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Background: To investigate the use of uniportal video-assisted thoracoscopic surgery (U-VATS) in the treatment of non-small cell lung cancer (NSCLC). Materials and Methods: A total of 82 patients with early NSCLC in our hospital from May 2019 to January 2021 were enrolled to this study. Forty-one patients treated with spontaneous breathing U-VATS were the research group (RG), and 41 with conventional thoracoscopy were the control group (CG). Fasting peripheral blood was drawn from patients before (T0), one (T1) and three days after surgery (T2), respectively. White blood cells (WBC), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), matrix metalloproteinase-9 (MMP-9) and T-lymphocyte subsets were measured in the blood. In addition, we counted the conversion rate to open chest and tracheal intubation in the RG, and compared the operation time, intraoperative bleeding, chest drainage, chest tube retention time, antibiotic application time, postoperative hospital stays and complications between groups. Finally, a 1-year prognostic follow-up was performed to record overall survival, chemotherapy rate, and recurrent metastasis rate. Results: At T1, WBC, IL-6, TNF-α, and MMP-9 were lower in the RG than in the CG, while immune function was better in the RG at T1 and T2 (P<0.05). Complication rates were lower in the RG than in the CG when compared (P>0.05). The prognosis of 1-year overall survival, chemotherapy rate, and recurrence rate were not different between the two groups (P>0.05). Conclusion: Spontaneous breathing U-VATS can effectively reduce the inflammation and enhance the stability of immune function in NSCLC patients undergoing surgery. [ABSTRACT FROM AUTHOR]

Macrophages perform critical functions for homeostasis and immune defense in tissues throughout the body. These innate immune cells are capable of recognizing and clearing dead cells and pathogens, and orchestrating inflammatory and healing processes that occur in response to injury. In addition, macrophages are involved in the progression of many inflammatory diseases including cardiovascular disease, fibrosis, and cancer. Although it has long been known that macrophages respond dynamically to biochemical signals in their microenvironment, the role of biophysical cues has only recently emerged. Furthermore, many diseases that involve macrophages are also characterized by changes to the tissue biophysical environment. This review will discuss current knowledge about the effects of biophysical cues including matrix stiffness, material topography, and applied mechanical forces, on macrophage behavior. We will also describe the role of molecules that are known to be important for mechanotransduction, including adhesion molecules, ion channels, as well as nuclear mediators such as transcription factors, scaffolding proteins, and epigenetic regulators. Together, this review will illustrate a developing role of biophysical cues in macrophage biology, and also speculate upon molecular targets that may potentially be exploited therapeutically to treat disease.

There are indications for immune dysregulation in PTEN Hamartoma Tumour Syndrome (PHTS), however information on the clinical immune phenotype is lacking. We aimed to assess the frequency of infections and autoimmune disease in PHTS patients. A retrospective cohort study including 81 paediatric and 109 adult PHTS patients and 73 female adult controls and self-reported data from yearly surveillance visits. Differences between adult patients and controls were assessed with odds ratios (OR). Of paediatric patients, 1% reported fungal infections, 23% tonsillectomy/adenoidectomy, 36% bacterial infections requiring antibiotics, and 2% autoimmune disease. Of adult patients, up to 67% repeatedly reported fungal infections, and 73% was ever affected which was similar to controls. Compared to controls, adult patients more often reported (signs of) viral infections: tonsillectomy/adenoidectomy (78%; OR = 7.4 (95%CI: 3.7–15.8)), frequent infections during childhood (43%; OR = 2.5 (95%CI: 1.3–5.2)), and flu or cold infections more often than others (49%; OR = 3.9 (95%CI: 2.0–8.0)). Autoimmune disease was also more frequent (24%, OR = 2.7 (95%CI: 1.1–7.3)) in adult patients, and antibiotics use (38%, OR = 4.7 (95%CI: 1.3–23.0)) in female adult patients. PHTS patients experience a broad clinical phenotype of immune dysregulation. At adult age, this consists of more often viral and bacterial infections and autoimmune disease, and repetitive fungal infections. [ABSTRACT FROM AUTHOR]

Many immune receptors transduce activation across the plasma membrane through their clustering. With Fcγ receptors (FcγRs), this clustering is driven by binding to antibodies of differing affinities that are in turn bound to multivalent antigen. As a consequence of this activation mechanism, accounting for and rationally manipulating immunoglobulin (Ig)G effector function is complicated by, among other factors, differing affinities between FcγR species and changes in the valency of antigen binding. In this study, we show that a model of multivalent receptor-ligand binding can effectively account for the contribution of IgG-FcγR affinity and immune complex valency. This model in turn enables us to make specific predictions about the effect of immune complexes of defined composition. In total, these results enable both rational immune complex design for a desired IgG effector function and the deconvolution of effector function by immune complexes.

