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At least 37 records · Page 2Linked to original sources

PubMed2002

Recurrent reproductive wastage and immunologic factors.

PROBLEM: The causes of recurrent reproductive wastage are varied and complex. The present study was designed to focus on the role of immunologic factors in cases where other causes were not evident. METHOD OF STUDY: Over 20 years, more than 1500 couples were evaluated in our clinic because of recurrent spontaneous abortion. Women were tested for anti-phospholipid antibodies and plasma contact proteins of the intrinsic pathway of blood coagulation after endocrine, organic, infectious and genetic etiologies of miscarriages were excluded. RESULTS: Anti-phosphatidylethanolamine antibodies, anti-annexin antibodies, and factor XII deficiency were more common factors in recurrent spontaneous abortion patients than were anti-cardiolipin antibodies in terms of induction of recurrent pregnancy losses. Paternal leukocyte immunotherapy of patients without such abnormalities was associated with a significantly improved success rate. CONCLUSIONS: Recurrent reproductive wastage can be minimized by individualized therapy based on comprehensive evaluation of immunologic factors, including several anti-phospholipid antibodies.

Abortion, Habitual↗

PubMed1992

Psychological factors, immunologic activation, and disease activity in rheumatoid arthritis.

The purpose of this study was to use structural equation modeling techniques to examine potential interrelationships among psychological factors, immunologic activation, and disease activity in rheumatoid arthritis (RA). The subjects were 80 male patients with a diagnosis of classic or definite RA. Measures included the Beck Depression Inventory, the Arthritis Helplessness Index, and the Arthritis Impact Measurement Scales (AIMS) pain score. Joint counts and immunophenotypic analyses of peripheral blood lymphocytes also were collected. Path analysis showed that percentage of HLA-DR+ cells in the peripheral blood and helplessness were related to join count. In addition, joint count had an effect upon depression. Depression had an effect upon pain, but there was no reciprocal effect of pain upon depression. This study describes a preliminary path model of interrelationships among psychological factors, immunologic activation, and disease activity in RA.

Aged↗

PubMed1993

An HLA-B regulatory element binds a factor immunologically related to the upstream stimulation factor.

HLA-A and -B are expressed by most cell types, and their levels can be increased by treatment with interferons (IFNs). The relative basal levels of HLA-A and -B expression can vary, and HLA-B loci are induced much more strongly by IFNs. Constitutive activity is dependent on an upstream enhancer (ENH) which contains a rel (KBF, NF kappa B) binding motif, and induction is mediated by an interferon response element (IRE) which binds members of the IRF family. Reported here is the identification of a regulatory element, 'R', which overlaps the IRE of HLA-B loci, but which is absent from the equivalent region of HLA-A or H2 class I genes. The core of the element, CACGAG, is bound by a nuclear factor which is recognized by an antiserum raised against the upstream stimulation factor (USF), a member of the helix-loop-helix/leucine zipper family. The use of reporter gene constructs shows that mutation of the R element results in increased induction by IFN alpha in some cell lines, which appears to be due to competitive binding of USF with IRF proteins.

Base Sequence↗

PubMed2005

Chronic graft loss. Immunological and non-immunological factors.

AIMS: Late loss of kidney grafts is an ongoing problem in the field of transplantation. This is caused by immunological and non-immunological factors, the main immunological driver of rejection is the immune response against HLA molecules that differ between donor and recipient. METHODS: To measure the anti-donor responses that a recipient can mount, we have been quantifying anti-donor T-cell frequencies in recipients of renal transplants for several years. Anti-donor direct and indirect pathway frequencies have been measured in vitro in kidney and heart transplant patients by Limiting dilution analysis and other methods. Further, to elucidate the role of CD4+CD25+ regulatory T-cells, these cells have been depleted in ex vivo assays of cellular function. Antigen specific CD4+CD25+ cell lines are being expanded in vitro with a view to using them in immunotherapeutic strategies. RESULTS: Frequencies of T-cells with direct pathway anti-donor specificity decline in most patients, while those with indirect anti-donor specificity increase in frequency in patients with late graft failure. In keeping with results from experimental models of transplantation tolerance, evidence for allospecific regulatory cells was found in some patients with good, stable transplant function. Interestingly, the regulatory cells appeared to have indirect allospecificity, and no evidence of direct pathway regulation was observed. CONCLUSIONS: The indirect pathway anti-donor alloresponse poses the major threat to long-term transplant survival. Indirect pathway regulatory T-cells arise in some patients. These data are consistent with the hypothesis that tolerance strategies require shrinkage of the direct, and regulation of the indirect, anti-donor response.

