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L M Hang

Publications and source records attributed to L M Hang.

14 recordsLinked to original sources
PubMed1997

Current concepts and advances in clinical laboratory testing for autoimmune diseases.

This review discusses the current concepts of immunological tolerance, physiological vs. pathological autoimmunity, autoimmune diseases, and laboratory tests helpful in diagnosis. The autoantibodies in organ-specific autoimmune diseases are directed against antigens of the injured organs, whereas the antinuclear antibodies (ANA) detected in systemic autoimmune diseases are detected against a vast array of nuclear and intracellular antigens and peptides necessary for DNA/RNA synthesis, repair, splicing, and transcription. Knowledge of the mean titer and presence or absence of specific ANA types will help predict the nature of the disease and the response to therapy. Noteworthy features of these "ANA profiles" are (1) patients with systemic lupus erythematosus frequently have multiple types of ANA but anti-dsDNA and anti-SM are diagnostic, (2) patients with drug-induced lupus have ANA restricted to antihistone, (3) patients with mixed connective tissue disease have ANA restricted to anti-RNP, (4) patients with CREST (calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome have ANA restricted to anticentromere, (5) ANA with anti-SS-A/Ro specificity is associated with vasculitis and nephritis, (6) ANA with anti-SS-B/La and anti-nRNP specificities is associated with milder clinical disease, (7) ANAs with anti-Jo-1 and PM-Scl specificities are associated with pulmonary fibrosis and poor prognosis. Technological advances in the fields of molecular immunogenetics are guiding the studies of autoimmune diseases from serological and histopathological evaluations toward search for subcellular risk factors such as chemical and biological agents and susceptibility genes. Knowledge of these factors will help (1) to identify disease susceptibility genes prior to clinical onset and irreversible tissue damage, (2) to avoid environmental risk factors, and (3) to devise specific immunosuppressive strategies.

Autoimmune Diseases↗
PubMed1986

Immunodeficiency associated with motor neuron disease treated with intravenous immunoglobulin.

A man with symptoms of amyotrophic lateral sclerosis and immunodeficiency was treated with intravenous immunoglobulin. After four weekly intravenous injections of 2.5 gm of immunoglobulin, his condition showed progressive improvement when measured by clinical, neurological, and physiological parameters. There was a noticeable increase in general physical well-being, an 80% reduction in fasciculations, and the normalization of sensory and motor nerve conduction velocities.

Humans↗
PubMed1986

Human leukocyte interferon in the treatment of rheumatoid arthritis.

Forty patients with symptoms of rheumatoid arthritis were treated with daily injections of 100 micrograms of human leukocyte interferon or saline placebo. Twenty patients received the interferon for nine weeks and were then switched to placebo for nine weeks, and 20 patients were started on placebo and were then switched to interferon. Treatment effectiveness was assessed on measures of symptom severity and activity impairment. On both measures the patients showed a rapid and constant improvement while being treated with interferon.

Activities of Daily Living↗
PubMed1985

Association of lpr gene with graft-vs.-host disease-like syndrome.

Hemopoietic cells have been reciprocally transferred between two lines of mice (MRL lpr/lpr and MRL +/+) that are congenic, differing only at the lpr (lymphoproliferation) and possibly closely linked genes. The lpr strain develops a significantly more severe and fast-paced lupus-like syndrome than +/+ strain, along with a substantially larger lymphoid mass. The results showed that: (a) hemopoietic cells of such mice were sufficient to induce the respective disease phenotypes in lethally irradiated syngeneic recipients; (b) cells of MRL +/+ mice maturing in an MRL lpr/lpr environment essentially retained the disease-producing characteristics of the donor, i.e., they induced late-life lupus without lymphadenopathy; but (c) MRL lpr/lpr cells transferred into irradiated MRL +/+ recipients unexpectedly failed to induce the early-life severe lupus and lymphoid hyperplasia of the donor, instead they caused a severe wasting syndrome resembling, in many respects, graft-vs.-host disease (GVHD). This GVHD-like syndrome developed after transfer of MRL lpr/lpr fetal liver, bone marrow, or spleen cells, and was not abrogated by elimination of T cells from the inocula. Thymectomy of the MRL +/+ recipients retarded, but did not prevent, the wasting disease. The unidirectional nature of this disease suggests that the lpr mutation conferred either a structural or regulatory defect that interfered, blocked, or altered the expression or structure of certain lymphocyte antigen(s). As a result, the MRL +/+ cells that did express this antigen(s) were recognized as foreign, and stimulated a graft-vs.-host reaction. These findings may allow definition of a new kind of rejection phenomenon caused by non-H-2 products, and may extend our understanding of the means by which the lpr gene adversely affects lymphocyte regulation and homeostasis.

Animals↗
PubMed1985

Induction of severe autoimmune disease in normal mice by simultaneous action of multiple immunostimulators.

Either of two immunostimulating factors (lpr, lipopolysaccharide) enhanced the pathogenic autoimmune responses of MRL/n mice, but the serologic and immunopathologic characteristics differed. In contrast, either factor acting alone, caused minimal immunopathology in normal mice, despite autoantibody induction. Combined immunostimulation, however, caused fatal glomerulonephritis in normal-background C57BL/6 mice. These results show the profound influence of the background genome on the effects of immunostimulating agents, and show that resistance to autoimmune disease in immunologically normal mice is not absolute.

