Serological profile of auto-immune haemolytic anaemia.
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Anemia, Hemolytic, Autoimmune↗
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Integrative multi-omics profiling of insomnia-related molecular features reveals microbiome, immune, and therapy-relevant heterogeneity in colorectal cancer.
Emerging evidence implicates insomnia as a potential risk factor in carcinogenesis, potentially involving systemic inflammation, circadian disruption, and microbiome alterations. However, the molecular associations linking insomnia-related features to colorectal cancer (CRC), particularly with respect to tumor biology, immune microenvironmental states, and therapy-relevant phenotypes, remain largely unexplored. Multi-omics integration of genomic, transcriptomic, and microbiome data from 3,026 CRC patients across seven independent cohorts, including a large, well-annotated Clinical Omics study of Colorectal Cancer in China (COCC) cohort, enabled insomnia-based molecular classification through unsupervised non-negative matrix factorization (NMF) clustering. The insomnia subtype (IS) was biologically characterized via pathway enrichment, immune deconvolution, microbial profiling, and single-cell transcriptomics. Furthermore, an insomnia score (ISscore) was developed and validated in multiple cohorts for risk stratification and assessment of treatment-response-related indicators in CRC. Unsupervised clustering revealed two distinct molecular subtypes (IS1/IS2), with IS2 demonstrating significantly poorer survival. IS2 exhibited marked activation of EMT/angiogenesis pathways versus cell cycle activation in IS1. The IS2 microenvironment showed increased immunosuppression-related infiltration and exhausted T cell signatures, together with intratumoral microbiome variation characterized by depletion of Ruminococcaceae UCG-002 and enrichment of Hungatella/Selenomonas. The ISscore system stratified survival risk and was associated with computational indicators of immunotherapy response. Single-cell analysis nominated PPIA-BSG as a potential cell-cell communication signal involving high-ISscore tumor cells, CXCL12+ endothelial cells, and CLEC9A+ dendritic cell subsets. This multi-omics characterization of insomnia-CRC interplay suggests that insomnia-related molecular features are associated with an immunologically distinct and microbiome-altered tumor ecosystem. The ISscore provides a reproducible framework for capturing insomnia-related molecular heterogeneity, supporting risk stratification and future evaluation of therapy-relevant phenotypes.IMPORTANCEChronic insomnia affects millions, but it is not typically considered a cancer risk factor. Our study, analyzing vast biological data from over 3,000 colorectal cancer patients, uncovers a potential link between a person's predisposition to insomnia and their risk of developing this disease. This suggests that the biological pathways related to sleep may play a role in cancer development. Understanding this connection opens up new avenues for identifying individuals at higher risk and developing novel prevention strategies for colorectal cancer.
colorectal cancer↗
Neutralizing antibody responses elicited in mice immunized with recombinant bacillus Calmette-Guérin producing the Schistosoma mansoni glutathione S-transferase.
Schistosomiasis is a group of severe parasitic diseases, in humans and domestic animals, that are especially of importance in the developing world. No efficacious vaccine is currently available. However, Ab-mediated immune responses against the 28-kDa glutathione S-transferase of Schistosoma mansoni (Sm28GST) appear to be involved in protection. This Ag was produced in recombinant Mycobacterium bovis bacillus Calmette-Guérin (BCG). The recombinant protein bound glutathione and expressed enzymatic activity, indicating that the active site of Sm28GST was folded properly. Single i.v., i.p., s.c., or intranasal immunizations with rBCG in BALB/c mice resulted in significant anti-SM28GST Ab responses, which were enhanced by a booster dose. The Ab responses remained high for at least 1 yr after immunization. Analyses of the isotype profiles indicated that i.v. immunized mice produced high titers of anti-Sm28GST IgG2a, and less IgG2b and IgG1. Mice immunized by the s.c. route initially also produced high levels of IgG2a and low titers of IgG1 and IgG2b, but the titers of the latter two isotypes increased gradually thereafter, tending toward a mixed profile. Intraperitoneal immunization provided a mixed profile directly after the first administration. High titers of anti-Sm28GST Abs also corresponded to high levels of neutralization of the enzymatic activity. These results indicate that rBCG induces strong IgG1, IgG2a, and IgG2b, and neutralizing Ab responses against Sm28GST, which has been found to correlate with protection against S. mansoni in humans.