Acute Disease↗

PubMed1976

Relationship of causative factors in spontaneous regression of cancer to immunologic factors possibly effective in cancer.

In a book written by Everson and Cole (1966) on spontaneous regression 176 examples of the phenomenon were encountered in the medical literature from 1900 to 1964, supplemented by cases referred by friends. No common denominator of explanations were found. Various types of trauma (e.g., biopsy, incomplete excision), transfusions, infection, hormone changes, drugs, etc. were encountered as possible causative factors. Most significant of all factors was encountered in the 13 examples of spontaneous regression of the bladder; in this series regression of the tumor occurred in 10 after transplantation of the ureters out of the bladder. A consideration and discussion of various reactions in human beings associated with therapeutic regressions have been reviewed hoping to develop a correlation between the two types of regression. At the time of publication of our monograph 9 years ago we were unable to suggest any mechanisms which might explain the regressions. However, since that time so many advances have been made in immunology that it appears now that a stimulation of the immune process might explain most of the regressions. We are just beginning to learn a few methods of stimulating the immune process. Use of BCG is one of the best examples of this stimulating process; other bacterial agents, or fractions, are known to have this action. No doubt there are innumerable others unknown, some of which might explain spontaneous regressions. It would appear that hormonal changes might be responsible for many of the regressions but this author doubts it explains many. More is known at the present time about cellular immunity than humoral immunity, but greater possibilities surely lie in humoral immunity. The blocking and unblocking activities developed by the Hellströms and associates are no doubt important. Immunoglobulins exert a very important role in the immune process; antibodies may consist of immunoglobulins but much more needs to be known before this relationship can be understood. The recent report (Amery, 1975) that levamisole (given at the time of resection of the lung for carcinoma) improves patient survival is exciting. Amery believes the drug may prevent the hematogenous spread of the tumor during surgery and/or may decrease the immunosuppression caused by a major operation.

Adult↗

PubMed2005

Immunological factors in the pathogenesis and treatment of age-related macular degeneration.

Recent findings indicate that immunological factors are involved not only in the pathogenesis of age-related macular degeneration (AMD), but also in its treatment. Earlier data showing the presence of inflammatory cells in affected areas of AMD retinas support this statement. Although a possible role for autoimmunity was initially suggested, it has never reached general acceptance. Microorganisms have also been implied in the pathogenesis of AMD. Both serum antibacterial antibody levels and positive DNA tests from neovascular membranes have pointed to a possible role for Chlamydia pneumoniae in the pathogenesis of AMD. New data is providing evidence for the hypothesis that deposits between Bruch's membrane and the retinal pigment epithelium (RPE) cell layer may act as a stimulus for the local activation of the complement system. This may lead to a further growth of the deposits due to the strong chemotactic activity of certain complement activation products (such as C5a) with an influx of inflammatory cells. The buildup of cells and extracellular deposits may lead to local ischemia resulting in the activation of RPE cells. These activated RPE cells are thought to release angiogenic stimuli leading to choroidal neovascularization, which is the most serious complication of AMD. The fact that immunosuppressive drugs such as triamcinolone acetonide and anecortave acetate are capable of inhibiting choroidal neovascularization is consistent with an inflammatory component in the pathogenesis of AMD. Specific immunotherapy directed at certain cytokines or growth factors is now being investigated at both the animal and patient levels. Various clinical trials involving engineered antibodies are now being applied to block angiogenic factors such as the vascular endothelial growth factor (VEGF). An approach using gene therapy to influence angiogenesis by inducing the production of the pigment epithelium-derived factor (PEDF) was able to block neovascularization in an experimental murine model. Besides trying to block ongoing processes in AMD, retinal transplantation is now also being investigated as a treatment option. The fact that the retina is possibly an immunoprivileged tissue in combination with experimental data showing that the subretinal space is an immunoprivileged site is an indication that transplantation would not suffer from the rejection process. A larger obstacle is the question whether transplanted retinal tissue will regain its functional properties.