Indoleamine 2,3 - dioxygenase ( IDO ) is an important immunoregulatory enzyme, which can degrade the level of the mammalian essential amino acid tryptophan ( TRP), catalyze the initiation and rate - limiting steps through the kynurenine pathway, and produce a variety of metabolites to participate in the immune response. On the one hand, IDO plays an immunosuppressive role in microenvironment and thus leads to infection and immune escape of tumor cells; on the other hand, IDO also exerts an inhibitory effect on the pathogens such as bacteria and parasites and thus protects the body from the harm of pathogens to a certain extent. Therefore, IDO is considered an important medium with the role of a double - edged sword in the development and progression of various liver diseases. This article reviews the latest research advances in IDO in viral hepatitis, liver fibrosis, liver cirrhosis, liver cancer, and hepatic echinococcosis. [ABSTRACT FROM AUTHOR]

The immune system consists of many specialized cell populations that communicate with each other to achieve systemic immune responses. Our analyses of various measured immune cell population frequencies in healthy humans and their responses to diverse stimuli show that human immune variation is continuous in nature, rather than characterized by discrete groups of similar individuals. We show that the same three key combinations of immune cell population frequencies can define an individual's immunotype and predict a diverse set of functional responses to cytokine stimulation. We find that, even though interindividual variations in specific cell population frequencies can be large, unrelated individuals of younger age have more homogeneous immunotypes than older individuals. Across age groups, cytomegalovirus seropositive individuals displayed immunotypes characteristic of older individuals. The conceptual framework for defining immunotypes suggested by our results could guide the development of better therapies that appropriately modulate collective immunotypes, rather than individual immune components.

The last common metazoan ancestor (LCMA) emerged over half a billion years ago. These complex metazoans provided newly available niche space for viruses and microbes. Modern day contemporaries, such as cnidarians, suggest that the LCMA consisted of two cell layers: a basal endoderm and a mucus-secreting ectoderm, which formed a surface mucus layer (SML). Here we propose a model for the origin of metazoan immunity based on external and internal microbial selection mechanisms. In this model, the SML concentrated bacteria and their associated viruses (phage) through physical dynamics (that is, the slower flow fields near a diffusive boundary layer), which selected for mucin-binding capabilities. The concentration of phage within the SML provided the LCMA with an external microbial selective described by the bacteriophage adherence to mucus (BAM) model. In the BAM model, phage adhere to mucus protecting the metazoan host against invading, potentially pathogenic bacteria. The same fluid dynamics that concentrated phage and bacteria in the SML also concentrated eukaryotic viruses. As eukaryotic viruses competed for host intracellular niche space, those viruses that provided the LCMA with immune protection were maintained. If a resident virus became pathogenic or if a non-beneficial infection occurred, we propose that tumor necrosis factor (TNF)-mediated programmed cell death, as well as other apoptosis mechanisms, were utilized to remove virally infected cells. The ubiquity of the mucosal environment across metazoan phyla suggest that both BAM and TNF-induced apoptosis emerged during the Precambrian era and continue to drive the evolution of metazoan immunity.

Objectives: To identify challenges in the vaccination of the elderly due to the influences of fake s news and common sense, in the light of systemic theory. Methods: This is a reflective study conceptualized in the systemic theory, neuro-endocrine immunological axis, on the challenges of vaccination of the elderly today. Results: The systemic theory emphasizes the need to stimulate the immune system of the elderly through vaccination, preventing diseases, but there is a resistance of this population to adhere to vaccination, due to fear, distrust and doubt, these uncertainties are due to the dissemination of fake news and the culture of common sense. Conclusion: The influences of fictitious information, fake news and common sense, generate challenges in immunization and reduce the adherence of the elderly, thus, health professionals are responsible for designing interventions for adherence to vaccination, demystifying wrong information.

