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I D Wilson

Publications and source records attributed to I D Wilson.

16 recordsLinked to original sources
PubMed1979

Evidence against the presence of circulating immune complexes in chronic inflammatory bowel disease.

Several investigators have reported the presence of circulating immune complexes in serum from patients with Crohn's disease and chronic ulcerative colitis. Because previous assays employed conditions which might have caused immunoglobulin aggregates to form in vitro, thus falsely suggesting the presence of immune complexes in vivo, we tested inflammatory bowel disease sera for immune complexes using four assays designed to minimize in vitro immunoglobulin aggregation. In three assays immune complexes were not detectable, while in a fourth, the Clq precipitin test, positive reactions occurred. These precipitin reactions did not have characteristics of immune complexes. Our data suggest that circulating immune complexes are either not present in patients with inflammatory bowel disease or that they occur infrequently or in low concentration.

Antigen-Antibody Complex↗
PubMed1979

Studies on the nature of heat-labile anti-complementary activity in normal human serum.

Heat-labile anti-complementary activity (ACA) appears in normal human serum during storage or heating as endogenous haemolytic activity disappears. Following gel filtration of unheated serum, two peaks of heat-labile ACA are present. The ACA of both whole and fractionated serum has previously been attributed to the presence of heat-labile immunoglobulin aggregates or immune complexes. Our data demonstrate that the heavy peak of ACA obtained by gel filtration does not bind to 125I-C1q or to Raji cells, and that its effect is abolished to C1INH, suggesting that it represents C1 rather than immunoglobulin aggregates or immune complexes. The lighter peak of ACA in fractionated serum has the functional characteristics of C1s and free C1s is demonstrable in fractions containing this activity. The ACA of whole serum likewise has functional characteristics of C1. The anti-complementary effect of C1 on guinea-pig complement would not be evident in the complement fixation assay until most endogenous haemolytic activity in human serum has been inactivated, either by heat or by storage. C1INH only partially inhibits this ACA in serum or in solutions containing isolated C1 in high concentrations. These observations indicate that heat-labile ACA in whole or fractionated sera is due to the presence of C1 and C1s and that this activity cannot be taken as evidence for the presence of immune complexes.

Agammaglobulinemia↗
PubMed1979

The effect of heat inactivation of serum on aggregation of immunoglobulins.

Heating serum at 56 degrees is used to inactivate complement in several immunological assays. During heating, both heat-labile and heat-stable anticomplementary activity (ACA) develop. While heat-labile ACA can be completely inactivated, heat-stable ACA increases progressively with continued heating. Heat-stable ACA develops in deaggregated IgG and in normal, but not in hypogammaglobulinaemic, human and porcine serum heated at 56 degrees suggesting that this ACA is due to formation of immunoglobulin aggregates. These aggregates would produce false-positive tests for immune complexes and could inhibit a variety of cell-mediated reactions in assays which incorporate heat-inactivated serum. Other temperatures were tested to determine whether endogenous haemolytic activity could be destroyed without forming immunoglobulin aggregates. At 53 degrees both endogenous haemolytic activity and heat-labile ACA were inactivated and formation of heat-stable ACA in normal serum was minimal. ACA, however, could be induced in deaggregated IgG at 53 degrees. Moreover, the degree of heat-induced aggregation of IgG in vitro at either temperature was directly proportional to IgG concentrations and inversely related to albumin concentrations. Thus, pathological sera with these protein alterations might form more aggregates during heating than normal sera. These data suggest the following: (1) heat inactivation of complement at 53 degrees for 90 min is preferable to the traditional 56 degrees; (2) in any assay where immunoglobulin aggregates might interfere, normal serum may be an inadequate control and correlations will need to be made between serum IgG and albumin concentrations and the results obtained in these assays.

Adult↗
PubMed1977

Lymphocytotoxic antibodies in patients with inflammatory bowel disease and their spouses--evidence for a transmissible agent.

Serum lymphocytotoxic antibodies (LCA) were detected in twenty-seven out of fifty-three (51%) patients with inflammatory bowel disease (IBD) and in twenty-three out of their fifty-three (43%) unaffected spouses. The prevalence of LCA in both groups was significantly increased (P less than 0.001) compared to that in age- and sex-matched controls (11%) or in control spouses (6%). Concordant expression of LCA occurred in sixteen out of the fifty-three (30%) patient-spouse pairs compared to only one out of the fifty-three (2%) control-spouse pairs (P less than 0.001). In contrast to the LCA results, heterophile antibody titres were similarly distributed in all four study groups. It is suggested that LCA may represent markers of infectious agents in IBD and that their occurrence in unaffected close contacts of patients may indicate transmission of such agents to these subjects.

Antibodies↗
PubMed1976

Immunoglobulins within human small-intestinal Paneth cells.