Anti-Inflammatory Agents↗

PubMed1979

Immunologic factors affecting the in-vivo and in-vitro survival of the Legionnaires' disease bacterium.

Immunologic factors affecting viability of the Legionnaires' disease (LD) bacterium were studied in vitro and in vivo in mice and guinea pigs. In bactericidal tests, fresh human serum quickly killed LD cells. Heating fresh serum to 56 degrees C for 30 min destroyed bactericidal activity; absorbing it with bentonite had little effect. Fresh normal human serum was more effective than guinea pig serum. Adding LD cells to fresh normal human serum caused a greater than 50% depletion in functional complement activity, apparently by activating the classic C-142 pathway, because human serum deficient in C4 was not bactericidal. Antibodies to the Knoxville 1 LD strain in guinea pigs showed enhanced complement-mediated bactericidal activity. Without complement, immune guinea pig or human sera prolonged in-vitro LD cell survival. Antibodies to Knoxville 1 in mice depressed in-vitro bactericidal activity of human complement against Knoxville 1. In-vitro bactericidal tests support in-vivo studies in subcutaneous chambers. Complement-deficient mice immunized with Knoxville 1 were (P less than 0.01) less resistant to homologous challenge than nonimmunized mice. Immunized guinea pigs had a greater than 80-fold increase in resistance to subcutaneous-chamber infection.

Animals↗

PubMed2004

Immunologic factors in the pathogenesis of osteonecrosis.

Osteonecrosis is a disease in which death of cellular elements of bone occurs as a result of diminished arterial blood supply. The pathogenetic mechanisms of osteonecrosis remain unresolved. Extravascular pressure and subsequent tamponade of the arterial vessels or an intravascular thrombosis have been suggested. Immunologic factors may also play an important role. In autoimmune disorders, small vessel vasculitis or other disease-associated features, as well as antiphospholipid antibodies, have been involved in the development of osteonecrosis.

Antibodies, Antiphospholipid↗

PubMed2002

European best practice guidelines for renal transplantation. Section IV: Long-term management of the transplant recipient. IV.2.2 Chronic graft dysfunction. Immunological factors (alloimmunity).

GUIDELINE: All recipients of an allogeneic kidney graft should take life-long maintenance immunosuppressive medication. Whereas there is no immunological test to diagnose chronic allograft dysfunction, circumstantial evidence suggests that immunological factors play an important role in its pathogenesis. This evidence is based on experimental data, the beneficial effect of sharing HLA antigens between donor and recipient and post-transplantation immunological monitoring studies.

Chronic Disease↗

PubMed1978

Immunologic factors determining survival of cadaver-kidney transplants. The effect of HLA serotyping, cytotoxic antibodies and blood transfusions on graft survival.

We assessed immunologic factors determining graft survival in 510 recipients of primary cadaver allografts at one center. The degree of HLA match grade did not directly affect graft survival (54 per cent in no-antigen match, and 42 per cent in three-antigen match, at two years). There was no correlation between the HLA match grade and the degree of stimulation of the mixed lymphocyte culture. Patients receiving more than five blood transfusions had a significantly better graft survival than nontransfused recipients (52 versus 23 per cent, respectively, at two years, P less than 0.001). The beneficial effect of transfusions was noted whether or not lymphocytotoxic antibodies were produced, provided adequate screening was performed before transplantation. Transfusions did not alter the degree of stimulation in the mixed lymphocyte culture. More liberal use of transfusions and frequent screening for cytotoxic antibodies would probably result in more effective cadaver-kidney transplantation.

Blood Transfusion↗

PubMed1978

A study of the role of immunological factors in the pathogenesis of the anaemia of acute malaria.

Children with acute Plasmodium falciparum malaria and anemia were investigated to see if immunological factors could be implicated in the pathogenesis of their anaemia. Direct Coombs tests using an anti-whole immunoglobulin antiserum were negative in all 12 children tested but two had positive tests with antisera to C3b and C3d. Low plasma levels of C3 and C4 were found but these were not significantly different from values found in a group of children with acute malaria who were not anaemic. Serum levels of immune complexes were normal at the time of their presentation at hospital with anaemia but were elevated one month later. Incubation of group O rhesus-negative red cells in a serum pool obtained from children with acute malaria and anaemia did not cause enhanced haemolysis or reduce their survival time on injection into mice. Splenic uptake of red cells was, however, significantly enhanced. We conclude that the anaemia of acute malaria is due mainly to destruction of red cells by malaria parasites and to enhanced erythrophagocytosis of normal cells.

