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PubMed1994

Immune and serologic profiles of HIV-infected and noninfected hemophilic children and adolescents. Hemophilia Growth and Development Study Group.

OBJECTIVES: To assess relationships among the effects of HIV on hemophilic children and adolescents' immunologic parameters and vaccine-related serology. METHODS: We analyzed data from extensive baseline immunologic evaluations of 207 HIV antibody-positive (HIV+) and 126 HIV antibody-negative (HIV-) hemophilic children and adolescents. RESULTS: HIV+ and HIV- participants differed significantly in T-lymphocyte subpopulation numbers, immunoglobulin levels, and seroprevalence rates for diphtheria toxoid, measles, and mumps antigens, IgG levels, IgM levels, and serologic titers to vaccine antigens showed little correlation with T-cell parameters. Proportionately more HIV+ participants were nonreactive to each and all of a panel of 7 skin test antigens (71% vs 28% anergic, RR 2.6). The odds of anergy increased 1.6 times for every decline of 200 CD4+ cells/microliters. CONCLUSIONS: HIV had significant, largely independent T- and B-lymphocyte effects on this pediatric cohort.

Adolescent↗
PubMed2003

Molecular profiling of the immune response in colon cancer using protein microarrays: occurrence of autoantibodies to ubiquitin C-terminal hydrolase L3.

We implemented a protein microarray approach to identify proteins that induce a humoral response in colon cancer. Solubilized proteins from the LoVo colon adenocarcinoma cell line were separated into 1760 fractions, arrayed onto nitrocellulose-coated slides, and hybridized with individual sera from 15 newly diagnosed patients with colon cancer, 15 with lung cancer, and 15 healthy subjects. 39/1760 fractions showed enhanced reactivity with sera from patients with colon cancer (p < 0.01) relative to healthy controls. A distinct pattern of reactivity was observed with sera from colon cancer relative to lung cancer. One fraction that exhibited reactivity with 9/15 colon cancer sera was subjected to mass spectrometry leading to the identification of ubiquitin C-terminal hydrolase isozyme 3 (UCH-L3) as a constituent. To validate the occurrence of autoantibodies to UCH-L3, independent analysis was done by means of Western blots. UCH-L3 antibodies were detected in 19/43 sera from patients with colon cancer, and in 0/54 sera from subjects with lung cancer (24), colon adenoma (15) or otherwise healthy (15). Our findings indicate the occurrence of an immune response to a broad set of antigens in colon cancer and the feasibility of identifying the antigenic targets using a combination of protein microarrays and mass spectrometry.

Autoantibodies↗
PubMed1993

Murine susceptibility to mercury. II. autoantibody profiles and renal immune deposits in hybrid, backcross, and H-2d congenic mice.

