HLA-DR alleles in patients with Sjögren's syndrome over-representing V beta 2 and V beta 13 genes in the labial salivary glands.

To identify genetic factors that play a role in the pathogenesis of patients with SS over-representing V beta 2 and V beta 13 genes in the lips, HLA-DR and -DQ alleles of 10 primary SS patients with predominant expression of V beta 2 and V beta 13 genes in the lips were analysed, using the polymerase chain reaction (PCR) and sequence specific oligonucleotide probes. The CDR3 amino acid sequences of cDNA clones encoding V beta 2 and V beta 13 genes were also determined by PCR. The results showed that the DRB4*0101 allele was significantly increased (80%) and that the frequency of DRB3 allele was decreased (0%) when compared to findings in healthy subjects (35.

Expression of sequences homologous to HTLV-I tax gene in the labial salivary glands of Japanese patients with Sjögren's syndrome.

Objective: To address the question of whether the human T cell leukemia virus type I (HTLV-I) gene is associated with the etiology of Sjögren's syndrome (SS).

Methods: RNA expression of HTLV-I gag, pol, env, and tax genes in labial salivary glands (LSGs) from SS patients who were seronegative for antibodies to HTLV-I was examined using reverse transcription and polymerase chain reaction techniques.

Results: The HTLV-I tax gene, but not the HTLV-I gag, pol, or env genes, was detected in LSG samples from 4 of 14 patients (29%).

Role of vascular cell adhesion molecule 1/very late activation antigen 4 and intercellular adhesion molecule 1/lymphocyte function-associated antigen 1 interactions in antigen-induced eosinophil and T cell recruitment into the tissue.

To determine the role of vascular cell adhesion molecule 1 (VCAM-1)/very late activation antigen 4 (VLA-4) and intercellular adhesion molecule 1 (ICAM-1)/lymphocyte function-associated antigen 1 (LFA-1) interactions in causing antigen-induced eosinophil and T cell recruitment into the tissue, we studied the effect of the in vivo blocking of VCAM-1, ICAM-1, VLA-4, and LFA-1 by pretreatment with monoclonal antibodies (mAb) to these four adhesion molecules on the eosinophil and T cell infiltration of the trachea induced by antigen inhalation in mice. The in vivo blocking of VCAM-1 and VLA-4, but not of ICAM-1 and LFA-1, prevented antigen-induced eosinophil infiltration into the mouse trachea. On the contrary, the in vivo blocking of VCAM-1 and VLA-4, but not of ICAM-1 and LFA-1, increased blood eosinophil counts after antigen challenge, but did not affect blood eosinophil counts without antigen challenge in sensitized mice.

Chronic salicylate intoxication and rhabdomyolysis in a patient with scleroderma and Sjögren's syndrome.

A 44-year-old woman with scleroderma and Sjögren's syndrome developed altered consciousness, acute renal failure, and rhabdomyolysis. She had no history of trauma, seizures, alcohol abuse, hyperthermia, or other possible causative factors for rhabdomyolysis. A high serum salicylate level indicated a diagnosis of salicylate intoxication.

Inhibitory effect of pemirolast, a novel antiallergic drug, on leukotriene C4 and granule protein release from human eosinophils.

To determine whether pemirolast, a new antiallergic drug, inhibits the activation of eosinophils, we investigated the effect of pemirolast on the release of leukotriene C4 (LTC4) and eosinophil cationic protein (ECP) from human eosinophils. Calcium ionophore A23187 caused both LTC4 and ECP release from human eosinophils, whereas PAF and FMLP induced only ECP release from the eosinophils. Pemirolast (10(-6) to 10(-3) M) inhibited A23187-induced LTC4 release from the eosinophils in a dose-dependent fashion with 77% inhibition at 10(-3) M.

Experimental toxoplasmosis in pregnant cats.

Cysts of the K strain of Toxoplasma gondii were administered orally to nine pregnant cats having no antibody to the organism at each of the three stages of gestation, namely early (14 days), middle (30 days), and late (40 and 51 days). Premature and weak or deformed fetuses were observed in the offsprings delivered by mother cats infected with Toxoplasma in the early or middle stage of gestation, while the cats infected at the late stage were delivered of apparently healthy fetuses. Mother cats developed parasitemia excreting Toxoplasma oocysts in their feces and formed the antibody to the organism after the oral administration.

Aerosolized recombinant interferon-gamma prevents antigen-induced eosinophil recruitment in mouse trachea.

In a murine model of airway late-phase reaction we have previously shown that antigen-induced eosinophil recruitment into the airways of sensitized mice is mediated by CD4+ T cells and interleukin-5. To determine whether interferon-gamma (IFN-gamma) regulates antigen-induced eosinophil recruitment into the airways, we studied the effect of aerosolized recombinant murine IFN-gamma on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. The administration of aerosolized rIFN-gamma prevented antigen-induced eosinophil infiltration in the trachea of sensitized mice.

Leukotriene B4 mediates substance P-induced granulocyte infiltration into mouse skin. Comparison with antigen-induced granulocyte infiltration.

Substance P, a potent proinflammatory peptide present in sensory neurons, causes granulocyte (neutrophil and eosinophil) infiltration into mouse skin by inducing mast cell degranulation. However, the mediator responsible for this granulocyte infiltration has not been determined. In this study, we determined which mediator from cutaneous mast cells mediates substance P-induced granulocyte infiltration in the skin by the use of two mediator antagonists; one for platelet activating factor (PAF) CV-6209 and the other for leukotriene B4 (LTB4) ONO-4057.

V gene analysis of anticardiolipin antibodies from MRL-lpr/lpr mice.