Acute Disease↗

PubMed2002

[Non-immunologic factor: immunosuppressive drug-induced nephrotoxicity].

Immunosuppressant-induced nephrotoxicity contributes to kidney graft loss in the long-term as one of the non-immunologic factors. We previously reported that correction of cyclosporine A (CsA)-induced hypomagnesemia reduced chronic CsA nephrotoxicity. This study was conducted to elucidate the mechanism of the beneficial effects of magnesium (Mg) on CsA nephrotoxicity and examine the role of the renin-angiotensin system in this mechanism. We particularly focused on CsA-induced interstitial mononuclear cell infiltration. CsA (15 mg/kg/day, s.c.) was administered daily to rats maintained on low sodium diets for 7, 14 and 28 days. The inhibitory effects of Mg supplementation and those of angiotensin converting enzyme inhibitor (ACEI) were compared for renal function, renal histology, mononuclear cell infiltration and gene expression profile. CsA lowered creatinine clearance and developed characteristic tubulointerstitial fibrosis that were mostly evident at day 28. CsA-induced impairment of renal function was ameliorated by Mg supplementation but not by ACEI. Monocyte/macrophage infiltration preceded the renal fibrosis and increased progressively with the duration of CsA administration. CsA markedly upregulated the expression of chemoattractant proteins, osteopontin and monocyte chemoattractant protein-1, concomitantly. These changes were markedly attenuated by Mg but only slightly by ACEI. CsA also promoted expression of fibrogenic molecules and extracellular matrices that were markedly attenuated by Mg but only slightly by ACEI. Similarly, CsA-induced tubulointestitial fibrosis was almost completely abolished by Mg supplementation but only partially attenuated by ACEI. These results suggested that Mg supplementation abolished CsA-induced precedent inflammatory cell influx possibly via inhibition of expression of chemoattractants and consequently suppressed tubulointerstitial fibrosis. In this beneficial mechanism, factors independent of renin-angiotensin system seem to be mainly involved.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1995

[The role of immunologic factors in the etiology of pregnancy-induced hypertension].

Pregnancy-induced hypertension (PIH) is a placental disease that mainly occurs in primigravidae, but its precise etiology is not yet known. It has long been considered that the protective effect of multiparity may be due to immunological factors. Here, we review epidemiologic data from the literature supporting the idea of a possible immunological basis of PIH. There are conflicting reports in the literature regarding the involvement of cellular and humoral mechanisms in the etiology of PIH, the impact of histocompatibility and the interactions between maternal and fetal genotype. Finally, the evidence for a common immunologic cause for pregnancy-induced hypertension and miscarriage is discussed.

Abortion, Spontaneous↗

PubMed1982

An immunoperoxidase study of immunological factors in high immune and low resistance granulomas in leprosy.

The epithelioid cell granuloma in high resistant tuberculoid (TT) leprosy was contrasted with the pure macrophage granuloma of anergic lepromatous leprosy (LL) by evaluating various immunological factors operating in these lesions. The immunoperoxidase technique using antisera to immunoglobulin IgG, IgM, complement C3, C3d and C1q and other products of macrophage secretion, lysozyme, plasminogen, a1 antitrypsin and C-reactive protein and of Ia antigens revealed peak levels in tissues of most of these factors in both types of granuloma. The tuberculoid response was linked to low antigenic load and Ia-like antigen and the lepromatous response was secondary to a high antigenic load in the absence of Ia antigen. Complement and other mediators were found intracellularly in both tuberculoid and lepromatous granulomas, but extracellularly only in tuberculoid lesions. This may indicate local hypersensitivity in the tuberculoid granuloma. It is suggested that the mediators in LL macrophages remain bound to lipids of mycobacterial degenerations in the phagocytic vacuole. Secretory cells were differently sited in the two types of granulomas: peripheral in epithelioid cell lesions and central around capillaries over the whole lesion in pure macrophage granulomas of LL. In tuberculoid leprosy many of the central vessels in the granuloma were obliterated. C1q was found in fibroblasts. However, the marked absence of fibrosis in any of the lesions of leprosy, except following severe reactions, casts some doubt on the link which has been postulated between epithelioid cells and fibroblasts as an explanation of fibrosis in granulomas.