Inorganic mercury causes systemic autoimmunity and/or immune-complex deposits in strains of mice carrying certain H-2 haplotypes, for example H-2s and H-2d. This study aimed at describing the genetic mechanisms regulating these reactions. Inbred SJL, C57BL/6J (B6), C57BL/10J (B10), and DBA mice, F1(SJL x DBA), F1(SJL x B6), and F2(SJL x B6) hybrids, and mice derived from a backcross of SJL or B6 mice to F1(SJL x B6) hybrids were given subcutaneous injections of either 1.6 mg HgCl2/kg body wt or 0.1 ml NaCl every third day for 6 weeks. SJL mice developed a high titer of serum antinucleolar antibodies (ANoA) of the IgG class targeting the nucleolar protein fibrillarin and a significantly increased titer of IgG and C3 colocalized as granular deposits in the renal mesangium and vessel walls. The B6 and DBA strains lacked ANoA and showed no increase in titers of immune deposits. Nine percent of mercury-treated F1(SJL x DBA) hybrids developed IgG-ANoA which were of a low titer, and only occasional hybrids showed an increased titer of granular mesangial IgG deposits. Mercury treatment induced ANoA of low titer in 41% of F1(SJL x B6) hybrids, and 24% had increased granular mesangial immune deposits. Four of 61 mercury-treated BC-[SJL x F1(SJL x B6)] mice showed ANoA which were of a high titer and targeted the nucleolar protein fibrillarin. ANoA were not found in 55 mercury-treated F2(SJL x B6) hybrids or in 56 mercury-treated mice derived from a backcross of B6 mice to F1(SJL x B6) hybrids. Increased mesangial immune deposits were regularly accompanied by vessel wall deposits in F1- and F2(SJL x B6) hybrids, but only 53% of BC(SJL x F1[SJL x B6]) mice with increased mesangial deposits had vessel wall deposits. Vessel wall immune deposits were only present in mice with increased mesangial deposits. A majority of mice which developed significantly increased titers of mesangial IC deposits showed no ANoA. In conclusion, the susceptibility in SJL mice to develop ANoA during mercury treatment, which has been shown to reside in the H-2A locus, was codominantly inherited in a cross with mice carrying the H-2b and H2d haplotypes. Non-H-2 genes dampened ANoA expression to a degree which varied between the strains. Since renal vessel and mesangial IC deposits developed in backcross mice lacking serum ANoA, these deposits must contain IC not related to fibrillarin-antifibrillarin.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Complement profile in childhood immune thrombocytopenic purpura: a prospective pilot study.

Immune thrombocytopenic purpura (ITP) is a frequent, usually acute hematologic complication of viral diseases in children. Its evolution is usually benign with spontaneous resolution. Some authors have raised the hypothesis of a possible role of the complement system in the pathogenesis of ITP. In the present study, we measured the complement system components in 25 children with ITP. The complement system was abnormal in most patients with ITP as compared with the control group: 20 of the 25 patients had at least one low-component level. The most affected components were properdin, factor H (p=0.005 and p=0.001, respectively), C1q, C9, and factor B. Our results may indicate a possible role for the complement system in the pathogenesis of pediatric ITP.

Adolescent↗
PubMed1988

Profiling of circulating immune complexes by high performance liquid affinity chromatography (HPLAC) on a protein A-silica matrix.

Protein A, a cell wall protein found in bacterial strains of Staphylococcus aureus, has been extensively used in the analysis and purification of immunoglobulins and immune complexes. By binding protein A to microparticulate silica (high performance liquid affinity chromatography, HPLAC), a rapid and efficient chromatographic system was obtained for the separation and analysis of circulating immune complexes. The method was applied to the separation of artificial immune complexes as well as to plasma samples from patients with immune complex associated diseases such as SLE and RA. It was possible to distinguish certain subpopulations of circulating immune complexes by performing pH gradients on the protein A silica HPLAC column.

Antigen-Antibody Complex↗
PubMed1992

Murine susceptibility to mercury. I. Autoantibody profiles and systemic immune deposits in inbred, congenic, and intra-H-2 recombinant strains.

