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Biomedical subjects

R I Carr

Publications and source records attributed to R I Carr.

At least 37 records · Page 2Linked to original sources
PubMed1984

Dietary protein antigenemia in humoral immunodeficiency. Correlation with splenomegaly.

Enhanced gastrointestinal absorption of dietary substances is an important feature of normal neonatal life that also exists in particular disease states such as selective IgA deficiency and atopic allergy. In these studies, it is shown that patients with hypogammaglobulinemia have increased absorption of dietary bovine antigens and that most patients have large amounts of these proteins present in the serum even after an overnight fast. The amounts of such proteins were found to be correlated with spleen size and/or peripheral lymphoid hypertrophy. Interestingly, three patients with X-linked agammaglobulinemia did not have detectable amounts of these proteins in the serum nor did they have splenomegaly or lymphadenopathy. It is speculated that hypogammaglobulinemic patients have a specific gastrointestinal mucosal lesion that permits the chronic excessive absorption of dietary antigens and may result in lymphoid hypertrophy.

Adult↗
PubMed1982

Humoral immunity in stage I mycosis fungoides: an increased incidence of lymphocytotoxic antibodies.

Thirteen patients with stage I mycosis fungoides (MF) were studied for the presence of circulating autoantibodies including cold-reactive lymphocytotoxic antibodies (LCA), antinuclear antibodies and rheumatoid factor antibodies to common food antigens, bovine gamma globulin and casein; and immune complexes as measured by cryoglobulins and I125 Clq binding. A significantly increased incidence (11/13) of LCA was found in the MF patients, and this may be related to the alterations in subpopulations of T cells seen in these patients. No significant increase in any other test was noted. there was no evidence of a diffuse hyperactivity of the humoral immune system as seen in systemic lupus erythematosus, which has a similar imbalance of T cell subpopulations.

Adult↗
PubMed1982

Interstitial and hemorrhagic pneumonitis induced by mycobacterial trehalose dimycolate.

Intraperitoneal injections of cord factor (trehalose dimycolate, TDM) provides a model for interstitial and hemorrhagic lung disease that is produced by a chemically defined substance. A single injection of 10 micrograms of TDM, in light mineral oil or hexadecane, into C57BL/6 mice produces interstitial and hemorrhagic pneumonitis. Following injection of TDM the pulmonary lesions increase gradually and become maximal by the seventh to ninth day, at which time 70% of the mice show both gross hemorrhages and dense mononuclear infiltrates; an additional 20% of the mice show only microscopic lesions. From day 14 onward the incidence and severity of the lesions decrease, and by day 28 the lungs are normal by both gross and light-microscopy examination. Only 5% of the mice succumb. Except for peritonitis other organs are not affected. Doses of 3.3 and 10 micrograms of TDM are equally effective in producing the lesions, but a dose of 1.0 microgram of TDM causes only mild interstitial inflammation and lesser doses do not induce lesions. A single subcutaneous injection of 10 micrograms of TDM causes lesions in only 20% of mice. Vehicle-injected mice do not develop lesions. Electron microscopy revealed that the majority of the infiltrating cells are monocytes and macrophages and that extensive interstitial damage is produced. The mechanism of the effects of TDM are unknown and is currently under study. Our preliminary data suggests that the phenomenon is dependent upon T-lymphocytes.

Animals↗
PubMed1980

The effect of high antigen density on solid-phase radioimmunoassays for antibody regardless of immunoglobulin class.

Human sera containing antibody to casein or to bovine serum albumin were used to assess the validity and utility of a solid-phase assay for quantitating antibody activity. Rabbit anti-human immunoglobulin radiolabeled with 125I and capable of reacting with all human immunoglobulin classes was used to detect antibody bound to antigen immobilized to polystyrene tubes by a new covalent technique. This method results in very high antigen concentrations in highly stable association with polystyrene tubes. Kinetic and absorption studies demonstrated that low avidity antibodies are better detected when antigen is immobilized by the covalent method than when passively adsorbed. Conditions are described for minimizing artifactual interactions and for obtaining results similar to those obtained with conventional, liquid-phase assays. Failure to reach equilibrium in solid-phase assays and other problems are proposed to explain, in part, the inability to obtain a better correlation between solid- and liquid-phase immunoassays.

Animals↗
PubMed1980

Cryoglobulinemia and decreased monocyte chemotaxis is malignant melanoma.

The sera fromm 13 patients with malignant melanoma were evaluated for immune complexes by cryoprecipitation and the 125I Clq binding assay. Cryoprecipitates were identified in 12/13 patients (92%) and cryoimmunoglobulins in 7/13 patients (54%). Either cryoimmunoglobulin or elevated Clq binding was identified in 8/13 patients (62%). Incubation of normal monocytes with the resuspended cryoimmunoglobulin of 7 melanoma patients produced greater than 50% reduction in the ability of th monocytes to respond to chemotactic stimuli (p < .01). Similar inhibition was seen with cryoimmunoglobulin from erythema multiforme patients, but not with 'medium alone, albumin, heat aggregated albumin or heat aggregated-IgG in similar concentrations. No soluble factors produced in vitro could be demonstrated to produce this inhibition. Inhibition of monocyte function by immune complexes may be an important component of impaired host response to malignant melanoma, or alternatively may represent an important mechanism for the accumulation of monocytes at sites of inflammation, analogous to migration inhibition factor.

Adolescent↗
PubMed1980

Immune complexes and antibodies to BCG in sera from patients with mycobacterial infections.