Animals↗
Complement activation and impaired capacity to solubilize immune complexes or to prevent their formation in essential mixed cryoglobulinemia.
The complement profile, the immune complex solubilizing capacity (ICSC), the immune complex precipitation inhibition capacity (ICPIC), the presence of cryoprecipitable material, and the presence of immune-aggregate- and non-immune-aggregate mediated C1q-binding activity was assessed in serum samples from 23 patients suffering from essential mixed cryoglobulinemia (EMC). No correlation between the levels of cryoglobulins and the clinical activity of EMC was found. The mean C1q-binding activity in EMC serum samples was abnormally elevated 28 +/- 29% (mean +/- SD). In six out of eight serum samples that contained C1q-binding material, evidence was obtained that such material was of the complexed immunoglobulin G (IgG) type. Among the levels of C1q, C1r, C2, C4, C3, C5, C6, C1-inhibitor, C3d, B, I, H, as well as the total hemolytic activity and the activity of the alternative pathway of the complement, the mean serum concentrations of C1, C2, and C4 and in consequence the mean total hemolytic activity were significantly reduced, whereas the mean levels of C3d were significantly elevated in the EMC serum samples. The capacity of the 23 EMC serum samples to solubilize preformed immune precipitates from bovine serum albumin (BSA) and rabbit anti-BSA antibodies as well as their capacity to prevent the formation of the precipitable form of such complexes was analyzed. Compared to the ICSC and the ICPIC of 30 normal human sera, the ICSC and the ICPIC of EMC serum samples were reduced to 57 +/- 24% and 38 +/- 33%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Sex-related differences in immune development and the expression of atopy in early childhood.
BACKGROUND: Sex and age are known to influence the clinical expression of asthma and allergic diseases. OBJECTIVE: We sought to evaluate whether immune response profiles also vary by sex and age. METHODS: We performed a prospective birth cohort study (Childhood Origins of Asthma) designed to evaluate interactions among age, sex, immune responses, and virus infections on the development of asthma and allergic diseases. Two hundred eighty-nine subjects were enrolled at birth, and 275 maintained prospective follow-up for 3 years. Cytokine response profiles at birth, 1, and 3 years of age; rates of wheezing, atopic dermatitis, and viral illnesses; and biomarkers of atopy, including total and specific IgE levels and peripheral eosinophil counts, were evaluated. RESULTS: PHA-induced IFN-gamma responses were higher in boys at 1 year of age (median, 35 vs 19 pg/mL; P < .001) and at 3 years of age (median, 282 vs 181 pg/mL; P = .07). Among children who wheezed during the third year of life, boys had increased IFN-gamma, IL-5, and IL-13 responses at age 3 years (P < .001, P = .008, and P = .01, respectively). Boys also demonstrated increased rates of sensitization (P = .05 at year 1), total IgE levels (P = .03 at year 1 and P = .006 at year 3), and peripheral eosinophil counts (2.62 vs 1.85; P = .05 at year 3). CONCLUSION: Sex-specific differences in immune responses develop during early childhood; some of these differences developmentally proceed, whereas others occur in parallel to the clinical expression of various atopic phenotypes. CLINICAL IMPLICATIONS: The differential expression of atopic diseases between boys and girls in early childhood is accompanied by sex-specific differences in immune response profiles.
Cells, Cultured↗
The correlation of DPM1 overexpression with immune infiltration and poor prognosis in hepatocellular carcinoma.
