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B T Shannon

Publications and source records attributed to B T Shannon.

32 records · Page 2Linked to original sources
PubMed1986

Progressive change in lymphocyte distribution and degree of hypergammaglobulinemia with age in children with hemophilia.

Fifty asymptomatic, pediatric hemophiliacs were examined for distribution of T-cell subsets, responsiveness to mitogen stimulation, interleukin-2 production, hypergammaglobulinemia, and the presence of antibody to virus including the human T-lymphotrophic virus type III (HTLV-III). Hemophilia A patients receiving factor VIII concentrate as replacement therapy had the most pronounced changes including decreased T4/T8 ratios and lower in vitro responsiveness to both phytohemagglutinin and pokeweed mitogen. Hemophilia A patients treated with cryoprecipitate and hemophilia B patients did not demonstrate these changes. Regardless of replacement therapy, hemophiliacs demonstrated a progressive decrease in the T4/T8 ratio and a progressive increase in the degree of IgG hypergammaglobulinemia as they aged. The amount of factor or cryoprecipitate or exposure to virus did not influence the T4/T8 ratio. These changes appear to be a result of chronic product exposure, which becomes more pronounced with increasing age.

Acquired Immunodeficiency Syndrome↗
PubMed1986

HTLV-III status and abnormalities in T lymphocyte distribution in children with hemophilia A.

Children with hemophilia A are at risk for the acquired immunodeficiency syndrome (AIDS). Clinically asymptomatic hemophiliacs demonstrate many immune abnormalities that might represent exposure to the AIDS agent through blood products or be a natural reaction to their therapy. In this study, we examined lymphocyte subset distribution in children with hemophilia A who had been exposed to HTLV-III as determined by antibody seroconversion. Seroconversion to HTLV-III was confirmed using Western blot analysis. The lymphocyte subsets studied included T4+ and T8+ cells. The distribution of lymphocyte subsets in children with hemophilia A was independent of seroconversion to HTLV-III. Children with hemophilia A treated with commercial factor VIII concentrate had normal numbers of circulating T4+ lymphocytes and significantly increased numbers of circulating T8+ lymphocytes compared with their nontransfused age-matched counterparts. An increased number of T8+ lymphocytes was not observed, however, in children treated exclusively with cryoprecipitate. These results suggest that HTLV-III alone cannot account for changes in lymphocyte subsets in hemophiliacs. Higher antigenic protein loads in factor VIII concentrate or additional factors might account for the increased absolute numbers of T8+ lymphocytes and represent a natural response to therapy.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Acquired spontaneous cytotoxicity of K562 in a subpopulation of monocytes.

Human peripheral blood monocytes were placed on a discontinuous density gradient of bovine serum albumin and fractionated into five subpopulations. Cells from each subpopulation were assayed for spontaneous cytotoxic activity against K562 tumor cells. Immediately following fractionation, monocytes were not cytotoxic. Following incubation for at least 48 hr, monocytes from two layers of the gradients clearly exhibited greater spontaneous cytotoxic activity than all others. The degree of cytotoxicity expressed by cells of these layers was enhanced by the addition of indomethacin and inhibited by prostaglandin E2 (PGE2). Monocytes acquiring spontaneous cytotoxicity did not secrete measurable levels of PGE2 and had increased levels of purine nucleoside phosphorylase after 72 hs of culture in vitro. Surface markers HNK-1 and Mac-1 normally associated with cytotoxic function, were detected on these cells by indirect immunofluorescence at isolation and after culture. The fraction with the greatest cytotoxic activity showed an increase in the proportion of cells displaying reactivity to HNK-1 after culture compared to initial isolation.

Antigens, Surface↗
PubMed1985

Gm and Km allotypes in Charcot-Marie-Tooth disease.

Gm and Km immunoglobulin allotypes were studied in 46 Caucasian patients with Charcot-Marie-Tooth disease (CMT). No significant association of Gm and Km phenotypes with CMT was found. Family studies revealed that Gm haplotypes and CMT were not inherited together, thus arguing against the involvement of immunoglobulin allotypes in CMT.

Charcot-Marie-Tooth Disease↗
PubMed1985

Effect of neonatal cerebrospinal fluid on monocyte chemotaxis.

We have reported in our previous study that macrophages constitute 58% of the total number of white cells in noninfected neonatal cerebrospinal fluid (CSF). CSF macrophages are probably derived from blood monocytes. To explain their predominance, we compared the chemotactic response of monocytes from cord and adult blood to neonatal (NCSF) and non-neonatal spinal fluids (NNCSF). Zymosan-activated serum (ZAS) was used as a positive control. Significance was accepted as p less than or equal to 0.05. We observed that both random migratory (RM) activity and chemotactic responses (CM) of cord monocytes to neonatal CSF and ZAS were greater than those of monocytes obtained from adult blood, resulting in a significant increase in the chemotactic differential (CD). Chemotactic responses of neonatal monocytes were significantly greater in the presence of neonatal CSF as compared to CSF from older children as indicated by CD. The CD of neonatal monocytes to neonatal CSF was greater than that of neonatal neutrophils. These findings are consistent with the presence of specific monocyte chemotaxins in noninfected neonatal CSF.

Adolescent↗
PubMed1983

Altered heterogeneity of monocytes in acute myelomonocytic leukemia.

