PubMed Health⌕ Search

Biomedical subjects

N K Day

Publications and source records attributed to N K Day.

At least 19 recordsLinked to original sources
PubMed1979

Familial herpes simplex infection associated with activation of the complement system.

A patient with severe recurrent herpes infection was evaluated for immunologic analysis including a profile of complement components. The peripheral blood lymphocytes from the patient responded by proliferation to herpes simplex antigen but failed to produce leukocyte migration inhibition factor. Herpes simplex antibody titers increased during active infection. Total hemolytic complement (TCH50), the third (C3), fifth (C5), sixth (C6) and seventh (C7) components of complement, and factor B were dramatically reduced; the first (C1), second (C2) and fourth (C4) components of complement were within normal limits. In family members with a history of recurrent herpes simplex, one or more of the later complement components (C5, C6 or C7) was reduced. This study demonstrates the activation of complement in these serums via the alternative pathway.

Adult↗
PubMed1979

Selective IgA deficiency and circulating immune complexes containing bovine proteins in a child with chronic graft versus host disease.

We have previously shown that a selective absence of serum and secretory immunoglobulin A (IgA) may lead to the development of circulating immune complexes which appear to contain bovine milk antigens. We report here that high levels of circulating immune complexes were found in the serum of a child who was treated for severe combined immunodeficiency by bone marrow transplantation but in whom the IgA-producing cells subsequently failed. As increasing amounts of complexes appeared over a two year period, the child had a parallel progression of an apparent chronic graft versus host disease including a Sjögrens syndrome and scleroderma. Very large amounts of complexes were eventually formed but the level fell 77 per cent after milk was excluded from the diet. Chemical studies on the complexes showed that the majority of complexes did contain bovine milk proteins, and fluorescence antibody staining of skin biopsy samples showed the presence of dense deposits of bovine casein in the dermis. The relationship between bovine protein-antigen antibody complexes and the chronic graft reaction remains uncertain.

Antibodies↗
PubMed1979

Virolysis of mouse mammary tumor virus by sera from breast cancer patients.

All type C retroviruses are lysed by human serum in apparently antibody-independent, complement-mediated reactions. In contrast, we have now determined that the mouse mammary tumor virus (MMTV), a type B retrovirus, is not disrupted by normal human serum. MMTV was lysed, however, when rabbit antibody to whole MMTV was added to the serum. By taking advantage of this dependence of MMTV lysis on specific antibody, a virolytic assay was developed, based on the measurement of reverse transcriptase released from disrupted virions, to search for evidence of antibodies to MMTV in human sera. Significantly greater virolytic activity was detected in the sera of patients with breast cancer than in sera of patients with benign disease (P less than 0.001) or colorectal cancer (P less than 0.001) or in sera from apparently healthy individuals (P less than 0.002). This assay thus appears to be able to detect a unique attribute, possibly the presence of an antibody crossreacting with MMTV, in serum in patient with breast cancer.

Antibodies, Viral↗
PubMed1979

Bovine antigens and the formation of circulating immune complexes in selective immunoglobulin A deficiency.

We have shown that levels of circulating immune complexes are closely associated with the presence of precipitating antibodies to bovine milk proteins in individuals with selective immunoglobin (Ig)A deficiency. To test whether milk proteins are involved in immune complex formation, sera of seven IgA-deficient individuals were studied for the appearance of complexes after milk ingestion. In three of the seven, an initial fall in the level of complexes was followed by an increasing value, which peaked at 120-150 min. In another three, there was a tendency toward the formation of two peaks of complexes, the first at 30-60 min and the second at 120-150 min after drinking milk. One subject, who had had recent treatment for two separate neoplasms, had a steady level of complexes that did not change during the course of this test. After drinking milk, the molecular weight of the complexes found in the sera of one individual at the start of the milk test fell from >19S to 7-11S, and in vitro additions of progressively increasing amounts of a mixture of milk proteins or bovine gamma globulin, to sera that contained complexes produced a progressive reduction in the level of complexes detectable. We conclude that the circulating immune complexes found in some patients who lack IgA contain bovine milk proteins and that periodic fluctuation of the molecular weight of such complexes, depending upon antigen ingestion, appears likely. It remains uncertain what effect the chronic circulation of complexes has upon the clinical state of this group of patients.