Purpose of reviewThe purpose is to review recent insights into the impact of HIV-associated immune activation on AIDS and non-AIDS morbidity and mortality.Recent findingsImmune activation has long been recognized as an important consequence of untreated HIV infection and predictor of AIDS progression, which declines but fails to normalize during suppressive antiretroviral therapy, and continues to predict disease in this setting. Thus, a major research agenda is to develop novel therapies to reduce persistent immune activation in treated HIV infection. Yet, the optimal targets for interventions remain unclear. Both the specific root causes of immune activation and the many interconnected pathways of immune activation that are most likely to drive disease risk in HIV-infected individuals remain incompletely characterized, but recent studies have shed new light on these topics.SummaryIn the context of this review, we will summarize recent evidence helping to elucidate the immunologic pathways that appear most strongly predictive of infectious and noninfectious morbidity. We will also highlight the likelihood that not all root drivers of immune activation - and the discrete immunologic pathways to which they give rise - are likely to produce the same disease manifestations and/or be equally attenuated by early antiretroviral therapy initiation.

Traditionally, cell analysis has focused on using molecular biomarkers for basic research, cell preparation, and clinical diagnostics; however, new microtechnologies are enabling evaluation of the mechanical properties of cells at throughputs that make them amenable to widespread use. We review the current understanding of how the mechanical characteristics of cells relate to underlying molecular and architectural changes, describe how these changes evolve with cell-state and disease processes, and propose promising biomedical applications that will be facilitated by the increased throughput of mechanical testing: from diagnosing cancer and monitoring immune states to preparing cells for regenerative medicine. We provide background about techniques that laid the groundwork for the quantitative understanding of cell mechanics and discuss current efforts to develop robust techniques for rapid analysis that aim to implement mechanophenotyping as a routine tool in biomedicine. Looking forward, we describe additional milestones that will facilitate broad adoption, as well as new directions not only in mechanically assessing cells but also in perturbing them to passively engineer cell state.

Dendrobium huoshanense is a valuable and versatile Chinese herbal medicine with the anecdotal claims of cancer prevention and anti-inflammation. However, its immunological activities are limited to in vitro studies on a few cytokines and immune cell functions. First, we investigated the effects of polysaccharides isolated from DH (DH-PS) on inducing a panel of cytokines/chemokines in mice in vivo and human in vitro. We found that DH polysaccharides (DH-PS) induced TH1, TH2, inflammatory cytokines and chemokines in mouse in vivo and human cells in vitro. Secondly, we demonstrated that DH-PS expanded mouse splenocytes in vivo including CD4(+) T cells, CD8(+) T cells, B cells, NK cells, NKT cells, monocytes/macrophages, granulocytes and regulatory T cells. Notably, DH-PS induced an anti-inflammatory molecule, IL-1ra, in mouse and human immune cells, especially monocytes. The serum level of IL-1ra elicited by the injection of DH-PS was over 10 folds of IL-1β, suggesting that DH-PS-induced anti-inflammatory activities might over-ride the inflammatory ones mediated by IL-1β. The signaling pathways of DH-PS-induced IL-1ra production was shown to involve ERK/ELK, p38 MAPK, PI3K and NFκB. Finally, we observed that IL-1ra level induced by DH-PS was significantly higher than that by F3, a polysaccharide extract isolated from another popular Chinese herbal medicine, Ganoderma lucidum. These results indicated that DH-PS might have potential applications for ameliorating IL-1-induced pathogenic conditions.

Copyright of Revista Enfermagem Digital Cuidado e Promoção da Saúde is the property of Revista Enfermagem Digital Cuidado e Promocao da Saude and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Substantial material, financial and human resources are dedicated to research on tumor biology. The validation of biomarkers, the development of novel diagnostic and therapeutic methods, the implementation of early detection programs in communities, and the promotion of healthy lifestyles have positively impacted on the prevention and control of this group of diseases. However, cancer remains a global health problem, due to the complex relationship between the host immune system and the cancer cells. It is a fact that the immune system´s effector mechanisms enable the detection and elimination of cancer cells. However, these immune mechanisms also promote the somatic evolution of tumors by selecting cellular clones resistant to immunity. This complex relationship conceptualized as cancer immunoediting develops mainly at the tumor microenvironment. Immunotherapy approaches are designed to reinforce antitumor immunity, while blocking immune escape mechanisms. This review starts a series of three articles that are going to review the molecular and cellular bases of the antitumor immune response, present the bases of tumor biology and, finally, address the implications of the complex relationship between the immune system and neoplasias for cancer immunotherapy.

