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Biomedical subjects

L R Hyman

Publications and source records attributed to L R Hyman.

At least 19 recordsLinked to original sources
PubMed1979

Presence of alpha-1-antitrypsin on mitogen-stimulated human lymphocytes.

Human lymphocytes that have undergone concanavalin A-induced blastogenetic transformation demonstrate surface alpha-1-antitrypsin by immunofluorescence when examined after 72 hr of culture, whereas unstimulated cells do not. These results may indicate a role for alpha-1-antitrypsin in lymphocyte blastogenesis.

Concanavalin A↗
PubMed1978

Diphenylhydantoin interstitial nephritis. Roles of cellular and humoral immunologic injury.

A child with diphenylhydantoin hypersensitivity developed an associated interstitial nephritis. Circulating autoantibody of the IgG class which reacted with normal human tubular basement membrane was linearly deposited along host renal TBM. Cell-mediated immunity to the DPH antigen was also present. In addition, deposits of DPH were demonstrated along the renal TBM. It is suggested that initial alteration of host renal TBM by DPH deposition with secondary immune injury directed at the DPH-TBM antigen may have altered the TBM or uncovered new antigenic sites, rendering it susceptible to further injury on an autoimmune basis.

Autoantibodies↗
PubMed1976

Immunopathogenesis of autoimmune tubulointerstitial nephritis. I. Demonstration of differential susceptibility in strain II and strain XIII guinea pigs.

Autoimmune tubulointerstitial nephritis (TN) was induced in strain XIII and Hartley but not strain II guinea pigs after immunization with rabbit tubular basement membranes (TBM) in CFA. Strain XIII guinea pigs developed extensive autoimmune TN associated with high anti-TBM (aTBM) antibody titers and linear deposits of IgG along renal cortical TBM after immunization with 10 mug to 10 mg of TBM. In addition, autoimmune TN was passively transferred to strain XIII animals by the i.p. injection of aTBM sera obtained from actively immunized Hartley guinea pigs. In contrast, strain II guinea pigs did not develop autoimmune TN after active immunization (10 mug to 10 mg) with rabbit TBM in CFA, and only produced high aTBM antibody titers with the highest immunnizing antigen dose. At this dose (10 mg) the strain II animals demonstrated linear deposits of IgG along renal cortical TBM but did not develop autoimmune TN. Further, recipient strain II guines pigs did not develop autoimmune TN after passive transfer of aTBM antisera despite renal cortical tubular deposition of aTBM antibodies. Both inbred guinea pig strains produced antibodies reactive with rabbit and rat renal basement membranes. No evidence for differences in nephritogenic TBM antigens could be demonstrated betweed strain XIII and strain II TBM. These observations indicate that 1) genetic factor(s) influence the production of antibodies reactive to autologous TBM, 2) after the deposition of antibodies on the TBM, additional or related genetic factor(s) determine the full expression of this autoimmune renal disease, and 3) aTBM antibody deposition on renal TBM is not sufficient to elicit autoimmune TN.

Animals↗
PubMed1976

Immunopathogenesis of autoimmune tubulointerstitial nephritis. II. Role of an immune response gene linked to the major histocompatibility complex.

Immunization of strain XIII guinea pigs with rabbit renal tubular basement membranes (TBM) in CFA consistently results in severe autoimmune tubulointerstitial nephritis (TN). Strain II guinea pigs similarly immunized do not develop this disease. F1 guinea pigs were found to be intermediate between inbred strain II and XIII animals with regard to extent of autoimmune TN and anti-TBM antibody production. The F1 X II backcrosses segregated into two groups with regard to antibody production and disease extent. Those backcrosses tissue typed as II+, XIII+ were similar to the F1 guinea pigs. Those backcrosses typed as II+,II+ demonstrated little disease and low anti-TBM titers similar to the inbred strain II animals. F1 X XIII backcrossed guinea pigs segregated into II+,XIII+ or XIII+,XIII+ subgroups on the basis of lymph node typing. The II+, XIII+ backcross animals resembled F1 guinea pigs with respect to anti-TBM response and disease extent; whereas the XIII+, XIII+ backcrosses developed severe disease and high anti-TBM titers as observed in the inbred strain XIII animals. These experiments suggest that susceptibility to autoimmune TN in the guinea pig is linked to the strain XIII major histocompatibility complex and that an immune response gene governing this susceptibility may be inherited as a single dominant or co-dominant trait.

Animals↗
PubMed1975

Alternative C3 pathway activiation in pneumococcal glomerulonephritis.

Glomerulonephritis following pneumococcal infection has been observed, but possible immunopathologic mechanisms have not been adequately explored. Multiple serologic studies as well as light, immunofluorescence and electron microscopic evaluation of kidney biopsy tissue from a 4 year old girl with pneumococcal glomerulonephritis were performed. Clinical studies at the onset of the disease showed normal serum C3 and C4 levels (third and fourth components of complement) with progression to selective C3 hypocomplementemia from days 2 to 58. A serum factor capable of breaking down C3 in normal human serum was present during the period of maximum C3 hypocomplementemia. Renal glomerular histology revealed a mesangial proliferative glomerulonephritis. Glomerular bound C3 and type 14 pneumococcal antigen were associated with similar, but less extensive, deposits of properdin. Minimal immunoglobulin M (IgM) and C4 were seen, but immunoglobulin G (IgG) and fibrinogen were absent. Ultrastructurally, subepithelial "humps" and intramembranous electron dense deposits were noted. It is hypothesized that the pneumococcal polysaccharide can activate the alternate complement pathway and may be responsible for a limited course of glomerulonephritis.

Antigens, Bacterial↗
PubMed1975

Drug-induced tolerance: selective induction with immunosuppressive drugs and their synergistic interaction.

Drug-induced tolerance to polyinosinic-polycytidylic acid was studied in NZB/W mice. A single injection of cyclophosphamide (CY) or methotrexate (MTX) induced tolerance when given 24 h after antigen, whereas azathioprine (AZ) and methylprednisolone (MP) did not. However, MP and MTX each synergized with a nontolerogenic dose of CY. In addition, MP and AZ further reduced the tolerance induced by low but tolerogenic doses of CY. Drug combinations in the induction of tolerance may have wide application in the fields of clinical immunology and transplantation.

Ammonium Sulfate↗