BACKGROUND: The DPM1 gene, crucial for glycosylation processes, has shown abnormal expression in various cancers, raising interest in its potential oncogenic role and as a biomarker in hepatocellular carcinoma (HCC). METHODS: Transcriptomic data were obtained from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. DPM1 expression levels were compared between HCC tissues and adjacent normal tissues. Clinical correlations were assessed using statistical analyses, including survival analysis and multivariate Cox regression. Immune microenvironment profiling was conducted to evaluate associations between DPM1 expression and immune cell infiltration patterns. RESULTS: Elevated DPM1 levels were associated with advanced tumor stages (P < 0.001), higher pathologic T stage (P < 0.001), increased histologic grade (P < 0.001), tumor positivity (P < 0.001), tissue inflammation (P < 0.001), and elevated alpha-fetoprotein levels (AFP > 400 ng/mL, P < 0.05). Multivariate Cox regression analysis identified DPM1 as an independent prognostic factor for reduced overall survival (HR = 1.990, 95% CI 1.390-2.848). Immunological analysis revealed that DPM1 expression was positively correlated with T helper cells (R = 0.268, P < 0.001) and Th2 cells (R = 0.295, P < 0.001), and negatively correlated with plasmacytoid dendritic cells (R=-0.291, P < 0.001) and cytotoxic cells (R=-0.284, P < 0.001). CONCLUSIONS: DPM1 serves as a promising prognostic biomarker in HCC, with its expression correlating with unfavorable clinical outcomes and immune landscape alterations. Future studies should further validate DPM1's impact on ferroptosis and immune evasion in HCC, and explore its potential as a therapeutic target.
DPM1↗
Reduced FOXP3 expression and its association with genetic ancestry in neuromyelitis Optica spectrum disorder: a Colombian cohort.
BACKGROUND: Autoimmune disorders are characterized by impaired immune tolerance, largely mediated by CD4⁺ regulatory T cells (Tregs), whose function depends on the transcription factor FOXP3. OBJECTIVES: To compare FOXP3 expression levels between patients with neuromyelitis optica spectrum disorder (NMOSD) and healthy controls from Bogotá, Colombia, and to explore their association with genetic ancestry. METHODS: FOXP3 expression was quantified from peripheral blood mononuclear cells using RNA-based analysis. Genomic ancestry proportions were estimated using ancestry-informative markers. RESULTS: FOXP3 mRNA expression was significantly reduced in NMOSD patients compared with controls (∼2.4-fold decrease in median expression; p = 0.027). Lower FOXP3 mRNA expression was associated with optic neuritis (p = 0.0059), but not with historical or current AQP4-IgG seropositivity. In a sensitivity analysis restricted to patients with documented historical AQP4-IgG seropositivity, the direction of reduced FOXP3 mRNA expression was preserved but did not reach statistical significance. In pre-specified exploratory ancestry-related analyses, African (p = 0.035) and Amerindian ancestry (p = 0.012) were associated with FOXP3 mRNA expression levels. CONCLUSIONS: Reduced FOXP3 mRNA expression in Peripheral Blood Mononuclear Cells (PBMCs) suggests an altered immune regulatory profile in NMOSD, potentially involving mechanisms beyond antibody-mediated immunity. The association between genetic ancestry and FOXP3 mRNA expression suggests that population-specific genetic background may influence immune regulatory pathways. These findings should be interpreted as exploratory and require validation in larger, clinically homogeneous cohorts.
Adolescent↗
Antibody response and antigen-specific gamma-interferon profiles of vaccinated and unvaccinated pregnant sheep experimentally infected with Brucella melitensis.