Adjuvants, Immunologic↗
PubMed1984

Association of elevated serum glycoprotein gp70 with increased gp70 immune complex formation and accelerated lupus nephritis in autoimmune male BXSB mice.

BXSB male mice, which spontaneously develop a systemic lupus erythematosus (SLE) like disease, were the only strain to have a significant incidence of abnormally elevated levels of gp70 in sera. Concentrations of gp70 in some mice were more than 10 times (greater than 500 micrograms/ml) those of young BXSB and any other murine strain. The presence of high serum levels of gp70 was significantly associated with hepatic sinusoidal lymphocytosis, a high incidence of which was only observed in male BXSB mice. Serum levels of gp70-anti-gp70 immune complexes were greatly increased in mice with high levels of gp70, presumably associated with increased anti-gp70 antibody production. Such mice developed fatal glomerulonephritis significantly earlier than those with lower levels of gp70. These results suggest that (1) hepatic inflammation of unknown aetiology occurring uniquely in male BXSB mice during the course of their SLE may be responsible for the enhanced expression of serum gp70 antigen, because of its nature as an acute phase reactant and (2) enhanced expression of gp70 antigen is associated with increased formation of anti-gp70 antibodies and exacerbation of lupus nephritis in male BXSB mice.

Animals↗
PubMed1981

Retroviral gp70 immune complexes in NZB x NZW F2 mice with murine lupus nephritis.

NZB x NZW (NZB x W) F1 hybrid mice spontaneously develop a disease most prominently characterized by immune complex glomerulonephritis (GN), which seems to be associated with both antibodies to DNA and to the serum retroviral envelope glycoprotein, gp70. To evaluate the contribution of each of these autoimmune responses to the pathogenesis of the GN, we studied NZB x W F2 mice in which the two responses appeared to segregate relatively independently. Use of this model permitted analysis of possible correlations between each response and the G.N. The presence of circulating anti-gp 70-complexed gp70 correlated significantly with the development of fatal GN and one could predict the course of renal disease by computing the rising serum levels of gp70 complexed with antibodies. In contrast, the presence of free antibodies to either double-stranded or single-stranded DNA was not significantly associated with the development of fatal GN. This association of anti-gp70 antibody production with these animals' early death from GN strongly suggests that the gene(s) governing production of antibodies to serum retroviral gp70 may be one of the major genes responsible for spontaneous renal disease segregated in NZB x W F2 generations.

Animals↗
PubMed1981

(NZW x BXSB)F1 hybrid. A model of acute lupus and coronary vascular disease with myocardial infarction.

Both sexes of the (NZW x BXSB)F1 mice developed an early systemic lupus erythematosus-like disease. In males, the disease resembled that in the BXSB male parent and was not affected by sex hormonal manipulation. In females, the disease duplicated that of (NZB x NZW)F1 females by virtue of a delayed onset and estrogen dependence. Autoantibody production, circulating Ig-bound gp 70 immune complexes, and deposition of Ig and gp 70 in the affected glomeruli were demonstrated in both males and females. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction, particularly in these F1 males, provides a useful model for the investigation of a possible immunologic component in coronary vascular disease.

Acute Disease↗
PubMed1975

The Schistosoma japonicum egg granuloma.

Although Schistosoma japonicum egg granulomas are generally considered to be similar to those of S. mansoni (which are largely immunologic reactions of the delayed hypersensitivity type) there are suggestions that the histopathology and perhaps the etiology of the lesions are different. In mice with light S. japonicum infections, at 5 weeks after infection (2 weeks after egg production began), the livers contained 36,000 eggs each, but there was no reaction to the eggs, nor any evidence of hepatosplenic disease. By 6 weeks, large abscesses replete with cosinophils occurred around some of the eggs, and there was periportal inflammation consisting predominantly of plasma cells. From this time on, major lesions occurred mainly around large aggregates of eggs, and there was hepatosplenomegaly and portal hypertension. Living S. japonicum eggs injected into the pulmonary microvasculature of mice did not evoke significant granulomatous reactions on either primary or secondary exposure. Even when the eggs were injected into the lungs of infected animals, which had large granulomas around egg aggregates in the liver, little or no inflammatory reaction was seen around the eggs distributed singly throughout the pulmonary vessels. When the priming dose of eggs or soluble egg antigens was injected subcutaneously with or without complete Freund's adjuvant, significant granuloma formation occurred around eggs subsequently injected into the lungs. On the basis, therefore, of differences in the parasite factor (eggs) and host factors (histopathology and responses to routes of injection) it is suggested that the immunologic factors responsible for granuloma formation around S. mansoni and S. japonicum eggs may differ significantly.

Animals↗
PubMed1974

Systemic cellular hypersensitivity induced by an intestinally absorbed antigen.

Neonatal mice given intact living Schistosoma mansoni eggs or soluble schistosome egg antigens intragastrically developed systemic cellular hypersensitivity as shown by markedly accelerated, augmented granulomatous inflammation around S. mansoni eggs subsequently injected intravenously into the pulmonary microvasculature. To achieve partial sensitization in adult mice schistosome eggs had to be administered intragastrically with bicarbonate; full sensitization occurred when the eggs were injected intraduodenally. These data indicate that under appropriate conditions intestinal administration of antigen can result in systemic cellular immune sensitization.

Animals↗