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PubMed2003

Correlated evolution between host immunity and parasite life histories in primates and oxyurid parasites.

Maturation time is a pivotal life-history trait of parasitic nematodes, determining adult body size, as well as daily and total fecundity. Recent theoretical work has emphasized the influence of prematurational mortality on the optimal values of age and size at maturity in nematodes. Eosinophils are a family of white blood cells often associated with infections by parasitic nematodes. Although the role of eosinophils in nematode resistance is controversial, recent work has suggested that the action of these immune effectors might be limited to the larval stages of the parasite. If eosinophils act on larval survival, one might predict, in line with theoretical models, that nematode species living in hosts with large eosinophil numbers should show reduced age and size at maturity. We tested this prediction using the association between the pinworms (Oxyuridae, Nematoda) and their primate hosts. Pinworms are highly host specific and are expected to be involved in a coevolutionary process with their hosts. We found that the body size of female parasites was negatively correlated with eosinophil concentration, whereas the concentration of two other leucocyte families-neutrophils and lymphocytes-was unrelated to female body size. Egg size of parasites also decreased with host eosinophil concentration, independently of female size. Male body size was unrelated to host immune parameters. Primates with the highest immune defence, therefore, harbour small female pinworms laying small eggs. These results are in agreement with theoretical expectations and suggest that life histories of oxyurid parasites covary with the immune defence of their hosts. Our findings illustrate the potential for host immune defence as a factor driving parasite life-history evolution.

Animals↗

PubMed2002

Interspecific neisserial high molecular weight proteins able to induce natural immunity responses are strongly correlated with in vitro bactericidal activity.

Human sera from healthy volunteers and patients convalescent from meningitis were used to search for widely cross-reactive antigens implicated in vivo protective responses. Using the type strain Neisseria meningitidis B16B6 and a wide variety of both N. meningitidis and N. lactamica strains, several cross-reactive antigens and bactericidal sera were found, although the cross-reactivity patterns did not correlate with bactericidal activity, a total correlation was found between bactericidal activity and reaction with one or two high molecular weight proteins (162 and 138 kDa), and a mouse serum against the purified proteins showed a high bactericidal activity. Our results suggest that the high molecular weight proteins found are immunogenic and cross-reactive, eliciting bactericidal responses during infection and as a result of natural immunity. These proteins should be taken into account in studies for future vaccine formulations.

Animals↗

PubMed1988

Correlation of in vitro immune defects with impaired gamma interferon response in human-immunodeficiency-virus-infected individuals.

65 patients belonging to known acquired-immune-deficiency-syndrome (AIDS) risk groups were tested for mitogen responsiveness to pokeweed mitogen, concanavalin A and phytohemagglutinin, percentages of peripheral blood CD4, CD8 and Leu7 lymphocyte subsets, serum neopterin levels, and gamma-interferon (gamma-IFN) concentrations in cell culture supernatants. Patients with clinical symptoms of human-immunodeficiency-virus infection showed reduced gamma-IFN production in vitro. The IFN concentrations were correlated significantly with mitogen-induced blastogenesis. High serum neopterin levels and decreased CD4/CD8 ratios were associated with diminished gamma-IFN levels. The percentage of Leu7 lymphocytes was increased in a group of patients with strikingly elevated gamma-IFN levels.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Subnormal serum concentration of 1,25-vitamin D in human immunodeficiency virus infection: correlation with degree of immune deficiency and survival.

Vitamin D metabolites, immunologic, virologic, and clinical parameters, and survival time were determined in 22 asymptomatic human immunodeficiency virus (HIV)-infected patients (CDC stage II/III), 31 symptomatic HIV-infected patients (CDC stage IV), and 28 HIV-seronegative controls. Significantly lower serum levels of 1,25-vitamin D (1,25D) were found in symptomatic patients (median, 34 pg/mL; 25th-75th percentile, 21-45) compared with controls (49 pg/mL; 39-59) and asymptomatic patients (45 pg/mL; 42-50). In HIV-infected subjects, the serum level of 1,25D was positively correlated with CD4+ cell counts in peripheral blood (r = .35, P < .05) and negatively correlated with the level of serum neopterin (r = -.36, P < .01). HIV-infected patients with abnormally low 1,25D (< 25 pg/mL) also had shorter survival times than other HIV-infected subjects (P < .01). Low 1,25D levels did not appear to be related to vitamin D deficiency.