The primary objective of the study was to evaluate the effects of a hydrolyzed polysaccharide, rice bran arabinoxylan compound (RBAC), on immune, hepatic, and renal function in HIV + individuals. A 6-month randomized double-blind placebo-controlled trial was utilized to conduct the intervention. Forty-seven HIV + individuals on stable antiretroviral therapy were enrolled and randomly assigned to one of the 2 study conditions (n = 22 RBAC and n = 25 placebo) and consumed 3 gram/day of either compound for 6 months. Participants were assessed at baseline and 3 and 6 months follow-up for CD4+ and CD8+, liver enzymes, and kidney function. No side effects were reported, and liver and kidney markers remained nearly completely within normal limits. The percentage change in CD4+ was similar for the placebo (+2.2%) and RBAC (+3.1%) groups at 6 months follow-up. The percentage change in CD8+ count significantly decreased from baseline to 6 months in the RBAC group (−5.2%), whereas it increased in the placebo group (+57.8%; p = 0.04). The CD4+/CD8+ ratio improved clinically in the RBAC group from 0.95 (SD = 0.62) at baseline to 1.07 (SD = 0.11) at 6 months, whereas it declined in the placebo group from 0.96 (SD = 0.80) at baseline to 0.72 (SD = 0.59) at 6 months. Our results showed a statistically significant decrease in CD8+ count and a clinically significant increase in CD4+/CD8+ ratio for the RBAC group compared to the placebo group. Thus, the results of this study suggest that the immunomodulatory and antisenescent activities of RBAC are promising for the HIV population. [ABSTRACT FROM AUTHOR]

Background: We evaluated the sequential changes of interleukin (IL)-10 and IL-13 serum levels with tuberculosis (TB)-related radiographic changes during pulmonary TB (PTB) treatment. Materials and Methods: In this cross-sectional study during two consecutive years, forty cases with PTB were recorded, and finally, 24 cases were completed the study. Serum levels of IL-10 and IL-13 were measured on admission time, and 6 months later. Furthermore, chest radiography was performed on admission and 6 months later in the treatment course. Results: Radiography at the baseline indicated pulmonary infiltration in all patients (n = 24). Fifteen (62.5%) cases had abnormal and 9 (37.5%) cases had normal radiography at the end of 6 months treatment course. IL-10 and IL-13 upregulated during the treatment time course, and their relationship with radiographic changes shifted from negative (r = -0.14 and P = 0.71) on admission to positive (r = 0.80 and P < 0.001) at the end of 6 months treatment course in normal radiography group. IL-10 level at the start of the treatment was 121.90 ± 88.81 in patients with normal and 82.68 ± 41.50 in patients with abnormal radiography (P = 0.31). Conclusion: Sequential increase in IL-10 and IL-13 during PTB treatment course may have a role in clearing the TB-related radiographic infiltration and preventing scar formation. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Liver macrophages are in a dynamic equilibrium of immune tolerance and immune response after continuous antigen stimulation. The immune response of liver macrophages to external antigen is closely associated with the immune homeostasis of the liver. This article reviews the association between the programmed necrosis pathway and the apoptotic pathway and elaborates on the important role of the activity of IKK complex in the interactive regulation of the programmed necrosis and apoptotic pathways. Further studies are needed to clarify the role of programmed necrosis in the response of liver macrophages to extrahepatic antigens. [ABSTRACT FROM AUTHOR]