Inbred, congenic, and intra-H-2-recombinant mouse strains were given subcutaneous injections of either 1.6 mg HgCl2/kg body wt or 0.1 ml NaCl thrice weekly for 5-6 weeks. Mercury-treated mice from strains carrying the H-2s haplotype developed antinucleolar antibodies (ANoA), which targeted the 34-kDa nucleolar protein fibrillarin, and in some instances also nucleolar proteins of 60-70 and 10-15 kDa, the latter corresponding to histones. Strains with H-2b and H-2d haplotypes were resistant to induction of ANoA. The susceptibility to development of AnoA/antifibrillarin antibodies (AFA) was mapped to the H-2A-region using intra-H-2-recombinant strains. We were not able to confirm earlier reports that expression of H-2E genes dampens the development of ANoA. Mercury treatment caused a substantial increase in the titer of antichromatin (ACA) and/or antihistone (AHA) antibodies in a fraction of SJL/J, A.SW, A.TH, B10.S, and B10.HTT mice (H-2s), and in A/J (H-2k) mice, whereas mice from the C57BL/6J and C57BL/10J (H-2b), and the DBA and BALB/c (H-2d) strains were low or nonresponders. The development of AHA and ACA could not be linked to the H-2 complex. A significant, substantial increase of granular mesangial and systemic vessel wall IgG deposits occurred in mice with serum ANoA/AFA. However, the B10.S(9R) and B10.HTT strains, which express the H-2E genes, developed only an intermediately increased titer of mesangial IgG deposits. Systemic vessel wall IgG deposits occurred in only 60-80% of the B10.S(9R) mice and in none of the B10.HTT mice. This contrasted with the high titer of mesangial IgG deposits and uniform development of systemic vessel wall IgG deposits observed in B10.S mice not expressing H-2E. Mice with mesangial IgG deposits showed a mild glomerulonephritis. There was no systemic vasculitis. The susceptibility to development of ANoA, AHA, ACA, and systemic, granular IgG deposits in the B10.S strain was influenced by the sex, since males showed less uniform development of these immunopathologic features than females.

Animals↗
PubMed2026

Spatially Distinct Bone Marrow Sites Are Asymmetrically Impacted by Inflammatory Cardiovascular Disease.

Cardiovascular disease, a leading cause of mortality globally, is increasingly recognized to involve complex bone marrow-driven inflammatory mechanisms, yet the impact on spatially distinct bone marrow sites and comorbidities remains poorly understood. To address this, we developed MarrowMet, a methodology for whole-body, site-specific quantification of bone marrow activity. The approach involves intravenously injecting the metabolic tracer 18F-fluorodeoxyglucose (18F-FDG) in mice, followed by bone excision to quantify site-specific bone marrow activity, with values then superimposed on a whole-body mouse atlas. After establishing that 18F-FDG bone marrow uptake strongly correlated with inflammatory activity, we applied MarrowMet to map site-specific activation patterns across diverse cardiovascular pathologies, including mouse models of inflammatory atherosclerosis, acute ischemic events, acute respiratory distress syndrome, metabolic syndrome, and aging. MarrowMet guided the selection of bone marrow regions of interest for in-depth mass cytometric analyses, with the skull and sternum emerging as critical sites exhibiting distinct immune and metabolic profiles in cardiovascular disease. These results challenge the prevailing view that femoral marrow represents systemic activity. Together, this work lays a foundation for whole-body exploration of bone marrow heterogeneity, yielding critical insights into cardiovascular disease and associated inflammatory responses, and MarrowMet can be readily adopted to profile other immune mechanisms in a variety of pathologies, including cancer and autoimmune diseases.

(18)F-FDG↗
PubMed1981

Idiotype profile of an immune response. I. Contrasts in idiotypic dominance between primary and secondary responses and between IgM and IgG plaque-forming cells.

The primary response of A/J mice to p-azobenzenearsonate-keyhole limpet hemocyanin (ABA-KLH) was investigated. A day-by-day analysis at the plaque- forming cell (PFC) level was performed, with inhibition by anti-cross- reactive idiotype (CRI) serum to determine percentage of CRI(+) PFC. A regular pattern in the dynamics of Id (idiotype) dominance was observed. Just as in the NP-b and NP-a systems (9, 12), the major Id (CRI) is more dominant in primary than in secondary or hyperimmune responses. This trend is more apparent in IgG PFC which are generally 80-95 percent CRI(+) at day 10 in the primary response but only 30-40 percent CRI(+) at day 10 in secondary or hyperimmune responses. A somewhat different pattern is seen with IgM PFC. These may reach a peak of 85 percent CRI(+) in the primary response, but secondary or hyperimmune IgM PFC, which are lower in numbers than IgG PFC, remain high in CRI content at approximately 70 percent. The PFC data on extent of id dominance in secondary or hyperimmune responses is fully compatible with previously reported serological data by others. Analysis of IgG PFC by hapten inhibition indicated that heterogeneity was in the order secondary PFC {greater than} primary PFC {greater than} hybridoma AK-2.2 PFC with H(75)/H(25) values of 22.9, 6.2, and 2.7, respectively; where H(75) and H(25) are the hapten concentrations required to give 75 percent and 25 percent of inhibition of PFC, respectively. Hapten inhibition data also suggested that secondary IgG PFC were 10 times higher in median binding avidity for ABA-L-tyrosine than primary IgG PFC. The kinetic analysis strongly indicated that CRI(+) IgM PFC were preferentially switched to IgG PFC in the primary response. In both studies, the CRI content of the earliest-appearing IgG PFC was significantly higher than that of IgM PFC on that day. For example, in one case IgM PFC were 60 percent CRI + on day 6 whereas IgG PFC were 100 percent CRI(+). The high Id dominance and selective isotype switching may have either a B or a T cell basis.