Acquired Immunodeficiency Syndrome↗

PubMed1983

Variation in immunoglobulin levels and circulating immune complexes in sarcoidosis. Correlation with extent of disease and duration of symptoms.

Sixty-three patients with clinically definite sarcoidosis confirmed histologically and/or by a positive Kveim test were studied according to the clinical and radiographic extent and known duration of their disease and symptoms. Immunoglobulin levels were not raised among patients with bilateral hilar lymphadenopathy (BHL) alone, but IgG and IgA were raised among patients with pulmonary sarcoidosis, most markedly among patients with long-standing active disease. Serum IgM was found elevated in extrathoracic sarcoidosis. West Indian males had the highest levels of IgG. The presence of circulating immune complexes reacting with conglutinin was strongly associated with a recent symptomatic onset of sarcoidosis; they were more prevalent in patients with BHL and erythema nodosum. In contrast, polyethylene glycol precipitable immunoglobulins were associated with long-standing active disease and with neurologic involvement.

Adult↗

PubMed1996

Experimental and clinical allogeneic heart transplant rejection: correlations between histology and immune reactivity detected by cytokine messenger RNA.

BACKGROUND: Cytokines produced by host cells infiltrating allogeneic transplants are critical determinants of graft rejection but information on cytokine production during graft rejection remains limited. No reported study on cytokine profiles has compared experimental allograft rejection induced by withdrawal of cyclosporine with clinical transplant rejection that occurs in the presence of therapeutic levels of cyclosporine. METHODS: Functional activities of allograft-infiltrating host cells in sequential endomyocardial biopsies obtained before, during, and after acute heart transplant rejection were determined with the use of the reverse transcriptase-polymerase chain reaction to detect cytokine messenger RNA. These results were correlated with histologic findings in both an experimental canine model of heart transplant and rejection and in clinical human heart transplant recipients. RESULTS: When experimental rejection was induced by withdrawal of immunosuppression, rejection was characterized by the presence of mRNA encoding CD4, CD8, interleukin-2 (but not interleukin-4), interleukin-2 receptor, and tumor necrosis factor-beta. These findings are consistent with a classic T-helper, T-cytotoxic cell-mediated response. However, the cytokine profile of human, clinical heart transplant rejection occurring in the presence of therapeutic levels of immunosuppression differed strikingly. In clinical rejection in human beings, histologic evidence of rejection was not associated with detectable interleukin-2 or interleukin-2 receptor mRNA. CONCLUSIONS: Human, clinical heart rejection can occur in the absence of locally produced interleukin-2; the degree of immunosuppression achieved with cyclosporine A may explain the different results obtained in the canine withdrawal model versus human clinical allograft rejection.

Adult↗

PubMed1995

Sequence evolution of the hypervariable region in the putative envelope region E2/NS1 of hepatitis C virus is correlated with specific humoral immune responses.

Sequence evolution of the hypervariable region 1 (HVR1) in the N terminus of E2/NS1 of hepatitis C virus (HCV) was studied retrospectively in six chimpanzees inoculated with the same genotype 1b strain, containing a unique predominant HVR1 sequence. Immediately after inoculation, all animals contained the same HVR predominant sequence. Two animals developed an acute self-limiting infection. Anti-HVR1 immunoglobulin G (IgG) was produced 40 to 60 days after inoculation and rapidly disappeared after normalization of transaminases. Another chimpanzee, previously infected with human immunodeficiency virus type 1, showed a delayed response to HVR1 epitopes after superinfection with HCV. No sequence variation of HVR1 was observed in these two animals during the transient viremia in the acute phase. Three other chimpanzees developed a chronic HCV infection. During follow up, sequence evolution occurred in two animals and their anti-HVR1 response remained at varying but detectable levels. The first mutations occurred immediately after the production of anti-HVR1 during the acute phase. However, IgM anti-HVR1 was not detectable. Remarkably, HVR1 sequences remained conserved for more than 6 years in another chronically infected animal. This correlated with the complete absence of detectable anti-HVR1 during this period. Seven years after inoculation, anti-HVR1 IgG was produced and coincided with an HVR1 alteration. These results strongly suggest the involvement of neutralizing anti-HVR antibodies in sequence evolution of HVR1 through immune selection.

