 4 siblings affected by hereditary spinocerebellar ataxia: clinical, immunological and genetic study.

One of 4 siblings affected by hereditary spinocerebellar ataxia (HSCA) of Marie's type developed Hodgkin's disease (HD): the stage was IV B, the patient was submitted to conventional chemo- and radiotherapy and achieved complete remission. An accurate clinical, genetic and immunological study was carried out on all his family, including a complete HLA typing, a chromosome study, the immunophenotyping of peripheral blood mononuclear cells (PBMC), the PBMC response to polyclonal mitogens, to interleukin 2 (IL-2), to the association of PHA + IL-2 and the evaluation of the IL-2 receptor expression. No association was clearly demonstrable between an HLA haplotype and HSCA, while the patient with HSCA and HD was HLA-B18- and DQw3-positive (the last at homozygous level), two antigens known to be strongly associated with HD, mainly among the Sardinian ethnic group.

Familial chronic B-cell malignancy. Hairy cell leukaemia in mother and daughter.

Two familial cases of hairy cell leukaemia are reported: a daughter, 44-years-old, with a very unusual ultrastructural pattern found in hairy cells, the "tubuloreticular inclusions", and her mother, 71-years-old, who was affected six years later. Routine laboratory investigations, cytochemical and cytogenetic studies including HLA typing, as well as in vitro proliferative response of peripheral blood mononuclear cells (PBMC) to polyclonal mitogens and to exogenous interleukin 2, were performed. The immunological characterization by assessing the cell surface phenotypic markers with monoclonal antibodies and transmission electron microscopy (TEM) investigations were also carried out.

Hairy cell leukemia with ultrastructural finding of 'tubuloreticular inclusions' in hairy cells: a possible marker of a virus-induced disease?

This report describes a case of hairy cell leukemia (HCL) with typical hematological and clinical findings. The most striking feature is the electron microscopic pattern of intracytoplasmic inclusions within hairy cells (HCs), which can be identified with the 'tubuloreticular inclusions', very unusual and not yet reported in HCL. The same structures were frequently detected in peripheral mononuclear cells from patients with acquired immune deficiency syndrome (AIDS) and with chronic lymphadenopathy syndrome (LAS), that are caused by the HTLV-III retrovirus.