Animals↗
PubMed1983

Idiotype profile of an immune response. II. Reversal of the relative dominance of major and minor cross-reactive idiotypes in arsonate-specific T-independent responses.

Two different cross-reactive idiotype (CRI) groups are distinguishable in the Ab response of A/J mice to the p-azobenzenearsonate (ABA) hapten: CRIA and CRIm. These two groups showed distinct patterns of relative dominance in the ensuing response depending on whether the inducing Ag was a T cell-dependent (TD) form of ABA, such as ABA-KLH or ABA-CGG, or a T-independent type 1 (TI-1) form, such as ABA-Brucella abortus or ABA-lipopolysaccharide (LPS), and on whether the response was elicited in vivo or in vitro. The CRI+ component of primary in vivo plaque-forming cell (PFC) responses to TD ABA Ags was largely (greater than 90%) CRIA+ as was, to a slightly lesser extent (greater than 75%) the CRI+ portion of secondary or hyperimmune serum Ab or PFC responses to the same Ags. In contrast, in vivo primary and hyperimmune PFC responses to ABA-Bru or ABA-LPS showed a significantly lower CRIA/CRI ratio, averaging 0.5-0.6, with some individual mice giving figures as low as 0.2, indicating predominance of CRIm over CRIA. Serological analysis of hyperimmune anti-ABA Abs from a group of 5 A/J mice immunized with ABA-Bru gave a figure of less than 0.5 for the CRIA/CRI ratio. The most striking disparity from the TD pattern was seen in primary in vitro PFC responses to the TI ABA Ags; here ratios of less than 0.2 were generally seen. Since T cell removal did not alter the Id pattern in the TI responses, CRIA-specific Ts cells do not account for the weak expression of CRIA in such responses. We propose a model that explains these results on the basis of differential expression of IdX dominance by two distinct B cell subpopulations--equatable to the Lyb-5+ and Lyb-5- B cell subsets--along with differential relative activation of these subsets in different types of responses. Examination of anti-ABA PFC responses of F1 progeny of CBA/N and A/J mice to ABA-Bru lends support to this hypothesis since CRIA expression was significantly lower in mice with the xid defect.

Animals↗
PubMed1991

Effects of SMS 201-995 on the pharmacokinetic profile and cellular immune and toxic effects of cyclosporine in male Wistar rats.

The immunosuppressant cyclosporine and the long-acting somatostatin analog SMS 201-995 (octreotide acetate) may have to be given simultaneously in diseases such as pancreatic transplantation. The aim of the study was to evaluate the effects of SMS 201-995 on the pharmacokinetics of cyclosporine, and to assess whether the addition of SMS 201-995 altered some of the cellular immune and toxic (renal, hepatic, glucose tolerance) effects of cyclosporine. Male Wistar rats were treated with cyclosporine 10 mg/kg/day, SMS 201-995 100 micrograms/kg b.i.d., a combination of the two drugs, or the vehicle alone. The addition of SMS 201-995 delayed the peak plasma levels of cyclosporine without affecting the through levels, and did not alter the effects of cyclosporine on the mononuclear cell subsets. This combination caused significant increases in plasma creatinine and hepatic enzymes, suggesting renal and hepatic toxicity, and severe glucose intolerance. If present in humans, the appearance of severe glucose intolerance with combined administration of SMS 201-995 and cyclosporine for pancreatic transplantation could be misinterpreted as rejection and lead to inappropriate interventions.