Amino Acid Sequence↗

PubMedDate not supplied

Environmental monitoring: correlating air measurements of substances with immune response.

In summary, data from animal models would suggest that air measurements of substances can be correlated with immune response, be it immunodepression or either of the two forms of immunostimulation-autoantibody formation or specific immunologic sensitization. However, became immunodepression and autoantibody formation are not specific for a given substance, and because they can be induced by a variety of other factors such as drugs and intercurrent viral infections, it would seem unlikely that correlations between air measurements and measurements of immunodepression or autoantibody formation could be very useful. In contrast, specific immunologic sensitization is a response that can only be induced by exposure to a specific agent. The major problem confronting investigators attempting to perform concentration-response studies in humans is accurate measurement of workplace exposures. If exposures could be reliably quantified, it is likely that concentration-response correlations could be determined for worker groups. This could prove useful for estimating exposure of groups based on aggregate immune response. It would be most useful, however, for determining threshold concentrations below which a very low proportion of workers--perhaps 1 in 100 or even 1 in 1000--would become sensitized. These threshold concentration levels of sensitizing substances could be used to develop permissible exposure levels in the workplace. Reducing workplace sensitization and diseases such as occupational asthma and hypersensitivity pneumonitis would be of obvious benefit to workers, management, government, and society at large.

Air Pollutants, Occupational↗

PubMed2004

Identifying biomarkers and surrogates of tumors (cancer biometrics): correlation with immunotherapies and immune cells.

The presence of inflammatory cells within cancer has been described for quite some time by pathologists, with generally improved outcome associated with their presence in various epithelial neoplasms. Most remarkably, this has included dendritic cells and T cells but more recently NK cells as well. Coupled with the rapid evolution of molecular technology, microarray analyses of primary tumors, serum and tumor proteomics, tumor capture analyses in the peripheral blood (together with quantitative RT-PCR), and novel histochemical markers and tissue microarrays, this provides the opportunity to establish a more effective means to study and classify into subsets various forms of cancer. Much of the current controversy in cancer diagnosis and pathologic assessment of prognosis lies in the application of these techniques in concert with other molecular tools including DNA microarrays, expression of histochemically defined cytokines, proangiogenic factors, and oncogene products, and correlating this with clinical relevance. Molecular detection technologies such as reverse transcriptase polymerase chain reaction, proteomics, and microarray analyses will be validated based on their integration with conventional cancer pathology and cancer diagnostics. Further work is needed to establish which cancer biomarkers and surrogates should be routinely measured and in which settings, and determining the appropriate sample size for such assays that can be validated in retrospective and prospective clinical studies. The ability to integrate these rapidly evolving strategies will consume much of our coordinate effort in cancer and cancer therapeutics for the near future.

Biomarkers, Tumor↗

PubMed2004

Increased immune transcript levels are correlated with acute graft-versus-host disease and cytomegalovirus response after allogeneic stem cell transplantation.