Complement System Proteins↗

PubMed2003

Immunologic factors in transplant arteriopathy: insight from animal models.

Transplant arteriopathy is the leading cause of long-term morbidity and mortality following heart transplantation. The pathologic hallmark of this disease is intimal proliferation. Animal models have demonstrated that immunologic factors, including cytokines, cellular adhesion molecules and inflammatory cells, play a significant role in the development of this arteriopathy. One goal of future studies will be to translate findings in animal models into effective treatments in humans.

Animals↗

PubMed2004

Viral and immunological factors associated with breast milk transmission of SIV in rhesus macaques.

BACKGROUND: The viral and host factors involved in transmission of HIV through breastfeeding are largely unknown, and intervention strategies are urgently needed to protect at-risk populations. To evaluate the viral and immunological factors directly related to milk transmission of virus, we have evaluated the disease course of Simian Immunodeficiency Virus (SIV) in lactating rhesus macaques (Macaca mulatta) as a model of natural breast milk transmission of HIV. RESULTS: Fourteen lactating macaques were infected intravenously with SIV/DeltaB670, a pathogenic isolate of SIV and were pair-housed with their suckling infants throughout the disease course. Transmission was observed in 10 mother-infant pairs over a one-year period. Two mothers transmitted virus during the period of initial viremia 14-21 days post inoculation (p.i.) and were classified as early transmitters. Peak viral loads in milk and plasma of early transmitters were similar to other animals, however the early transmitters subsequently displayed a rapid progressor phenotype and failed to control virus expression as well as other animals at 56 days p.i. Eight mothers were classified as late transmitters, with infant infection detected at time points in the chronic stage of the maternal SIV disease course (81 to 360 days). Plasma viral loads, CD4+ T cell counts and SIV-specific antibody titers were similar in late transmitters and non-transmitters. Late breast milk transmission, however, was correlated with higher average milk viral loads and more persistent viral expression in milk 12 to 46 weeks p.i. as compared to non-transmitters. Four mothers failed to transmit virus, despite disease progression and continuous lactation. CONCLUSION: These studies validate the SIV-infected rhesus macaque as a model for breast milk transmission of HIV. As observed in studies of HIV-infected women, transmission occurred at time points throughout the period of lactation. Transmission during the chronic stage of SIV-infection correlated with a threshold level of virus expression as well as more persistent shedding in milk. This model will be a valuable resource for deciphering viral and host factors responsible for transmission of HIV through breastfeeding.

Animals↗

PubMed1989

[Immunological factors in the evolution of the epidemic process in meningococcal infection].

The results obtained in 1987 in the study of the immunostructure of the population of Yaroslavl with respect to meningococcal polysaccharides, groups, A, B, C, and lipopolysaccharide are presented in comparison with earlier results obtained in 1976. The regulating role of the immunological factor in the evolution of the epidemic process of meningococcal infection has been confirmed. The level of antibodies to meningococcal polysaccharides, groups A and B, has been found to reflect the intensity of the circulation of the infective agent among the population. The comparison of the results of investigations carried out in 1976 and 1987 has revealed the essential role of the lipopolysaccharide antigen in the formation of the postinfection immunity of the population to meningococcal infection, irrespective of the group of the infective agent.

Adolescent↗

PubMedDate not supplied

Immunological factors governing resistance and susceptibility of mice to Leishmania major infection.

Infection with Leishmania sp. is particularly suitable for the study of immunoregulatory mechanisms associated with host susceptibility or resistance. The clinical spectrum of this infection results from parasite virulence factors and host immune responses, some of which acting in a host protective manner while others exacerbate the disease. In the mouse model, factors governing resistance to Leishmania major infection mainly depends on the IFN-gamma activation of the leishmanicidal function of macrophages, and the Fas/ FasL-dependent T-cell cytotoxicity against infected macrophages. On the other hand, the immunological factors of susceptibility involve: I) the early upregulation of IL-4 production induced by the LACK antigen, II) the upregulation of IL-2 production, III) the high production of TGF-beta as macrophage deactivating factor, and IV) the production of IL-10 by the L. major infected macrophages, inhibited their microbicidal activity.

Animals↗