Animals↗
PubMed2005

TH1/TH2 cytokine profile of the immune response in limb component transplantation.

BACKGROUND: The purpose of this study was to define the cytokine secretion pattern during limb allograft rejection and to determine its correlation to differential tissue antigenicity of limb allograft components. METHODS: Twenty-five C57Bl/6 mice (H-2Kb) were randomized to six groups. The experimental groups were recipients of vascularized Balb/c mice (H-2Kd) allografts consisting of skin, muscle, whole limb, or limb with the skin removed or nonvascularized nerve allografts. The unmodified rejection response was studied by histology, flow cytometry, and ELISPOT assay to quantify IFN-gamma (Th1) and IL-4 (Th2) production. RESULTS: The greatest Th1 response was seen in the recipients of allografts composed of skin (973.3 +/- 93 spots/million spleen cells; mean +/- SEM), followed by whole limb (961.3 +/- 86/million), nerve (613.3 +/- 245/million), limb with skin removed (483 +/- 246/million), and then muscle (460 +/- 234/million). Recipients of skin, whole limb, and nerve allografts had the highest IFN-gamma:IL-4 ratios, or greatest Th1 deviation, of 3.1 +/- 0.4, 3.0 +/- 0.2, and 2.9 +/- 0.6, respectively. These were significantly greater than those that received muscle (0.9 +/- 0.3) and limb allografts with skin removed (1.0 +/- 0.4) (p < 0.05). CONCLUSIONS: The skin component produced the greatest Th1 activation of the immune response and appears to be a critical component of the overall antigenicity of the whole limb allograft, as evidenced by the Th2 shift seen when the skin was removed. Muscle produced the least Th1 differentiation, with nerve being intermediate.

Animals↗
PubMed2000

[Regulation of defence and allergic reaction in infections with parasites].

Cytokines regulate development, differentiation and expression of effector function of the immune system. The profile of immune reactions depends on cytokine contents at the recognition of parasite. However, parasites themselves can modify immunological events and favourite these, which allow them to survive. The host immune defence can be transformed into the chronic reaction. Inflammatory reactions result from the recruitment of different cells, to the site where worms are localised. The eosinophil and mast cell migration preferentially is induced. These cells play also a major role in immediate allergic responses. Mast cells can bind allergen-specific IgE to their FcepsilonRI, the high affinity receptor for IgE. Eosinophils, through their receptors for IgG1, IgG2, IgA and IgE are mainly involved in the cytotoxic reaction directed against parasites. Crosslinking of these receptors by antigen binding will lead to subsequent release of stored mediators and cytokines. Granular materials released from mast cell accelerate inflammatory reaction and in the case of intestinal worm parasites may be involved in the expulsion phenomenon. However these cells may also induce Th2 related immunological response because they produce and release of IL-4. Eosinophils are required into the tissue and release cytotoxic and stress proteins including reactive oxygen species. Parasites are destroyed but accelerated reaction results in the destruction of host proteins and cells. Antibodies, cytokines, chemokines and adhesion molecules are essential for elevation of defence against parasites. The role of cytokines, emphasizing IL-5, and function of eosinophils, mast cells and IgE are discussed in terms of induction and effector mechanisms during parasite infections.

Allergens↗
PubMed1995

Immunotherapy with transfer factor of recurrent herpes simplex type I.