Copyright of HNO is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study investigated the role of childhood parental deprivation in the association between quality of life (QOL) and the Epstein–Barr virus (EBV) antibody titer, a marker of cellular immune functioning, using data from 734 adults living in seven communities in rural Fujian, China. Parental deprivation was defined if either of their parents had died, divorced, or left them for migratory work for more than 1 year before they turned (a) 16 years of age (childhood and adolescence), or (b) 3 years of age (early childhood). A mixed‐effects regression analysis with a random effects model revealed that parental deprivation during early childhood was positively associated with the EBV antibody titer (coefficient = 0.33, p = 0.007), whereas parental deprivation during the first 16 years was not. Further analysis incorporating an interaction term between QOL and parental deprivation revealed a significant interaction between QOL and parental deprivation during early childhood; a significant association between QOL and the EBV antibody titer was found only among those who reported parental deprivation during early childhood. This study suggests that parental deprivation during the period of immune system development may be linked with physiological responses to stressors later in life. [ABSTRACT FROM AUTHOR]

IntroductionSeveral gene expression signatures have been proposed and demonstrated to be predictive of outcome in breast cancer. In the present article we address the following issues: Do these signatures perform similarly? Are there (common) molecular processes reported by these signatures? Can better prognostic predictors be constructed based on these identified molecular processes?MethodsWe performed a comprehensive analysis of the performance of nine gene expression signatures on seven different breast cancer datasets. To better characterize the functional processes associated with these signatures, we enlarged each signature by including all probes with a significant correlation to at least one of the genes in the original signature. The enrichment of functional groups was assessed using four ontology databases.ResultsThe classification performance of the nine gene expression signatures is very similar in terms of assigning a sample to either a poor outcome group or a good outcome group. Nevertheless the concordance in classification at the sample level is low, with only 50% of the breast cancer samples classified in the same outcome group by all classifiers. The predictive accuracy decreases with the number of poor outcome assignments given to a sample. The best classification performance was obtained for the group of patients with only good outcome assignments. Enrichment analysis of the enlarged signatures revealed 11 functional modules with prognostic ability. The combination of the RNA-splicing and immune modules resulted in a classifier with high prognostic performance on an independent validation set.ConclusionsThe study revealed that the nine signatures perform similarly but exhibit a large degree of discordance in prognostic group assignment. Functional analyses indicate that proliferation is a common cellular process, but that other functional categories are also enriched and show independent prognostic ability. We provide new evidence of the potentially promising prognostic impact of immunity and RNA-splicing processes in breast cancer.

One of the leading causes of infectious diarrhea in newborn calves is the apicomplexan protozoan Cryptosporidium parvum ( C. parvum ). However, little is known about its immunopathogenesis. Using next generation sequencing, this study investigated the immune transcriptional response to C. parvum infection in neonatal calves. Neonatal male Holstein-Friesian calves were either orally infected (N = 5) or not (CTRL group, N = 5) with C. parvum oocysts (gp60 subtype IIaA15G2R1) at day 1 of life and slaughtered on day 7 after infection. Total RNA was extracted from the jejunal mucosa for short read. Differentially expressed genes (DEGs) between infected and CTRL groups were assessed using DESeq2 at a false discovery rate < 0.05. Infection did not affect plasma immunohematological parameters, including neutrophil, lymphocyte, monocyte, leucocyte, thrombocyte, and erythrocyte counts as well as hematocrit and hemoglobin concentration on day 7 post infection. The immune-related DEGs were selected according to the UniProt immune system process database and were used for gene ontology (GO) and pathway enrichment analysis using Cytoscape (v3.9.1). Based on GO analysis, DEGs annotated to mucosal immunity, recognizing and presenting antigens, chemotaxis of neutrophils, eosinophils, natural killer cells, B and T cells mediated by signaling pathways including toll like receptors, interleukins, tumor necrosis factor, T cell receptor, and NF-KB were upregulated, while markers of macrophages chemotaxis and cytosolic pattern recognition were downregulated. This study provides a holistic snapshot of immune-related pathways induced by C. parvum in calves, including novel and detailed feedback and feedforward regulatory mechanisms establishing the crosstalk between innate and adaptive immune response in neonate calves, which could be utilized further to develop new therapeutic strategies., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Veshkini, Dengler, Bachmann, Liermann, Helm, Ulrich, Delling, Kühn and Hammon.)