We have examined the prevalence of circulating immune complexes in sera from patients with mycobacterial infections. Sera from 68 percent of patients with active M. tuberculosis and 58 percent of patients with M. intracellulare infections had significantly elevated Clq binding activity (Clq-BA). In general there was a fall in Clq-BA with treatment. Only 15 percent of M. tuberculosis patient with a bacteriological cure, 22 percent of non-tubercular patients with chronic obstructive pulmonary disease, and 3 percent of normal individuals had an elevated Clq-BA. Antibodies to a BCG-derived antigen were demonstrated in most of the individuals studied in all groups but, significantly elevated levels were seen only in patients with mycobacterial infections. In certain patients there appeared to be an inverse relationship between Clq-BA and BCG binding, suggesting that perhaps BCG-related antigens participated in the immune complexes found. Other possible antigen-antibody complexes are discussed.

Adolescent↗
PubMed1980

Circulating immune complexes and serum immunoglobulins in acute poststreptococcal glomerulonephritis.

Acute poststreptococcal glomerulonephritis (APSGN) is a disease thought to be induced by the renal deposition of circulating immune complexes. In order to test this possibility, serum samples from 119 patients with APSGN were studied for Clq binding activity (ClqBA), levels of IgG, IgM, IgA, C3 and antibody titers to streptococcal enzymes. These parameters were analyzed in relation to the clinical and laboratory data of the acute nephritic syndrome and with respect to the time elapsed from streptococcal infection and from the onset of nephritis. Elevated ClqBA was found in 66.7% of the patients in the first week of the disease and this frequency decreased progressively to 17.6% after the second week. Normal ClqBA was found in patients after the third week of nephritis. Serum levels of IgG and IgM were elevated in over 95% of the patients. Levels of IgG in excess of 2400 mg/dl were detected in 71.1% of the cases. No correlation could be found between the ClqBA and the clinical or immunoserological findings of the disease. The data support the hypothesis that circulating immune complexes are responsible for the nephritis that follows streptococcal infection.

Acute Disease↗
PubMed1979

Acute poststreptococcal glomerulonephritis in Maracaibo. II: Studies on the incidence, nature, and significance of circulating anti-immunoglobulins.

Antiglobulins were measured in the sera of 82 patients with acute poststreptococcal glomerulonephritis and correlated with C1q binding activity, serum levels of immunoglobulins and C3, site of infection, antibody titres to streptococcal enzymes, and the duration of the nephritis and interval from infection. Raised serum antiglobulins were found in 89.2% of the patients. In addition, raised titres were detected at any time during the course of the disease and very early after streptococcal infection. The finding of antiglobulins soon after the infection suggests the possibility that they appear as a primary event in the disease.

Acute Disease↗
PubMed1979

Anti-DNA activity of IgG F(ab')2 from normal human serum.

The components of normal human serum (NHS) which bound DNA in a standard assay for anti-DNA antibody were characterized. IgG was the major detectable protein isolated from NHS by affinity chromatography on DNA-cellulose. A second adsorption of the whole serum IgG with DNA-cellulose did not remove additional gamma-globulin indicating that only a very small fraction of the IgG was capable of binding DNA. This binding activity was largely restricted to denatured DNA. IgG (Fab')2 bound DNA as well as the intact molecules demonstrating the antibody-like nature of the IgG binding. These results suggest that IgG antibody to denatured DNA is a normal component of human serum.

Animals↗
PubMed1978

A laboratory evaluation of immune complexes in patients on inhalant immunotherapy.

Patients with allergic rhinitis receiving maintenance inhalant immunotherapy and two control groups were studied for evidence of circulating immune complexes. The first control group contained patients with allergic rhinitis who had never received immunotherapy. The second control group contained normal volunteers. Patients in the treatment group had no proteinuria. When compared with the control group, the treatment group had no statistically significant differences in incidence of Clq binding immune complexes, cryoglobulinemia, rheumatoid factor, or complement depletion. This initial study suggests that maintenance immunotherapy does not result in an increase of circulating immune complexes.

Antigen-Antibody Complex↗
PubMed1978

Evidence of an autologous immune complex pathogenic mechanism in acute poststreptococcal glomerulonephritis.

Clinical and experimental studies have suggested a role for antiimmunoglobulins in the pathogenesis of glomerulonephritis associated with streptococcal infection. We attempted to localize anti-IgG in the kidneys of 22 patients who had renal biopsies performed 7 to 66 days after the onset of acute poststreptococcal glomerulonephritis (APSGN). In addition to routine localization of immunoglobulins and C3, specimens were stained with neuraminidase-treated, heat-aggregated, and unmodified IgG. Twelve biopsies showed staining with fluorescein-labeled human neuraminidase-treated IgG. A lesser number gave positive staining with the other IgG preparations. Following treatment of slides with 0.01 M citrate buffer, seven previously negative biopsies showed positive staining with neuraminidase-treated IgG. The demonstration of anti-IgG by these methods was possible in 19 out of 22 biopsies. It correlated best with the presence of C3 and IgG, and to a lesser extent with IgM, in the renal glomerulus. These results and our previous finding of elevated levels of serum anti-IgG early in the course of APSGN, and as early as 8 days following the antecedent streptococcal infection, support a role for anti-IgG in the immune pathogenesis of APSGN. Although our series of studies support the hypothesis that anti-IgG is formed to an IgG modified enzymatically by streptococcal product, the formation of this autoantibody to IgG incorporated in an exogenous (streptococcal antigen-antibody) complex can not be ruled out.

Adolescent↗