It is well known that the immune response in sheep against Brucella melitensis is subject to individual variation, depending on diverse factors. It bears asking whether these factors (e.g. clinical disease, active infection, state of previous immunity), when affecting a group, can cause variation in the performance of different diagnostic tests. To clarify some of the circumstances in which this immune response can vary, we examine the immune-response profile of sheep protected against the clinical disease by prior vaccination with strain Rev. 1 in comparison with the profile of unprotected females showing the classical brucellosis symptoms. An experimental infection was provoked at midpregnancy under controlled conditions of both non-vaccinated (n=7) and previously Rev.1-vaccinated ewes (n=5). Their immune response was monitored from 7 to 9 weeks before abortion or normal birth to 30 weeks afterwards. Antibody response was assessed by classical tests (Rose Bengal test, complement fixation test (CFT)) in comparison with other diagnostic tests (indirect ELISA (iELISA), competitive ELISA (cELISA), fluorescence polarization assay (FPA), immunocapture test (ICT)). In addition, the cell-mediated immune response was indirectly evaluated by the in vitro antigen-specific release of gamma-interferon. The antibody levels and antigen-specific gamma-IFN profile of the non-vaccinated ewes having the disease and excreting the pathogen was notably high and differed significantly (P<0.05 or P<0.01) from those of vaccinated ewes that neither contracted brucellosis nor excreted the pathogen. In general, all the tests detect the infection in the non-vaccinated ewes with substantial effectiveness. It can be concluded that the high levels of circulating antibodies and of antigen-specific gamma-IFN are related to active Brucella infection. Similarly, the state of protection against the disease, but not necessarily against infection, due to a previous immunization with the Rev. 1 vaccination, appears to be responsible for a low level of detectable immune response. Nevertheless, the design of the study limits conclusions to pregnant ewes and cannot be extrapolated to non-pregnant ewes or rams. Likewise, the study provides no information on animals which are carriers of B. melitensis.
Animals↗
Comparison of two different nutritive conditions against the changes in peripheral blood mononuclear cells of periparturient dairy cows.
To clarify the relationship between cellular immune status and nutritive condition in periparturient dairy cows, feeding content, blood profiles, and immune condition were observed in cows from two dairy herds with different types of feed content. Immunological analyses such as leukocyte population and peripheral blood mononuclear cell (PBMC) mRNA of IFN-gamma, TNF-alpha, IL-4, and IL-10, quantified by real-time RT-PCR were performed. With regard to feed content during dry periods, there were six cows in the herd with insufficient non-structural carbohydrate (NFC) intake (group I) and six cows in the herd with sufficient NFC intake (group II). Significantly lower levels of blood glucose were observed in group I between weeks -12 and 16 compared with group II. Serum cholesterol level was significantly lower in group I between weeks 2 and 10 than in group II. The numbers of CD3+ and CD4+ T cells in group I were significantly lower than those in group II in weeks 6 and 14. The numbers of CD21+ B cells were significantly lower in group I than in group II in weeks -16, -12, 2, and 10. On the other hand, the CD4+/CD8+ ratio in group II was significantly higher than group I between weeks 2 and 14. The IFNgamma/IL-4 mRNA rate in group I was significantly lower than group II in week 6. We concluded that cellular immune depression occurrs after calving in dairy cows with low nutritional status in the periparturient period.
Animal Feed↗
Protection against respiratory syncytial virus infection by DNA immunization.
Respiratory syncytial virus (RSV) remains a major cause of morbidity and mortality in infants and the elderly and is a continuing challenge for vaccine development. A murine T helper cell (Th) type 2 response associates with enhanced lung pathology, which has been observed in past infant trials using formalin-inactivated RSV vaccine. In this study, we have engineered an optimized plasmid DNA vector expressing the RSV fusion (F) protein (DNA-F). DNA-F was as effective as live RSV in mice at inducing neutralizing antibody and cytotoxic T lymphocyte responses, protection against infection, and high mRNA expression of lung interferon gamma after viral challenge. Furthermore, a DNA-F boost could switch a preestablished anti-RSV Th2 response towards a Th1 response. Critical elements for the optimization of the plasmid constructs included expression of a secretory form of the F protein and the presence of the rabbit beta-globin intron II sequence upstream of the F-encoding sequence. In addition, anti-F systemic immune response profile could be modulated by the route of DNA-F delivery: intramuscular immunization resulted in balanced responses, whereas intradermal immunization resulted in a Th2 type of response. Thus, DNA-F immunization may provide a novel and promising RSV vaccination strategy.
Animals↗
Consensual immunity: success-driven development of T-helper-1 and T-helper-2 responses.
Non-germline-encoded T- and B-cell receptors allow humans to effectively deal with rapidly mutating pathogens. Here, we argue that, in addition to determining the antigenic specificity of immune responses, the same receptor systems can also regulate the T-helper-1/T-helper-2 profile of immunity. Such a mechanism--based on feedback from distinct effector cells to dendritic cells, rather than on instruction from pathogens--uses the effectiveness of particular effector cells at targeting and destroying a pathogen as a reliable, experience-based criterion to induce and maintain the appropriately polarized response.