Ovarian follicular development is a critical determinant of reproductive performance in litter bearing species like pigs, wherein economic gains depend on litter size. The study aimed to gain insight into the differentially expressed genes (DEGs) and signalling pathways regulating follicular growth and maturation in Ghoongroo pigs. Transcriptome profiling of porcine small follicles (SF) and large follicles (LF) was conducted using NovaSeq600 sequencing platform and DEGs were identified using DESeq2 with threshold of Padj. < 0.05 and log 2 fold change cut off 0.58 (LF vs. SF). Functional annotations and bioinformatics analysis of DEGs were performed to find out biological functions, signalling pathways and hub genes regulating follicular dynamics. Transcriptome analysis revealed 709 and 479 genes unique to SF and LF stages, respectively, and 11,993 co-expressed genes in both the groups. In total, 507 DEGs (284 upregulated and 223 downregulated) were identified, which encoded for diverse proteins including transcription factors (TFs). These DEGs were functionally linked to response to stimulus, lipid metabolic process, developmental process, extracellular matrix organisation along with the immune system process, indicating wide-ranging mechanisms associated with follicular transition. The enriched KEGG pathways in LF stage consisted of ovarian steroidogenesis, cholesterol and retinol metabolism, cell adhesion molecules, cytokine receptor interaction and immune signalling pathways, depicting intra-follicular control of varied ovarian function. The hub gene analysis revealed APOE, SCARB1, MMP9, CYP17A1, TYROBP as key regulators of follicular development. This study identified candidate genes and TFs providing steroidogenic advantage to LFs which makes them fit for selection into the ovulatory pool of follicles., Competing Interests: Declaration of Competing Interest None., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: We evaluated the sequential changes of interleukin (IL)-10 and IL-13 serum levels with tuberculosis (TB)-related radiographic changes during pulmonary TB (PTB) treatment. Materials and Methods: In this cross-sectional study during two consecutive years, forty cases with PTB were recorded, and finally, 24 cases were completed the study. Serum levels of IL-10 and IL-13 were measured on admission time, and 6 months later. Furthermore, chest radiography was performed on admission and 6 months later in the treatment course. Results: Radiography at the baseline indicated pulmonary infiltration in all patients (n = 24). Fifteen (62.5%) cases had abnormal and 9 (37.5%) cases had normal radiography at the end of 6 months treatment course. IL-10 and IL-13 upregulated during the treatment time course, and their relationship with radiographic changes shifted from negative (r = −0.14 and P = 0.71) on admission to positive (r = 0.80 and P < 0.001) at the end of 6 months treatment course in normal radiography group. IL-10 level at the start of the treatment was 121.90 ± 88.81 in patients with normal and 82.68 ± 41.50 in patients with abnormal radiography (P = 0.31). Conclusion: Sequential increase in IL-10 and IL-13 during PTB treatment course may have a role in clearing the TB-related radiographic infiltration and preventing scar formation.

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Substantial material, financial and human resources are dedicated to research on tumor biology. The validation of biomarkers, the development of novel diagnostic and therapeutic methods, the implementation of early detection programs in communities, and the promotion of healthy lifestyles have positively impacted on the prevention and control of this group of diseases. However, cancer remains a global health problem, due to the complex relationship between the host immune system and the cancer cells. It is a fact that the immune system's effector mechanisms enable the detection and elimination of cancer cells. However, these immune mechanisms also promote the somatic evolution of tumors by selecting cellular clones resistant to immunity. This complex relationship conceptualized as cancer immunoediting develops mainly at the tumor microenvironment. Immunotherapy approaches are designed to reinforce antitumor immunity, while blocking immune escape mechanisms. This review starts a series of three articles that are going to review the molecular and cellular bases of the antitumor immune response, present the bases of tumor biology and, finally, address the implications of the complex relationship between the immune system and neoplasias for cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Clinical Healthcare is the property of Chinese Journal of Clinical Healthcare and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The Psychoneuroimmunoendocrinology studies the interaction between psychic processes and the Nervous, Endocrine and Immune systems and, in an integrative way, the health-disease process interrelationships. Several researches show the close relation between the somatic diseases emergence and development with certain psychological alterations, among them stress, anxiety and depression. This work is aimed at systematizing the theoretical elements which demonstrate the interrelation between the psyche, the Nervous System, Endocrine and Immune System in the health - illness process and to present the clinical evidences which support its validity. [ABSTRACT FROM AUTHOR]