Adult↗
PubMed1979

Genetic control of the eighth component of complement.

Using isoelectric focusing in polyacrylamide gel and a hemolytic assay for development of patterns, extensive, structural polymorphism in human C8 has been delineated. Two alleles, C8A and C8B, have been identified in orientals, with gene frequencies of 0.655 and 0.345. In blacks, what appears to be a third common allele was found, so that frequencies were 0.692, 0.259, and 0.049 for C8A, C8B, and C8A1. In whites, C8A1 was rare with a frequency of 0.003, and frequencies for C8A and C8B were 0.649 and 0.349. Inheritance was autosomal codominant in family studies and the distribution of types in random unrelated populations fit the Hardy-Weinberg equilibrium in all groups. C8 allotypes have been determined for two previously studied families, each with a homozygous C8-deficient propositus. This study suggests that C8 deficiency is a silent or null allele of the C8 structural locus, and that half normal levels of C8 cannot be used as a single criterion for the establishment of heterozygous C8 deficiency. C8 allotypes, as well as 18 other autosomal markers, were also determined for 24 families. The C8 structural locus is not closely linked to these markers, including the human histocompatibility loci complex.

Alleles↗
PubMed1979

Hypocomplementemia associated with naturally occurring lymphosarcoma in pet cats.

Eighty cats were classified by indirect immunofluorescence and histologic diagnosis into four categories: normal, feline leukemia virus (FeLV) infected; normal noninfected; lymphosarcoma-FeLV infected; lymphosarcoma, no FeLV present. All viremic cats with lymphosarcoma were found to be hypocomplementemic and activation of the complement system had occurred via the classical pathway. Sera of cats with lymphosarcoma in the absence of FeLV had varying levels of total hemolytic complement (TCH50) ranging from normal to hypocomplementemic. Approximately 50% of the cats that were viremic but histologically and clinically free of disease had TCH50 levels within normal range, and the remainder exhibited varying degrees of hypocomplementemia.

Animals↗
PubMed1979

Forssman-like antibody levels in sera of patients with lung cancer.

Sera of normal individuals or patients with lung cancer were assayed for Forssman-like antibody by a quantitative and specific method using ethylenediaminetetraacetate-containing buffer to inactivate complement in the test serum. It was shown that although Forssman-like antibody levels were distributed widely, (a) the levels of young (20 to 45 years of age) normal subjects of Blood Groups A and AB were lower than those of Blood Groups O and B, (b) the levels of old (60 to 80 years of age) normal subjects were lower than those of young normal subjects of Blood Groups O and B, and (c) the levels of old lung cancer patients were lower when compared to age-matched normal individuals of their blood group.

ABO Blood-Group System↗
PubMed1978

Murine complement component 3: genetic variation and linkage to H-2.

Two electrophoretic variants of murine complement component 3 (C3) were detected by using high-voltage electrophoresis of fresh mouse serum in agarose gels. Most of the inbred strains tested were homozygous for the S allele (for the slow-migrating variant); only four out of 46 strains had the alternative F allele (fast variant). Pen-bred Swiss-Webster animals belonged to one of three phenotypes--S, F, or SF--and the genes responsible for this variation segregated in a strictly Mendelian manner. In three such crosses, with 5* offspring, C3 segregated with H-2 in 46 instances, corresponding to a recombination frequency of approximately equal to 0.12.

Animals↗
PubMed1978

Milk precipitins, circulating immune complexes, and IgA deficiency.