B-Lymphocytes↗
Isotypic analysis of grass pollen-specific immunoglobulins in human plasma. 1. Specialization of certain classes and subclasses in the immune response.
The specificity and isotypic profile of humoral immune responses to Dactylis glomerata (Cocksfoot) pollen was studied by isoelectric focusing (IEF)-immunoprint analysis using 26 human plasma samples with high levels of Dactylis pollen-specific IgG4 (IgG4+ plasma) and 25 human plasma samples with low levels of specific IgG4 (normal plasma). Over 60 individual protein components in an aqueous pollen extract were separated by IEF and immunoprinted onto nitrocellose (NC). Following plasma incubation, bound IgE, IgG1-4, IgA1, IgA2 and IgM antibodies were detected on separate immunoprints with isotype-specific antibodies. Binding patterns of IgG4 and the majority of IgG1 and IgA2 antibodies in the IgG4+ plasma group very closely paralleled the binding patterns produced by the IgE antibodies from the same plasma and are described as the 'allergen repertoire'. In contrast, IgE, IgG4, IgG1 and IgA2 antibody reactivities to the 'allergen repertoire' were insignificant in the normal plasma group. These results suggest a qualitative, as well as a quantitative relationship between the immune responses which involve these 4 isotypes. Characteristic IgG2 and IgM antibody binding patterns, predominantly to non-allergenic antigens, were shared by the plasma from both groups, while IgG3 and IgA1 antibody binding patterns were highly variable from one plasma to another in both groups. One possible origin of the allergic diseases at the immunoglobulin heavy chain gene level is discussed.
Antibody Formation↗
Relationship of hypergammaglobulinemia, circulating immune complexes, and histocompatibility antigen profiles in patients with cystic fibrosis.
Among patients with cystic fibrosis (CF), those in the subset who develop hypergammaglobulinemia and circulating immune complexes often have relatively severe disease and a decreased likelihood of survival. Because Fc receptors have an important role in the removal of immune complexes and because defective Fc receptor function has been associated with inheritance of the histocompatibility antigens HLA DR2 and HLA DR3, we postulated that HLA DR2 and/or HLA DR3 might be genetic markers for this subset of patients with CF. However, in a group of 20 carefully documented patients with CF, we found no association of HLA DR2 or HLA DR3 with serum immunoglobulin, immune complex levels, or evidence of rapidly progressive disease.
Adolescent↗
Complement profiles in monkeys subjected to aggregate (immune complex) anaphylaxis, and following injection of soluble and particulate polysaccharides.
Complement profiles were established in four groups of Macaca irus monkeys: (I) Aggregate (immune complex) anaphylaxis was induced following immunization, with ovalbumin. Upon challenge, systemic arterial pressure decreased from 115 to 50 mm Hg (mean values) in 10 min. The complement profiles revealed decreases in: C1q to less than 10% of initial value within 5 min; C4 proportional to hypotension; C3 slowly to 60% at 24 h; C5, C6, C7, C8 and factor B to about 80% of initial value in 5--30 min. Conversion products of C3 and factor B were detected on the day of anaphylaxis. In conclusion, mainly the classical and to a lesser extent the alternative pathway, were activated. Following injection of (II) native B 512 dextran, (III) biodegradable starch microspheres, and (IV) saline, no significant changes of complement profiles were seen. Conversion products of C3 and factor B were, however, demonstrable in groups II and III without appearance of clinical signs.
Anaphylaxis↗
Protective immunity induced by the full-length cDNA encoding paramyosin of Chinese Schistosoma japonicum.