Human peripheral blood monocytes isolated from normal donors and patients with acute myelomonocytic leukemia (AMML) were separated on a discontinuous density gradient of bovine serum albumin (BSA) into five fractions. Cells from each fraction were assayed for cell surface markers, prostaglandin E2 (PGE2) production, ability to affect proliferation in response to antigen by autologous peripheral blood lymphocytes previously depleted of monocytes, and ability to regulate immunoglobulin (Ig) synthesis by allogeneic B-lymphocytes. Fractions 1-5 from normal donors contained 11, 10, 23, 34, and 22%, respectively, of the total number of monocytes. In contrast, in 6 patients with AMML fraction 3 was considerably larger (52%) than any other fraction, in 1 patient comprising 87% of her monocytes. Cells from each fraction differed markedly in accessory function. In general, cells from fraction 3 were poorer as helper cells than cells from other fractions. They also produced after stimulation larger amounts of PGE2 than did cells from other fractions of the gradient. These data show that PBL contain a subpopulation of monocytes, which either helps poorly or suppresses in vitro immunologic function of T-cells (proliferation) and B-cells (lg synthesis), and that this subpopulation is increased in the blood of patients with AMML.

B-Lymphocytes↗
PubMed1982

Heterozygosity at Gm loci associated with humoral immunity to osteosarcoma.

Serum samples from 50 Caucasian patients with osteosarcoma were tested for the presence of antibodies to osteosarcoma-associated antigens (OSAA) and typed for nine Gm markers. A highly significant association was found between Gm 3;5,13,14 and unresponsiveness to OSAA, and between 1,3,17;5,13,14,21 and responsiveness to OSAA. These results suggest the existence of complementary immune response genes which in the heterozygous condition permit a response to OSAA.

Antibody Formation↗
PubMed1981

Quantitation of glycosaminoglycans of rabbit lung during delayed-type hypersensitivity reactions and granuloma formation.

The specificity and kinetics of hyaluronic acid (HA) accumulation in relation to other glycosaminoglycans (GASs) were determined in rabbit lungs during an allergic granulomatous response to BCG, an allergic nongranulomatous response to tuberculoprotein, and during a foreign-body granulomatous response to carrageenan. Hyaluronic acid was the only GAG detected in the lung lavage fluids. Hyaluronic acid occurred in the airways on day two of the allergic granulomatous response, but its presence in the airway did not correlate with ensuing granuloma formation in the parenchyma. Generalized increases in GAG of the parenchyma also peaked on day two of the DTH responses. Generalized increases in GAG peaked on day five during the foreign-body granulomatous response to carrageenan. A persistently elevated level of HA in the lung tissue correlated with granuloma formation but not with the intensity of the response.

Animals↗
PubMed1980

Selective suppression of granuloma formation and delayed hypersensitivity in rabbits.

The relationship between dermal delayed hypersensitivity (DH) and granulomatous hypersensitivity was studied in rabbits sensitized with killed mycobacteria. Specific antigen challenge of sensitized animals resulted in extensive pulmonary granulomatous inflammation and induced suppression of both dermal DH and dermal granuloma formation. Whereas suppression of DH was concomitant with pulmonary granuloma formation, as is the case in a number of granulomatous diseases, a causal relationship between the two did not exist. Both DH and dermal granulomatous hypersensitivity were significantly suppressed whether or not the antigen challenge was of a granulomagenic (particulate) or nongranulomagenic (soluble) form. The data presented indicate that granulomatous hypersensitivity and DH are selectively suppressed with regard to different anatomical sites.

Animals↗
PubMed1980

Participation of hyaluronic acid in the macrophage disappearance reaction.

Hyaluronic acid accumulates in the peritoneal cavity of mice during the macrophage disapperance reaction. Macrophages reappear in the exudates during the depletion of hyaluronate. The disappearance reaction is simulated by the intraperitional (i.p.) injection of hyaluronic acid into normal mice. The disapperance reaction largely is inhibited by the simultaneous injection (i.p.) of specific hyaluronidase with the challenge dose of BCG. We propose that hyaluronic acid makes a major contribution to the macrophage disappearance reaction.

Animals↗
PubMed1980

Additional evidence for the role of hyaluronic acid in the macrophage disappearance reaction.

A slight macrophage disappearance reaction was elicited in C3H/Hej mice, a low responder strain. Low levels of hyaluronic acid accumulated in the peritoneal fluid during the disappearance reaction, in keeping with the low response. The macrophage disappearance reaction was not simulated by the intraperitoneal injection of large amounts of hyaluronate into nonsensitized C3H/Hej mice. This suggested that these macrophages were refractory to hyaluronic acid. Subsequent experiments demonstrated that low concentrations of hyaluronic acid did not agglutinate these cells, in vitro, nor inhibit their migration to the extent obtained with macrophages from the responder mice (C57BL/6 strain), thus providing evidence that the low responder mice had at least two defects with respect to the disappearance reaction: 1) they accumulated less hyaluronic acid in their peritoneal fluid, and 2) their macrophages were refractory towards hyaluronic acid. Generalized defects in membranes of various cell types of C3H/Hej mice, involving receptors for lymphokines in the case of mesothelial cells, or hyaluronic acid receptors on macrophages may serve as the central defect and explain the above observations.

Agglutination↗