Twenty-two patients with selective IgA deficiency were studied for the presence of serum precipitins to bovine milk, bovine and fetal calf serum, and circulating immune complexes. Fifty-nine percent had circulating immune complexes, 50% had milk precipitins, 23% had precipitins to bovine serum, and 13% had precipitins to fetal calf serum. All patients with precipitating antibodies against milk or against bovine or fetal calf serum had circulating immune complexes and the precipitin titers correlated with the amount of circulating immune complexes. After one IgA-deficient patient had drunk 100 ml of milk, studies of sequential serum samples showed the presence of casein in the circulation at 60 min and the appearance of increasing amounts of immune complexes for 120 min. These findings are interpreted to indicated that in human beings the IgA system may provide a major barrier to absorption of immunogens from the gastrointestinal tract.

Adult↗
PubMed1978

The presence of active C1 (C-1) on peripheral human lymphocytes.

We have shown that the first component of complement C1 is present in an active form on the surface of washed human peripheral lymphocytes but not on platelets or erythrocytes. This active C1 (C-1) was detected by its ability to transfer to sensitized cells carrying C4, i.e., EAC4, forming EAC-1,4. Active C1 was also able to consume C4. Treatment of these lymphocytes with 0.02 M EDTA removed C-1. EDTA-treated lymphocytes were able to bind exogenous purified human C-1. Comparative studies with sentized erythrocytes (EA) and EDTA treated lymphocytes showed that although fewer molecules of exogenous C1 could bind to the EDTA-treated lymphocytes than to EA, the consumption of C4 by C-1 bound to lymphocytes was significantly higher than that observed with EAC-1. When lymphocytes obtained from 2 patients with chronic lymphocytic leukemia and hypocomplementemia were tested, the release of C1, the C4 consumption and the binding of C-1 to EDTA-treated cells were highly inefficient.

Blood Platelets↗
PubMed1978

Detection of immune complex-like materials in cancer patients' sera: a comparative study of results obtained with the C1q deviation and C1q binding tests.

In a collaborative study involving three laboratories, randomly coded sera from 47 patients and healthy donors were tested for soluble immune complexes by two versions of the C1q BT and by the C1q DT. Analysis of ranked data showed a close correlation between results obtained in all laboratories as well as good reproducibility on testing coded duplicate samples included in each panel of sera. However, with the use of values for normal donors established independently in each laboratory, the tests did not always agree in discriminating normal from abnormal sera, particularly with sera from cancer patients. Results reflected to some extent the methods used to inactivate the endogenous C1 complex in the test sera. Studies of 130 additional cancer patients revealed that 44 (34%) gave abnormal C1q BT values when inactivated with EDTA but only 35 (27%) were abnormal when heat inactivated (56 degrees for 30 min). Similarly 12 of 65 sera (18%) from patients with nonneoplastic diseases and 10 of 80 (13%) from healthy donors gave significantly abnormal results after addition of EDTA. Eight (12%) of the disease and six (8%) of the healthy controls' sera were similarly outside normal limits when heat inactivated. Repeated freezing and thawing of sera or changes in the concentration of PEG used to precipitate complex-bound 125I-C1q influenced C1q BT results more than duration of storage at -70 degrees C or changes ascribed to presence or absence of rheumatoid factors and CRP.

Antigen-Antibody Complex↗
PubMed1977

Circulating immune complexes detected by 125I-Clq deviation test in sera of cancer patients.

The presence of circulating immune complexes in freshly drawn sera of patients with various forms of malignancies was detected by the 125I-Clq deviation test of Sobel et al. More than 50% of the 459 cancer sera showed a high inhibition of 125I-Clq uptake by sensitized sheep erythrocytes when compared with sera of 50 healthy laboratory personnel. The levels were compared with levels of total hemolytic complement and immunochemical determinations of Cl1 and C3. A correlation between high levels of circulating immune complexes and low levels of Clq was suggested. These immune complexes were separated by sucrose density gradient ultracentrifugation at low pH and were found to be heavier than 19S. Fluctuation of levels of immune complexes was evident when serial samples from the same patient were tested. Decrease of levels of immune complexes and a concomitant increase of Clq were detected after Calmette-Gueérin bacillus and autologous tumor cell treatment in some melanoma patients.