BACKGROUND: Donor T cells are primarily responsible for graft-versus-host disease (GVHD). Three effector pathways have been described for T-cell cytotoxicity: granzyme B/perforin, Fas/Fas ligand (FasL), and secreted molecules such as tumor necrosis factor (TNF)-alpha. Therefore, this study evaluates the gene expression pattern in the peripheral blood of patients after allogeneic stem cell transplantation and correlates the results to acute GVHD. METHODS: Real-time quantitative reverse transcriptase-polymerase chain reaction was used to quantify the gene expression of granzyme B, perforin, FasL, and TNF-alpha in peripheral blood from 53 patients. RESULTS: Samples were available from 27 of the 38 patients with acute GVHD diagnoses. Increased gene expression (>50%) during acute GVHD was detected in 23 of 27, 26 of 27, and 24 of 27 patients for granzyme B, perforin, and FasL, respectively. TNF-alpha showed a diffuse correlation. The median increases were as follows: granzyme B, 7.2x (1.6-183.2); perforin, 5.8x (1.6-254.9); and FasL, 8.5x (1.5-895.6). We also showed that all of the 10 patients with increasing levels of granzyme B, perforin, and FasL during steroid treatment demonstrated persistent or deteriorating GVHD. Patients with increasing transcription levels during cytomegalovirus (CMV) reactivation responded significantly better to therapy than those with declining levels. A total of 13 of 17 patients with increasing levels versus 0 of 11 patients with decreasing levels responded well to CMV treatment (P<0.01). CONCLUSION: Although not specific for acute GVHD, quantitative assessment of immune transcripts may be of value in diagnosing and monitoring acute GVHD. It may also serve as a guide for the clinician in detecting patients who respond poorly to CMV therapy.

Acute Disease↗

PubMed1978

Immune complexes in sarcoidosis: a correlation with activity and duration of disease.

Samples of serum from patients with sarcoidosis were examined for the presence of immune complexes, using the Raji cell line. An indirect immunofluorescent technique was used to detect the binding of immune complexes to the complement receptors of Raji cells. Preliminary studies indicated that the method was sensitive and specific. We studied 44 patients with sarcoidosis who were separable into the following three distinct clinical groups: (1) acute disease (one year or less); (2) chronic active disease (five years or more); and (3) resolved disease (five years or more). In the 26 patients with acute disease, 12 had circulating immune complexes; immune complexes were present in two of the ten patients with chronic active disease. In contrast, immune complexes were absent in patients with resolved disease and normal control subjects. In patients with active disease, there was no apparent correlation between the presence of immune complexes and the stage of disease; however, immune complexes were present in five of the 11 patients with extrapulmonary disease, in seven of 12 patients with elevated concentrations of gamma-globulin, and in four of five of those patients with autoantibodies to lymphocytes.

Acute Disease↗

PubMedDate not supplied

Serological levels of apoptotic bodies, sFAS and TNF in lupus erythematosus.

In our study we have investigated the presence of apoptotic bodies, soluble FAS receptor and TNF (tumor necrosis factor) in three clinical forms of lupus erythematosus. Determinations were performed in attack period of: systemic lupus erythematosus (SLE) for 20 patients, 20 patients with subacute cutaneous lupus erythematosus (SCLE), 20 patients with chronic discoid lupus erythematosus (DLE). Determinations were performed by ELISA (for apoptotic bodies, kit Boehringer, normal values 400-800 mU), (for sFAS, kit R&D Systems, normal values 4500-17000 pg/ml) (for TNF, ELISA kit R&D Systems, normal values 0.4-3.6 pg/ml). Results in SLE: apoptotic bodies were increased in 16 cases (980-1030); sFAS in 18 cases (17000-24000 pg/ml) TNF was increased in all 20 cases (40-140 pg/ml). In SCLE with multiple cutaneous lesions and without internal organs disturbance the apoptotic bodies were increased in 10 cases (960-1030 pg/ml), sFAS in 9 cases (17000-22000 pg/ml), and TNF alpha in 9 cases. In DLE, apoptotic bodies were increased in 2 patients (980-1010 pg/ml), sFAS in 3 patients (17000-20000 pg/ml) and TNF in 2 patients (20-40 pg/mil). Investigated values were slightly correlated with immune parameters (anti dsDNA antibodies), but they were correlated with the presence of renal disturbances or extension of cutaneous lesions. We consider that the presence of increased apoptotic bodies as a result of peripheral mononuclear cells apoptosis appear as a nauto-limiting mechanism in a pathological immune response. The increase of sFAS in lupus patients serum might be interpreted as an alteration of apoptosis respectively a deficit in apoptosis which has as a first consequence the persistence of B and T lymphocytes, activated, in the pathogen immune response.