The full-length cDNA encoding paramyosin of Chinese S. japonicum (Sjc97) has been cloned and sequenced for the first time. The homology of the nucleotide sequence of paramyosin and the deduced amino acid sequence between Chinese, Philippine, Japanese strains and S. mansoni (Sm97) were 99.7, 99.8 and 96% at amino acid level, respectively; 99.4, 99.2 and 91% at nucleotide level, respectively. The immunogenicity and protective efficacy of a DNA vaccine encoding Sjc97 was evaluated in C57BL/6 mice. Mice immunized intramuscularly with pCMV-Sjc97 resulted in predominantly IgG2a and IgG2b immune responses, and immune sera were able to mediate antibody-dependent macrophage mediated cytotoxicity in vitro. Cytokine profiles in immunized C57BL/6 mice demonstrated Th1 bias, with IFN-gamma and IL-2 production and lack of IL-4 and IL-5. Immunization with pCMV-Sjc97 conferred a significant level of protection against cercariae in C57BL/6 mice. These results demonstrate that the nucleic acid encoding Sjc97 was able to induce a Th1 type immune response and confer protective efficacy in C57BL/6 mice when administrated via the intramuscular route.
Animals↗
Immune responsiveness and lymphokine production in patients with tuberculosis and healthy controls.
The aim of the present study was to determine the profile of immune responsiveness that differentiates patients with tuberculosis (TB) from healthy tuberculin-positive controls. Forty-five patients with pulmonary TB and 16 healthy tuberculin-positive controls, all human immunodeficiency virus negative, were studied. Patients had decreased reactivity to tuberculin, diminished proliferative response to purified protein derivative (PPD), lower concentrations of interleukin-2 (IL-2) and gamma interferon in PPD-stimulated cultures, no increase in the percentage of gamma/delta cells in PPD-stimulated cultures, and higher immunoglobulin G antimycobacterial antibodies compared with control subjects. Furthermore, controls exhibited decreased production of IL-4 by PPD-stimulated cells. Multivariate discriminant and factor analyses demonstrated divergent patterns of immune reactivity against mycobacterial antigens. The association of IL-4 and immunoglobulin G antibody levels in patients, in contrast to the high reactivity to tuberculin, increased proliferation to PPD, and higher levels of IL-2 and gamma interferon observed in healthy controls suggested that most TB patients exhibit a TH2 pattern of immune responsiveness while tuberculin-positive healthy individuals have a TH1 pattern.
Adolescent↗
Transforming growth factor-beta and p-21: multiple molecular targets of decorin-mediated suppression of neoplastic growth.
Decorin is a member of the small leucine-rich proteoglycan (SLRP) gene family that has recently become a focus in various areas of cancer research. The decorin protein consists of a core protein and a covalently linked glycosaminoglycan chain. Decorin binds to collagens type I, II and IV in vivo and promotes the formation of fibers with increased stability and changes in solubility. Further, the decorin core protein binds to growth factors, including transforming growth factor-beta (TGF-beta), to other intercellular matrix molecules such as fibronectin and thrombospondin, and to the decorin endocytosis receptor. Decorin may directly interfere with the cell cycle via the induction of p21WAF1/CIP1 (p21), a potent inhibitor of cyclin-dependent kinases (CDKs). Here, we discuss interactions of decorin with TGF-beta and with p21, both of which are relevant to carcinogenesis and tumor progression. TGF-beta is released by tumors of various histogenetic origins and promotes immunosuppression in the host and tumor immune escape by induction of growth arrest and apoptosis in immune cells, by downregulation of MHC II antigen expression and by changes in the cytokine release profiles of immune and tumor cells. Moreover, TGF-beta may modulate tumor growth in an autocrine and paracrine fashion, may mediate drug resistance, and may facilitate tumor angiogenesis. Decorin binds to TGF-beta, thus inhibiting its bioactivity, and is a direct or indirect negative modulator of TGF-beta synthesis. Ectopic expression of decorin results in the regression of rat C6 gliomas, an antineoplastic effect attributed to the reversal of TGF-beta-induced immunosuppression. On the other hand, de novo expression of decorin in colon cancer cells and some other tumor cells, even though not in glioma cells, results in an upregulation of p21 expression and a cell cycle arrest, presumably in a TGF-beta-independent manner. Decorin expression is downregulated in many tumors but upregulated in the peritumoral stroma. By virtue of its growth regulatory and immunomodulatory properties, decorin promises to become a novel target for the experimental therapy of human cancers.
Animals↗