We analyzed the VH and V kappa genes of 14 hybridomas producing anticardiolipin antibodies (aCL) from MRL-lpr/lpr mice, in an attempt to address the question of whether aCL are generated by Ag-driven stimulation or by polyclonal B cell activation. Five of six aCL from one mouse and both aCL from the other mouse carried 98 to 100% homologous VH and V kappa genes, respectively, thereby indicating that aCL were derived from the oligoclonal B cell precursor in that individual mouse. Of nine clones, six (67%) used the VH gene of the J558 family, and three (43%) of seven clones used the V kappa gene of the V kappa 23 group.

[Episodic angioedema with eosinophilia].

In 1984, Gleich et al. originally reported a novel syndrome of episodic angioedema with eosinophilia. The syndrome is characterized by recurrent angioedema, urticaria, weight gain, elevated IgM levels, marked blood eosinophilia, and eosinophil infiltrates in the dermis.

[Effect of cytokines on eosinophil differentiation and proliferation].

IL-3, IL-5, and GM-CSF are eosinopoietic cytokines that induce the proliferation and differentiation of eosinophils. However, the regulatory mechanism of eosinopoiesis is largely unknown. A combination of IL-3 and IL-5 induces selective proliferation and differentiation of eosinophils from mononuclear cell fractions of human cord blood.

Interferon gamma regulates antigen-induced eosinophil recruitment into the mouse airways by inhibiting the infiltration of CD4+ T cells.

We have previously shown that antigen-induced eosinophil recruitment into the tissue of sensitized mice is mediated by CD4+ T cells and interleukin 5. To determine whether interferon gamma (IFN-gamma) regulates antigen-induced eosinophil recruitment into the tissue, we studied the effect of recombinant (r) murine IFN-gamma and of anti-IFN-gamma monoclonal antibody (mAb) on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. The intraperitoneal administration of rIFN-gamma prevented antigen-induced eosinophil infiltration in the trachea of sensitized mice.

Right common iliac arterio-intestinal fistula caused by tubercular peritonitis: report of a case.

A 59-year-old female was admitted with massive hematemesis and melena. A hematological examination revealed that the red blood cell count was 1.31 x 10(6)/mm3, Hb 3.

In vitro interleukin-5 production of peripheral blood mononuclear cells is increased in patients with asthma.

To determine whether the capacity of interleukin-5 (IL-5) production is increased in patients with asthma, we studied in vitro IL-5 production from peripheral blood mononuclear cells (PBMC) in 27 asthmatics (16 allergic asthmatics and 11 nonallergic asthmatics) and 10 normal subjects. IL-5 production of phytohemagglutinin (PHA)-stimulated PBMC was significantly greater in asthmatics than in normal subjects (p < 0.02).

The development of hypercalcemia in a patient with an ovarian tumor producing parathyroid hormone-related protein.

Hypercalcemia developed in a 34-year-old woman with a clear cell carcinoma of the ovary. Osseous involvement with the tumor cells was not present. Primary hyperparathyroidism was absent.

Role of CD4+ T lymphocytes and interleukin-5 in antigen-induced eosinophil recruitment into the site of cutaneous late-phase reaction in mice.

Previous studies suggested that the eosinophil recruitment into the site of cutaneous late-phase reaction (LPR) was dependent on IgE antibody and mast cells. In this study, we determined the role of CD4+ T cells and CD8+ T cells in causing antigen-induced eosinophil recruitment of LPR in mouse skin. Eosinophil infiltration into the subcutaneous tissue of ovalbumin (OVA)-sensitized BALB/c mice was biphasic, reaching the first peak at 6 h after the subcutaneous challenge with OVA and the second peak at 24 to 48 h.

[Effects of growth factors on proliferation of cultured human peritoneal mesothelial cells].

Loss of ultrafiltration during continuous ambulatory peritoneal dialysis (CAPD) is often caused by the structural peritoneal membrane alteration, namely the disappearance of mesothelial cells and the proliferation of peritoneal collagen fibers. The interleukin hypothesis has been proposed to explain the etiology of peritoneal fibrosis. The CAPD procedure has been shown to induce macrophages and lymphocytes in the peritoneum, resulting in the production of interleukin-1 (IL-1) and interferon-gamma (IFN-gamma), which may be promote to the development of peritoneal fibrosis.

[Studies on pseudo-Chediak-Higashi granules formation in acute promyelocytic leukemia].

Leukemic cells from acute promyelocytic leukemia containing pseudo-Chediak-Higashi (P-CH) granules in a 38-year-woman were studied with ultrastructural and cytochemical techniques to evaluate the origin and nature of the granules. Wright-Giemsa stain revealed giant granules to be azurophilic. Cytochemical stain revealed p-CH granules ot the basic of their peroxidase and glycoprotein content.

CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea.

In order to determine the role of CD4+ and CD8+ T-cells and of interleukin-5 (IL-5) in causing antigen-induced eosinophil infiltration into the site of airway late-phase reaction, we examined the effect of the in vivo depletion of CD4+ and CD8+ T-cells on the eosinophil infiltration of the trachea induced by antigen inhalation in mice. We also studied the effect of anti-murine IL-5 monoclonal antibody (mAb) on the antigen-induced eosinophil infiltration in the trachea. The eosinophil infiltration into the trachea of ovalbumin (OVA)-sensitized BALB/c mice began to increase 9 h after OVA inhalation and persisted for more than 48 h.

[Effect of a leukotriene B4 antagonist on substance P-induced granulocyte infiltration in mouse skin].

Substance P causes granulocyte (neutrophil and eosinophil) infiltration in mouse skin by inducing mast cell degranulation. However, the mediator responsible for this granulocyte infiltration has not been determined. In this study, we examined the effect of a leukotriene B4 (LTB4) antagonist ONO-4057 on substance P-induced granulocyte infiltration in the skin of BALB/c mice.