Apoptosis↗

PubMed2004

Costs of resistance: genetic correlations and potential trade-offs in an insect immune system.

Theory predicts that natural selection will erode additive genetic variation in fitness-related traits. However, numerous studies have found considerable heritable variation in traits related to immune function, which should be closely linked to fitness. This could be due to trade-offs maintaining variation in these traits. We used the Egyptian cotton leafworm, Spodoptera littoralis, as a model system to examine the quantitative genetics of insect immune function. We estimated the heritabilities of several different measures of innate immunity and the genetic correlations between these immune traits and a number of life history traits. Our results provide the first evidence for a potential genetic trade-off within the insect immune system, with antibacterial activity (lysozyme-like) exhibiting a significant negative genetic correlation with haemocyte density, which itself is positively genetically correlated with both haemolymph phenoloxidase activity and cuticular melanization. We speculate on a potential trade-off between defence against parasites and predators, mediated by larval colour, and its role in maintaining genetic variation in traits under natural selection.

Analysis of Variance↗

PubMed1977

Effectiveness of murine leukemia chemotherapy according to the immune state: reconsideration of correlations between chemotherapy, tumour cell killing, and survival time.

Cyclophosphamide (CPM) chemotherapy (134 mg/kg) of L1210 leukemia is less efficient in mice previously immunodepressed by antithymocyte serum (ATS) than in non-ATS pretreated mice. On the other hand, administration of a higher dose of CPM (403 mg/kg), which kills a greater number of leukemic cells but induces an immunodepression, according to the skin graft test, results in a shorter survival time than does the administration of a lower dose of CPM (134 mg/kg), capable of killing fewer leukemic cells but not inducing such an immunodepression. Thus, it appears that: (1) the antileukemic effect of the same dose of a chemotherapeutic drug is less efficient in immunodepressed than in nonimmunodepressed hosts, and (2) calculation of the number of neoplastic cells killed by a given chemotherapy by extrapolation from the survival time may lead to erroneous conclusions.

Animals↗

PubMed1977

Cellular and humoral immunity in non-Hodgkin's lymphoma: correlation of immunodeficiencies with clinicopathologic factors.

Immune function was evaluated in 28 non-Hodgkin's lymphoma patients in an attempt to correlate the occurrence of immunodeficiency with the prognostic clinicopathologic factors, lymph-node histology, and clinical stage of disease. Anergy to a battery of recall antigens occurred infrequently (4/28) and only in patients who had Stage IV disease (4/8) (p = less than .004), but did not correlate with lymph-node histology. In contrast to anergy, cellular immunodeficiencies were often detected by lack of response to keyhole limpet hemocyanin immunization in patients regardless of stage. Reductions in at least two of three Ig fractions were found in a third of the patients, with, again, a significantly greater incidence in Stage IV patients (p = less than .005). No significant correlation with histologic type was possible. The response to phytohemagglutinin in vitro was reduced in the patients, but this was of no correlative value.

Antigens↗

PubMed2006

Supplementation with active hexose correlated compound increases the innate immune response of young mice to primary influenza infection.

The emergence of H5N1 avian influenza and the threat of new or adapted viruses in bioterrorism have created an urgent interest in identifying agents to enhance the immune response to primary virus infection. Active hexose correlated compound (AHCC) is a natural mushroom extract reported to increase natural killer (NK) cell activity, survival, and bacterial clearance in young mice. However, the effects of AHCC on the response to viral infections have not been studied. In this study, young C57BL/6 mice were supplemented with 1 g AHCC/(kg body weight x d) for 1 wk prior to and throughout infection with influenza A (H1N1, PR8). Supplementation increased survival, decreased the severity of infection, and shortened recovery time following intranasal infection with flu, as determined by the recovery of body weight and epithelial integrity in the lungs. AHCC increased NK activity in lungs at d 1 (P < 0.05) and d 4 (P < 0.01) and in the spleen at d 2 postinfection (P < 0.01). Supplementation increased the percentage (P < 0.05) and number (P < 0.01) of NK1.1+ cells in the lung and reduced the infiltration of lymphocytes and macrophages compared with controls (P < 0.01). These data suggest that AHCC supplementation boosts NK activity, improves survival, and reduces the severity of influenza infection in young mice. Bolstering innate immunity with dietary bioactives may be one avenue for improving the immune response to primary flu infection.