Antigen-Antibody Complex↗
PubMed1976

Linkage of gene for C2 deficiency and the major histocompatibility complex MHC in man. Family study of a further case.

Close linkage between HL-A and C2 deficiency was first reported by FU and co-workers in 1974. We present here a pedigree of a 31-year-old C2-deficient individual with clinical manifestations of Hodgkins disease. The following markers were tested: C2 levels, factor B polymorphism, blood groups, and enzyme typing. In addition to close linkage between HL-A and C2 deficiency, both parents were heterozygous for Bf (HL-A linked, electrophoretic variation of B). The two HL-A haplotypes closely linked to C2 deficiency are different: 2, W18 and W24, W18. They share, however, the SD2 antigen W18 and the LD type 7a.

Adult↗
PubMed1976

Evidence for immune complexes involving anti-lymphocyte antibodies associated with hypocomplementaemia in chronic lymphocytic leukaemia (CLL).

Unmeasurable total haemolytic complement (C) was observed in serum of a patient with untreated chronic lymphocytic leukaemia and recurrent non-hereditary angioedema. Analysis of C components immunochemically demonstrated a marked reduction of C1q and C1s inhibitor, undetectable C1r, C1s and an elevated B. Haemolytic C1, C4 and C2 were less than 5 percent of normal, functional C1s inhibitor was absent. Cryoglobulin and C1q precipitins were present in the serum. Of special interest was the presence of high levels of cold-reactive antilymphocyte antibody, determined by both C-dependent cytotoxicity and indirect immunofluorescence. The antibody exhibited specificities for both autologous lymphocytes and lymphocytes from normal donors; cytotoxic activity for autologous leukaemia cells was removed by absorption with normal isologous tonsil lymphocytes. Specific enrichment of this antibody relative to the serum level was demonstrated in the cryoglobulin and its isolated 19S fractions. Free lymphocyte surface antigen was also demonstrated by gel diffusion using specific rabbit antilymphocyte antiserum. These data strongly suggest the presence of pathogenetically significant circulating complexes of lymphocyte surface antigen and specific antibody in certain patients with CLL.

Angioedema↗
PubMed1975

C1-bypass complement-activation pathway in patients with chronic urticaria and angio-oedema.

During the routine screening of 152 patients with urticaria or angio-oedema for hypocomplementaemia, 4 patients were found to have low serum levels of the third component of complement (C). These patients were noteworthy and differed from previous reports of patients with urticaria-like skin lesions and hypocomplementaemia because of the absence of immune-complex disease. In addition to the low C3, 2 of these patients were unique on the basis of low serum levels of haemolytic C1, C1q, C1s, and properdin factor B, but normal concentrations of C4 and C2. These C abnormalities may reflect a new clinical entity, and these cases form the first description in man of the C1-bypass complement-activation pathway.

Adult↗
PubMed1975

Mixed lymphocyte culture determinants and C2 deficiency: LD-7a associated with C2 deficiency in four families.

Four families with C2 deficiency were studied. Among eight HL-A haplotypes involved with C2 deficiency, five were HL-A 10,W18. Three homozygotes for C2 deficiency from different families were mutually nonreactive in mixed lymphocyte cultures (MLC) and the heterozygotes from the fourth family failed to react to the homozygous cells. It appeared that identical MLC determinants were associated with all the genes from the different families that related to C2 deficiency. Further experiments identified the MLC determinant, LD-7a, as being involved. These results suggest marked linkage disequilibrium between the genes for C2 deficiency and the major histocompatibility complex (MHC). Studies of possible recombinants have offered tentative evidence for the positioning of the locus for C2 deficiency with respect to other segments of the MHC.

Chromosome Mapping↗