Human duodenal, jejunal, and ileal samples obtained at necropsy and by peroral and surgical biopsy, were studied by light microscopy using the unlabelled antibody enzyme method for imunocytochemical staining of lysozyme and immunoglobulins. Paneth cells contained IgA and IgG, but not IgD IgE, or IgM. Staining intensity indicated that IgA and IgG were present in amounts greater than in other epithelial cells. There was pronounced variation in the immunoglobulin content of Paneth cells. Rat Paneth cell containing IgA and lysozyme and are capable of the phagocytosis and degradation of microorganisms. These observations suggest that human Paneth cells may have similar functional capabilities.

Duodenum↗
PubMed1976

Immunocytochemical identification and localization of immunoglobulin A within Paneth cells of the rat small intestine.

Light microscopic immunocytochemistry was used to identify Paneth cells by their lysozyme content and to detect immunoglobulin antigens within a subpopulation of these cells. Antisera specific for the heavy chains of rat or human immunoglobulin A and for immunoglobulin light chain antigens produced specific staining of rat Paneth cells. The distribution of immunoglobulin staining varied between adjacent Paneth cells in the same crypt and between Paneth cells in adjacent crypts, as well as between Paneth cell populations of different animals. No staining of rat Paneth cells was detected using antisera specific for the heavy chain of immunoglobulins G or M. The specific staining of Paneth cells for immunoglobulin A and light chain antigens was blocked by absorption of each antiserum with its respective purified antigen. Absorption of these antisera with purified rat lysozyme did not affect staining and thereby eliminated the possibility of immunologic cross-reactivity between lysozyme and immunoglobulin antigens. It is suggested, in light of current concepts of Paneth cell function, that the immunoglobulin staining of Paneth cells may reflect their ability to phagocytize immunoglobulin A-coated microorganisms or immune complexes containing immunoglobulin A.

Animals↗
PubMed1975

Lymphocytotoxic antibody in inflammatory bowel disease. A family study.

The prevalence of lymphocytotoxic antibody in inflammatory bowel disease is 40 per cent. Twenty-seven of 90 relatives of 23 probands with the disease (30 per cent) demonstrated lymphocytotoxic antibody, as contrasted with only three of 69 control family members (4 per cent) (P less than 0.0001). Decreased lymphocytotoxicity against lymphocytes from patients with inflammatory bowel disease as compared to normal donor lymphocytes previously demonstrated in the serum of probands was also observed in the serums from family members of the probands. Nineteen of the 48 household contacts of probands (40 per cent) were positive for antibody, whereas eight of 42 nonhousehold contacts (19 per cent) demonstrated it (P less than 0.05). Eight of 16 spouses (50 per cent) of probands showed antibody. The increased prevalence of lymphocytotoxic antibody in family members of probands and its occurrence mainly in household contacts (consanguineous and non-consanguineous) may indicate the exposure of probands and their family members to a common environmental agent.

Adult↗
PubMed1975

Serum lymphocytotoxins in inflammatory bowel disease. Studies of frequency and specificity for lymphocyte subpopulations.

Serum cold-reactive lymphocytotoxin (LCT) was detected in twenty-two of fifty-six (40%) patients with inflammatory bowel disease (IBD). The frequency of LCT detection was similar in Crohn's disease and ulcerative colitis. Cytotoxicity testing against T or B cell-enriched peripheral blood lymphocytes from normal donors, together with absorption experiments, indicated that LCT in IBD was reactive against determinants on both cell subpopulations. Reactivity against T cells from patients with common variable immunodeficiency was significantly less than with normal donor T cells. LCT in IBD could not be related to prior allogeneic sensitization and its presence appeared to be unrelated to disease activity or drug therapy. No correlation was found between LCT and peripheral blood T- or B-cell numbers. The present findings suggest the need for further investigation of the role of infectious agents in the pathogenesis of IBD.

Absorption↗
PubMed1975

Serum immunoglobulin M concentrations following bowel resection in chronic inflammatory bowel disease.

Serum immunoglobulin alterations were characterized in 20 patients with chronic inflammatory bowel disease (CIBD) undergoing bowel resection and in 11 control subjects undergoing intra-abdominal operations. Serum immunoglobulin M (IgM) values became elevated during the 2nd week in both groups with individual serum IgM concentrations reaching as high as 9 times preoperative values. The IgM increment, which was 19 S polyclonal immunoglobulin, was significantly greater in the CIBD group than in controls. Because of a recent suggestion that this IgM rise might be related to the pathogenesis of CIBD, the affinity of this IgM for colon was studied in two ways. Serum anticolon antibody titers did not change after surgery nor did IgM, isolated from serum after surgery and labeled with 125I, bind to homogenates of normal or CIBD colon. Titers of heterophile antibody and antibodies directed against Escherichia coli, Bacteroides, and blood group antigens increased in many patients. In most instances, these increments were shown to be antibody of the IgM class by reduction with 2-mercaptoethanol. These data indicate that the IgM changes after abdominal surgery (1) are not specific for CIBD patients, (2) do not represent antibody directed against colon antigens, and (3) include increased titers of several IgM antibodies. These findings might be explained by a response to bacterial or tissue antigens released at or after the time of surgery.

ABO Blood-Group System↗