Adjuvants, Immunologic↗

PubMed2004

Hematopoietic stem cell dose correlates with the speed of immune reconstitution after stem cell transplantation.

In the current study, we tested whether higher numbers of hematopoietic stem cells correlate with the speed of immune reconstitution in a congenic transplantation model (C57BL/Ka, CD45.1, Thy1.1-->C57BL/6, CD45.2, Thy1.2) using purified hematopoietic stem cells (c-Kit(+)Thy1.1(low)Lin(-/low)Sca-1(+)). There were 3 different doses of stem cells used (400, 1000, and 5000). Phenotypic analyses in peripheral blood and spleen demonstrated that higher numbers of infused stem cells are associated with more rapid regeneration of T cells (CD4(+), CD8(+), naive CD4(+), naive CD8(+)) and B cells at early time points. The numbers of T and B cells eventually became equivalent between different dose groups at late time points. Production of interleukin-2 and inter-feron-gamma per T cell was similar regardless of stem cell dose even when tested at the time when there were significant differences in peripheral T-cell counts. The improved immune recovery was attributed to a more rapid regeneration of donor-type immune cells. Higher numbers of total thymocytes and signal joint T-cell receptor excision circles were observed in the higher dose stem cell recipients, suggesting that accelerated regeneration of T cells was due to enhanced thymopoiesis.

Animals↗

PubMed1988

Evolution of expression of hepatitis B surface and core antigens (HBsAg, HBcAg) in resected primary and recurrent hepatocellular carcinoma in HBsAg carriers in Taiwan. Correlation with local host immune response.

Studies were conducted on the evolution of hepatitis B virus (HBV) surface and core antigens (HBsAg and HBcAg) in the tumors of both primary and recurrent hepatocellular carcinoma (HCC) in 27 HBsAg carriers; these were followed for up to 8 years after the resection of the primary tumor. Twenty-seven primary and 34 recurrent tumors were included. HBV antigens were detected in the tumor of the primary HCC in ten cases (37%): six (22.2%) had both antigens (Group I) and four (14.8%) had HBsAg alone (Group II). The remaining 17 cases were negative for both antigens (Group III). Intrahepatic tumor recurrence occurred in 17 cases; both HBcAg and HBsAg were found in the recurrent HCC in four of five HBcAg-positive cases (Group I). In contrast, HBcAg was detected in none of the other 12 cases (Group II, 0 of one; Group III, 0 of 11), and HBsAg in only one (Group II, 0 of one; Group III, one of 11), P less than 0.03 and P less than 0.02, respectively. Groups I, II, and III had extrahepatic recurrence in two, four, and seven cases, respectively. HBcAg was detected in none, while HBsAg was found in only one case (7.7%). The frequent detection of both antigens in the primary HCC and even in the intrahepatic recurrences suggests that HBV replication in HCC may occur more commonly than previously perceived, especially in the small HCC. Failure to detect HBV antigens in the extrahepatic recurrences suggests that the switch-off of the viral gene expression, particularly the core gene, may be an event related to the extrahepatic growth of HCC. HBV antigen expression in HCC is associated with more evident lymphocyte infiltration; this local host immune response may in turn result in a negative selection and expansion of the antigen-negative HCC cell clones. This suggestion is in accord with the fact that HBV antigens, particularly HBcAg, are rarely detected in advanced HCC.

Carcinoma, Hepatocellular↗