This clinical trial of Transfer Factor, an immunomodulator, in the treatment of herpes simplex type I, proved this agent to be more effective as regards duration of acute phase recurrences as well as the frequency of the reappearance of relapses of this disease. The evaluation was made in 20 patients whose disease had been treated before with other therapeutic agents (including acyclovir) which permitted them to be their own controls for the comparative data obtained and submitted to statistical analysis of the two parameters mentioned, duration of the acute phase and frequency of relapses. Patients with compromised cellular immunity or with any additional disease were excluded from the study. Transfer factor, one unit, was administered subcutaneously daily for 3 to 4 days during the acute phase of the disease, and subsequently at 15-day intervals for the first 6 months; followed by a continuation of monthly injections until the termination of the study period. In six of the 20 patients there was a recurrence of the disease while receiving maintenance dosages of TF. These patients were again given the full initial dosage schedule and reinstated again with the maintenance dosage. In the initial eight patients, an immune status profile was obtained, and all results were found to be in the normal range. This was considered sufficient evidence that the criteria for the selection of patients excluded any with detectable variations in the profile of the immune status, and it was decided to eliminate this as a prerequisite for participating in the study. The results showed an important improvement in the response to transfer factor immune modulation therapy. A statistically significant reduction in the frequency of recurrences within a one month period, the Student t test gave a p = 0.0001 in TF treated patients. The average duration in days of the acute phase also showed an important difference in favor of the TF treatment. The U Mann-Whitney test gave a p = 0.0005. These results suggest that, at present, TF may be considered the therapeutic agent of choice in the treatment of herpes simplex type 1 disease.

Adolescent↗
PubMed1993

[The immune status and hormonal profile of patients with idiopathic thrombocytopenic purpura].

Immune and endocrine parameters were studied in patients with autoimmune thrombocytopenic purpura treated with glucocorticosteroids. Initial differences were registered in the levels of endogenic cortisol, lymphocyte cortisol-resistant fraction, circulating immune complexes and populations of immature lymphocytes for the therapy responders and resistant patients. The findings may be used in rating the efficacy of the on-going treatment.

Adolescent↗
PubMed2004

Distortion of the self-reactive IgG antibody repertoire in multiple sclerosis as a new diagnostic tool.

To date, none of the myelin-associated Ag targets definitively discriminates between the immune response observed in multiple sclerosis (MS) patients and healthy subjects. However, it has been shown recently that analysis of global immune Ab profiles such as natural autoantibody reactivities can help to distinguish between normal individuals and patients suffering from various immune diseases. The aim of our study was to compare the global IgG immune response against brain self-Ags in sera from 82 MS patients and 27 healthy subjects. The analysis of the immune profiles was performed by Western blotting, and data were subjected to linear discriminant analysis. Particular patterns of IgG reactivity were found in healthy subjects, Sjögren patients, and MS patients. Moreover, this approach separated the three clinical forms of MS with a high concordance rate with the clinical data (kappa value, 77.8%). Our study suggests, for the first time, that serum IgG Ab repertoires are able to distinguish MS patients. In addition, our data suggest that patterns of IgG reactivity could model the pathological processes underlying the various forms of MS. Further characterization of such discriminant Ags could provide useful information regarding their potent role in pathogenesis or regulatory processes in MS.

Adult↗
PubMed2006

Innate immune response gene expression profiles of N9 microglia are pathogen-type specific.

Glial cells, particularly microglia, are thought to play a pivotal role in initiating and guiding innate immune responses to CNS infections and in perpetuating inflammation and pathology in CNS diseases such as multiple sclerosis and Alzheimer's disease. We describe here the development and use of a new microarray designed to specifically profile transcript expression of innate immunity genes. Microarray analysis validated by quantitative PCR demonstrated an extensive range of pattern recognition receptor gene expression in resting N9 microglia, including Toll-like receptors, scavenger receptors and lectins. Stimulation with LPS or infection with virus modulated pattern recognition receptor, cytokine, chemokine and other innate immune transcripts in a distinct and stimulus-specific manner. This study demonstrates that a single glial cell phenotype has an innate capability to detect infection, determine its form and generate specific responses.

Alphavirus Infections↗